A team of Michigan State University scientists - using a new cooling method they created - has uncovered the inner workings of a key iron-containing enzyme, a discovery that could help researchers develop new medicines or understand how enzymes repair DNA.
Taurine/alpha-ketoglutarate dioxygenase, known as TauD, is a bacterial enzyme that is important in metabolism. Enzymes in this family repair DNA, sense oxygen and help produce antibiotics.
Specifically, the MSU team was interested in how iron and oxygen atoms reacted together in the enzyme. Understanding how TauD works, which serves as a model for many other proteins, has implications in the scientific and medical fields, said Robert Hausinger, MSU professor of microbiology and molecular genetics.
"This is a broad enzyme family with similar mechanisms," he said. "Understanding how TauD works sheds light on how many other enzymes function from bacteria to humans. This can be applicable to a wide variety of essential enzymes of medical and agricultural interest."
For example, Hausinger said, understanding how the enzyme works can help scientists design inhibitors to prevent it from doing its job, which is a key step in preventing diseases. Also, understanding how the iron inserts oxygen atoms into other molecules provides insight into how enzymes metabolize the majority of medical drugs or environmental pollutants in the human body.
As understanding how enzymes work can be very complicated - such reactions often are complex, fast and require multiple steps - the MSU team developed a new method to follow the TauD reaction. The difficult part for researchers was to slow down the reaction enough that the individual steps can be observed; one way to slow down an enzymatic reaction is to cool it.
The team used a stream of cold nitrogen gas to slow down the reaction at -36 C (-33 F). To prevent freezing and to keep the reaction going, the scientists used ethylene glycol - the same antifreeze that goes in vehicles.
Once the reaction started, the team used lasers - in an advanced method called Raman spectroscopy - to follow the vibrations of iron and oxygen atoms in TauD to determine how the reaction progressed. They found never seen before steps in the TauD reaction, overturning conventional thought.
The project was a collaboration between the laboratories of Hausinger and Denis Proshlyakov of MSU's Department of Biochemistry and Molecular Biology, with support from MSU colleague Piotr Grzyska and Evan Appelman of the Argonne National Laboratory in Chicago.
The research, supported by the National Institutes of Health, was recently published in the Proceedings of National Academy of Science Early Edition.
Source:
Jason Cody
Michigan State University
понедельник, 20 июня 2011 г.
воскресенье, 19 июня 2011 г.
Light Shed On Modern Pandemic By Ancient Retrovirus
Human resistance to a retrovirus that infected chimpanzees and other nonhuman primates 4 million years ago ironically may be at least partially responsible for the susceptibility of humans to HIV infection today.
These findings, reported by a team of researchers at Fred Hutchinson Cancer Research Center in Science, provide a better understanding of this modern pandemic infection through the study of an ancient virus called Pan troglodytes endogenous retrovirus, or PtERV1.
"This ancient virus is a battle that humans have already won. Humans are not susceptible to it and have probably been resistant throughout millennia," said senior author Michael Emerman, Ph.D., a member of the Human Biology and Basic Sciences divisions at the Hutchinson Center. "However, we found that during primate evolution, this innate immunity to one virus may have made us more vulnerable to HIV."
Evidence of human immunity to this ancient retrovirus first emerged with the sequencing of the chimpanzee genome. "When the chimp genome was sequenced, a team of scientists at the University of Washington led by Evan Eichler found the largest difference overall between the chimp and human genomes was the presence or absence of PtERV1," Emerman said. "Chimps have 130 copies of PtERV1 and humans have none."
It is believed that retroviruses have been entering the genome for many millions of years, and so humans share many retroviral DNA fragments with their primate cousins. Such vestiges of primitive infection, rendered inactive by eons of genetic mutation, make up about 8 percent of the human genome.
Innate protection against PtERV1 in humans could be credited, the researchers believe, to the presence of an ancient, rapidly evolving antiviral defense gene called TRIM5a, which produces a protein that binds to and destroys the virus before it can replicate within the body.
"We know that PtERV1 infected chimps, gorillas and old-world monkeys 4 million years ago but left no traces of having infected humans. Our theory is that this is because humans had this innate viral defense system," Emerman said.
To test their hypothesis, Emerman and co-authors Harmit Singh Malik, Ph.D., an evolutionary biologist and an assistant member of the Center's Basic Sciences Division, and Shari Kaiser, a graduate student in Emerman's laboratory, used DNA sequences from the chimp genome to reconstruct a small part of the PtERV1 virus.
They reassembled about one-fifth of the virus by taking dozens of PtERV1 sequences and aligning them to create an "ancestral" sequence, teasing out areas of commonality between them. They then used this information to make a partial viral genome. During reconstruction the viral segment was debilitated, enabling only one round of infection in cells. Working with cells in the laboratory, the researchers found that the human antiviral protein TRIM5a effectively neutralizes this extinct retrovirus, which never successfully fixed into the human genome.
"However, while TRIM5a may have served humans well millions of years ago, the antiviral protein does not seem to be good at defending against any of the retroviruses that currently infect humans, such as HIV-1," Emerman said. "In the end, this drove human evolution to be more susceptible to HIV." For example, the researchers found that changes in TRIM5a that make it better at fighting HIV actually inhibit its ability to stop PtERV1 and vice versa, which indicates that this antiviral gene may only be good at fighting off one virus at a time.
Uncovering the story of TRIM5a's role in battling one ancient retrovirus while increasing human susceptibility to modern-day HIV "is a lot like doing archaeology -- figuring out how humans have become who we are today and why we are or are not susceptible to modern viruses that presently circulate," Emerman said.
In fact, this emerging area of research, which seeks to better understand modern infections by studying ancient viruses, is known as "paleovirology." "Ultimately," said co-author Malik, "if we want to understand why our defenses are the way they are, the answers inevitably lie in these ancient viruses more so than the ones that have affected us only recently, such as HIV."
This work was supported by National Institutes of Health grants to Emerman, a Searle Scholar Award to Malik and a National Science Foundation graduate fellowship to Kaiser.
At Fred Hutchinson Cancer Research Center, our interdisciplinary teams of world-renowned scientists and humanitarians work together to prevent, diagnose and treat cancer, HIV/AIDS and other diseases. Our researchers, including three Nobel laureates, bring a relentless pursuit and passion for health, knowledge and hope to their work and to the world. For more information, please visit ffhcrc/.
Contact: Kristen Woodward
Fred Hutchinson Cancer Research Center
These findings, reported by a team of researchers at Fred Hutchinson Cancer Research Center in Science, provide a better understanding of this modern pandemic infection through the study of an ancient virus called Pan troglodytes endogenous retrovirus, or PtERV1.
"This ancient virus is a battle that humans have already won. Humans are not susceptible to it and have probably been resistant throughout millennia," said senior author Michael Emerman, Ph.D., a member of the Human Biology and Basic Sciences divisions at the Hutchinson Center. "However, we found that during primate evolution, this innate immunity to one virus may have made us more vulnerable to HIV."
Evidence of human immunity to this ancient retrovirus first emerged with the sequencing of the chimpanzee genome. "When the chimp genome was sequenced, a team of scientists at the University of Washington led by Evan Eichler found the largest difference overall between the chimp and human genomes was the presence or absence of PtERV1," Emerman said. "Chimps have 130 copies of PtERV1 and humans have none."
It is believed that retroviruses have been entering the genome for many millions of years, and so humans share many retroviral DNA fragments with their primate cousins. Such vestiges of primitive infection, rendered inactive by eons of genetic mutation, make up about 8 percent of the human genome.
Innate protection against PtERV1 in humans could be credited, the researchers believe, to the presence of an ancient, rapidly evolving antiviral defense gene called TRIM5a, which produces a protein that binds to and destroys the virus before it can replicate within the body.
"We know that PtERV1 infected chimps, gorillas and old-world monkeys 4 million years ago but left no traces of having infected humans. Our theory is that this is because humans had this innate viral defense system," Emerman said.
To test their hypothesis, Emerman and co-authors Harmit Singh Malik, Ph.D., an evolutionary biologist and an assistant member of the Center's Basic Sciences Division, and Shari Kaiser, a graduate student in Emerman's laboratory, used DNA sequences from the chimp genome to reconstruct a small part of the PtERV1 virus.
They reassembled about one-fifth of the virus by taking dozens of PtERV1 sequences and aligning them to create an "ancestral" sequence, teasing out areas of commonality between them. They then used this information to make a partial viral genome. During reconstruction the viral segment was debilitated, enabling only one round of infection in cells. Working with cells in the laboratory, the researchers found that the human antiviral protein TRIM5a effectively neutralizes this extinct retrovirus, which never successfully fixed into the human genome.
"However, while TRIM5a may have served humans well millions of years ago, the antiviral protein does not seem to be good at defending against any of the retroviruses that currently infect humans, such as HIV-1," Emerman said. "In the end, this drove human evolution to be more susceptible to HIV." For example, the researchers found that changes in TRIM5a that make it better at fighting HIV actually inhibit its ability to stop PtERV1 and vice versa, which indicates that this antiviral gene may only be good at fighting off one virus at a time.
Uncovering the story of TRIM5a's role in battling one ancient retrovirus while increasing human susceptibility to modern-day HIV "is a lot like doing archaeology -- figuring out how humans have become who we are today and why we are or are not susceptible to modern viruses that presently circulate," Emerman said.
In fact, this emerging area of research, which seeks to better understand modern infections by studying ancient viruses, is known as "paleovirology." "Ultimately," said co-author Malik, "if we want to understand why our defenses are the way they are, the answers inevitably lie in these ancient viruses more so than the ones that have affected us only recently, such as HIV."
This work was supported by National Institutes of Health grants to Emerman, a Searle Scholar Award to Malik and a National Science Foundation graduate fellowship to Kaiser.
At Fred Hutchinson Cancer Research Center, our interdisciplinary teams of world-renowned scientists and humanitarians work together to prevent, diagnose and treat cancer, HIV/AIDS and other diseases. Our researchers, including three Nobel laureates, bring a relentless pursuit and passion for health, knowledge and hope to their work and to the world. For more information, please visit ffhcrc/.
Contact: Kristen Woodward
Fred Hutchinson Cancer Research Center
суббота, 18 июня 2011 г.
Moving Closer To Solving Lou Gehrig's Disease Mystery
Chemists from UCLA and the University of Florence in Italy may have solved an important mystery about a protein that plays a key role in a particular form of amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, a progressive, fatal neurodegenerative disorder that strikes without warning.
Joan Selverstone Valentine, UCLA professor of chemistry and biochemistry, has studied the protein - copper-zinc superoxide dismutase - since the 1970s, long before it was implicated in ALS in 1993. Since the link was discovered, Valentine's laboratory has made more than two dozen mutant, ALS-causing enzymes, most of which have only one wrong amino acid out of 153, to try to understand their properties and learn what makes them toxic.
"Some of the mutant proteins are very different from the normal protein, but others are virtually identical to the normal protein - yet they all cause the disease," said Valentine, a member of UCLA's Molecular Biology Institute. "That was the real mystery. You wrack your brain: What is similar among all these proteins" They seem so different. How can they all cause the same disease""
Now Valentine and her colleagues, including Ivano Bertini, professor of chemistry at the University of Florence and director of the European Magnetic Resonance Center, think they know. In ALS patients, the protein's copper and zinc may not be there at all. They present evidence for this hypothesis in new research published in Proceedings of the National Academy of Sciences, online and available in the journal's July 3 print edition.
"If we keep the metals entirely out of the protein, we can explain the toxicity, since even the normal protein forms aggregate at physiological conditions when the metals are gone," Valentine said. "It was such a puzzle, but this hypothesis can solve it."
If scientists can figure out why ALS patients lack the copper and zinc, that would be a major advance that could lead to treatment, she said.
The research team is testing the hypothesis. Valentine, who was elected to the National Academy of Sciences in 2005 and to the American Academy of Arts and Sciences this year, praised her colleagues. "This research is the result of a long, successful international collaboration between UCLA and the University of Florence," she said. "Our colleagues in Italy are exceptional scientists."
Co-authors on the Proceedings of the National Academy of Sciences research are Lucia Banci, a professor of chemistry at the University of Florence who is affiliated with the FiorGen Foundation; Armando Durazo, a UCLA graduate student of chemistry and biochemistry; Stefania Girotto, a postdoctoral scholar at the University of Florence; Edith Butler Gralla, a senior research chemist at UCLA; Manuele Martinelli and Miguela Vieru, graduate students at the University of Florence; and Julian P. Whitelegge, an adjunct professor at the Semel Institute for Neuroscience and Human Behavior at UCLA and UCLA's Brain Research Institute.
Copper-zinc superoxide dismutase, which was discovered in the 1960s, is an antioxidant enzyme that protects cells from free radicals, unstable atoms or molecules that can cause cell damage. The link with ALS came when researchers sequenced the genes of people who have the inherited form of ALS and found that some of them have mutations in the gene that codes for this enzyme. While the inherited form represents only a fraction of all ALS cases, this marked the first time there was any indication of a cause for any form of ALS, Valentine said.
For many years, Valentine's laboratory has studied the normal version of the protein. While the normal protein has copper and zinc, scientists can make it with no metals. When it is first made inside the cell, it has no metals and only acquires them later, Valentine said.
"We studied what happens to the protein if you have the metals, if you have no metals and if you have part of the metals," she said.
The research of the UCLA-University of Florence team has indicated it is the metal-free protein that is likely to be toxic. The protein misfolds when the copper and zinc are not present, but folds properly when they are there.
"Before copper and zinc are inserted, the protein can misfold under physiological conditions," Valentine said.
There is evidence that ALS is associated with this misfolding of the protein, which becomes toxic in some way that is not known and has properties similar to misfolded proteins associated with other neurodegenerative disorders like Alzheimer's and Parkinson's diseases, Valentine said.
Is there a way to slow down this process to give the cell more time to eliminate the misfolded proteins in all of these diseases" Would a strategy to reduce or prevent protein misfolding work against these and other diseases" These are avenues for further investigation by researchers.
When Valentine first began working on copper-zinc superoxide dismutase, she was not a biochemist but a biological inorganic chemist and hardly knew what ALS was. She was interested in the enzyme, which is unique in that it has copper and zinc so close together.
Her laboratory isolated and characterized the enzyme, but Valentine was less interested in its biological properties than in the inorganic chemistry. She was more interested, for example, in how the protein influenced the reactivity of the copper or zinc, or how the copper and zinc influenced the structure of the enzyme. She and her colleagues were among the pioneers in taking the copper and zinc out and putting other metals in to see what would happen. Her laboratory put more emphasis on biological factors over time.
"When I moved to UCLA in 1980, we started working on copper-zinc superoxide dismutase in yeast, a model organism, using the then new tools of molecular biology to redesign the protein and make new mutant forms of the protein that would have different inorganic properties," she said. "We were making mutant forms of this enzyme to study, but with no connection to disease."
"I remember the day in March 1993 that the announcement came - it was on the front page of The New York Times - that ALS has been linked to superoxide dismutase (SOD), but the article didn't say which superoxide dismutase; I was hoping it was our enzyme. It took me all day to track down the scientists to find out which SOD it actually was. It was our SOD. It was a very exciting day."
"When we made the mutant proteins, each one seemed to be totally different," she said. "Some of the mutant proteins that cause the disease are identical to the normal protein in every property we measure."
Valentine and Bertini have known each other since she was a graduate student and he was a research associate at Princeton University. Initially, they were both inorganic chemists who did not intend to do biological research. They have just published an authoritative new textbook called "Biological Inorganic Chemistry: Structure and Reactivity," with co-authors Harry Gray at the California Institute of Technology and the late Edward Stiefel from Princeton University. The textbook is designed for both undergraduate and graduate students.
"All of us who work in the field hope our research will lead to a treatment of ALS," Valentine said. "What we really want is to diagnose and prevent ALS before its onset. We're still a long way from that, but we're making progress."
Valentine's research was federally funded by the National Institutes of Health.
UCLA is California's largest university, with an enrollment of nearly 37,000 undergraduate and graduate students. The UCLA College of Letters and Science and the university's 11 professional schools feature renowned faculty and offer more than 300 degree programs and majors. UCLA is a national and international leader in the breadth and quality of its academic, research, health care, cultural, continuing education and athletic programs. Four alumni and five faculty have been awarded the Nobel Prize.
Contact: Stuart Wolpert
University of California - Los Angeles
Joan Selverstone Valentine, UCLA professor of chemistry and biochemistry, has studied the protein - copper-zinc superoxide dismutase - since the 1970s, long before it was implicated in ALS in 1993. Since the link was discovered, Valentine's laboratory has made more than two dozen mutant, ALS-causing enzymes, most of which have only one wrong amino acid out of 153, to try to understand their properties and learn what makes them toxic.
"Some of the mutant proteins are very different from the normal protein, but others are virtually identical to the normal protein - yet they all cause the disease," said Valentine, a member of UCLA's Molecular Biology Institute. "That was the real mystery. You wrack your brain: What is similar among all these proteins" They seem so different. How can they all cause the same disease""
Now Valentine and her colleagues, including Ivano Bertini, professor of chemistry at the University of Florence and director of the European Magnetic Resonance Center, think they know. In ALS patients, the protein's copper and zinc may not be there at all. They present evidence for this hypothesis in new research published in Proceedings of the National Academy of Sciences, online and available in the journal's July 3 print edition.
"If we keep the metals entirely out of the protein, we can explain the toxicity, since even the normal protein forms aggregate at physiological conditions when the metals are gone," Valentine said. "It was such a puzzle, but this hypothesis can solve it."
If scientists can figure out why ALS patients lack the copper and zinc, that would be a major advance that could lead to treatment, she said.
The research team is testing the hypothesis. Valentine, who was elected to the National Academy of Sciences in 2005 and to the American Academy of Arts and Sciences this year, praised her colleagues. "This research is the result of a long, successful international collaboration between UCLA and the University of Florence," she said. "Our colleagues in Italy are exceptional scientists."
Co-authors on the Proceedings of the National Academy of Sciences research are Lucia Banci, a professor of chemistry at the University of Florence who is affiliated with the FiorGen Foundation; Armando Durazo, a UCLA graduate student of chemistry and biochemistry; Stefania Girotto, a postdoctoral scholar at the University of Florence; Edith Butler Gralla, a senior research chemist at UCLA; Manuele Martinelli and Miguela Vieru, graduate students at the University of Florence; and Julian P. Whitelegge, an adjunct professor at the Semel Institute for Neuroscience and Human Behavior at UCLA and UCLA's Brain Research Institute.
Copper-zinc superoxide dismutase, which was discovered in the 1960s, is an antioxidant enzyme that protects cells from free radicals, unstable atoms or molecules that can cause cell damage. The link with ALS came when researchers sequenced the genes of people who have the inherited form of ALS and found that some of them have mutations in the gene that codes for this enzyme. While the inherited form represents only a fraction of all ALS cases, this marked the first time there was any indication of a cause for any form of ALS, Valentine said.
For many years, Valentine's laboratory has studied the normal version of the protein. While the normal protein has copper and zinc, scientists can make it with no metals. When it is first made inside the cell, it has no metals and only acquires them later, Valentine said.
"We studied what happens to the protein if you have the metals, if you have no metals and if you have part of the metals," she said.
The research of the UCLA-University of Florence team has indicated it is the metal-free protein that is likely to be toxic. The protein misfolds when the copper and zinc are not present, but folds properly when they are there.
"Before copper and zinc are inserted, the protein can misfold under physiological conditions," Valentine said.
There is evidence that ALS is associated with this misfolding of the protein, which becomes toxic in some way that is not known and has properties similar to misfolded proteins associated with other neurodegenerative disorders like Alzheimer's and Parkinson's diseases, Valentine said.
Is there a way to slow down this process to give the cell more time to eliminate the misfolded proteins in all of these diseases" Would a strategy to reduce or prevent protein misfolding work against these and other diseases" These are avenues for further investigation by researchers.
When Valentine first began working on copper-zinc superoxide dismutase, she was not a biochemist but a biological inorganic chemist and hardly knew what ALS was. She was interested in the enzyme, which is unique in that it has copper and zinc so close together.
Her laboratory isolated and characterized the enzyme, but Valentine was less interested in its biological properties than in the inorganic chemistry. She was more interested, for example, in how the protein influenced the reactivity of the copper or zinc, or how the copper and zinc influenced the structure of the enzyme. She and her colleagues were among the pioneers in taking the copper and zinc out and putting other metals in to see what would happen. Her laboratory put more emphasis on biological factors over time.
"When I moved to UCLA in 1980, we started working on copper-zinc superoxide dismutase in yeast, a model organism, using the then new tools of molecular biology to redesign the protein and make new mutant forms of the protein that would have different inorganic properties," she said. "We were making mutant forms of this enzyme to study, but with no connection to disease."
"I remember the day in March 1993 that the announcement came - it was on the front page of The New York Times - that ALS has been linked to superoxide dismutase (SOD), but the article didn't say which superoxide dismutase; I was hoping it was our enzyme. It took me all day to track down the scientists to find out which SOD it actually was. It was our SOD. It was a very exciting day."
"When we made the mutant proteins, each one seemed to be totally different," she said. "Some of the mutant proteins that cause the disease are identical to the normal protein in every property we measure."
Valentine and Bertini have known each other since she was a graduate student and he was a research associate at Princeton University. Initially, they were both inorganic chemists who did not intend to do biological research. They have just published an authoritative new textbook called "Biological Inorganic Chemistry: Structure and Reactivity," with co-authors Harry Gray at the California Institute of Technology and the late Edward Stiefel from Princeton University. The textbook is designed for both undergraduate and graduate students.
"All of us who work in the field hope our research will lead to a treatment of ALS," Valentine said. "What we really want is to diagnose and prevent ALS before its onset. We're still a long way from that, but we're making progress."
Valentine's research was federally funded by the National Institutes of Health.
UCLA is California's largest university, with an enrollment of nearly 37,000 undergraduate and graduate students. The UCLA College of Letters and Science and the university's 11 professional schools feature renowned faculty and offer more than 300 degree programs and majors. UCLA is a national and international leader in the breadth and quality of its academic, research, health care, cultural, continuing education and athletic programs. Four alumni and five faculty have been awarded the Nobel Prize.
Contact: Stuart Wolpert
University of California - Los Angeles
пятница, 17 июня 2011 г.
Exercise To Avoid Gallstones!
A new University of Illinois study shows that exercise-trained mice get far fewer gallstones than sedentary mice and identifies potential mechanisms to explain why this occurs.
The study, recently published in the Journal of Applied Physiology, can be viewed online at: jap.physiology/cgi/reprint/01292.2007v1.
"For the first time, we have direct evidence that physical activity reduces gallstone formation, adding to the ever-increasing number of reasons that people should get more exercise," said Kenneth Wilund, a faculty member in the U of I Division of Nutritional Sciences and an Assistant Professor in Kinesiology and Community Health.
Gallbladder disease affects 10 to 25 percent of adults in the United States, although some persons who are affected may not have symptoms. It has the second highest cost of any digestive disease at $5.8 billion annually and results in over 800,000 hospitalizations each year.
Gallstones form when bile cholesterol levels become high enough to precipitate, fall out of solution, and solidify, Wilund said.
In the study, 50 mice from a gallstone-susceptible strain were fed a high-fat diet containing cholic acid, which helps increase cholesterol absorption. They were then divided into two groups. One group of mice ran on treadmills 45 minutes per day five days a week; the other group did not exercise.
After 12 weeks, the scientists removed the animals' gallbladders, pooling the stones from each group and weighing them. The gallstones in the sedentary group weighed two and a half times more than the stones in the exercised group.
"You could see through the gallbladders in the exercise-trained group, whereas the gallbladders in the sedentary group were full of stones," Wilund said.
To understand more about why this happened, the scientists then measured the expression of selected genes in the liver and intestine that are involved in cholesterol absorption and may affect gallstone development.
"In the exercised mice, we saw an increase in the expression of two genes (LDLr and SRB1) that help bring cholesterol into the liver to 'clear' it from the circulation. But we also found that a protein called Cyp27 was upregulated about two a half times; this resulted in there being more bile acids to solubilize the increased cholesterol so it didn't turn into gallstones.
"Taken together, the differences in gene expression between the exercised and sedentary mice in this study show how exercise training could simultaneously improve cholesterol levels while also inhibiting gallstone formation," he said.
Previous observational studies have suggested that people who are physically fit have fewer gallstones and lower cholesterol, but laboratory studies had not confirmed the link.
Wilund said these mice are a useful model because humans have a similar set of genes that regulate liver and bile cholesterol metabolism. He also said that human studies would be difficult to perform because of the number of years it takes for people to develop gallstones.
"We certainly found the changes in gene expression in the exercised animals very intriguing," he said. "The results add to a body of evidence that supports the importance of physical activity for good health."
Co-authors of the study are Laura A. Feeney, Emily J. Tomayko, and Hae R. Chung of the University of Illinois and Kijin Kim of Keimyung University in Daegu, Korea. Funding was provided by the University of Illinois Research Board.
Source: Phyllis Picklesimer
University of Illinois at Urbana-Champaign
The study, recently published in the Journal of Applied Physiology, can be viewed online at: jap.physiology/cgi/reprint/01292.2007v1.
"For the first time, we have direct evidence that physical activity reduces gallstone formation, adding to the ever-increasing number of reasons that people should get more exercise," said Kenneth Wilund, a faculty member in the U of I Division of Nutritional Sciences and an Assistant Professor in Kinesiology and Community Health.
Gallbladder disease affects 10 to 25 percent of adults in the United States, although some persons who are affected may not have symptoms. It has the second highest cost of any digestive disease at $5.8 billion annually and results in over 800,000 hospitalizations each year.
Gallstones form when bile cholesterol levels become high enough to precipitate, fall out of solution, and solidify, Wilund said.
In the study, 50 mice from a gallstone-susceptible strain were fed a high-fat diet containing cholic acid, which helps increase cholesterol absorption. They were then divided into two groups. One group of mice ran on treadmills 45 minutes per day five days a week; the other group did not exercise.
After 12 weeks, the scientists removed the animals' gallbladders, pooling the stones from each group and weighing them. The gallstones in the sedentary group weighed two and a half times more than the stones in the exercised group.
"You could see through the gallbladders in the exercise-trained group, whereas the gallbladders in the sedentary group were full of stones," Wilund said.
To understand more about why this happened, the scientists then measured the expression of selected genes in the liver and intestine that are involved in cholesterol absorption and may affect gallstone development.
"In the exercised mice, we saw an increase in the expression of two genes (LDLr and SRB1) that help bring cholesterol into the liver to 'clear' it from the circulation. But we also found that a protein called Cyp27 was upregulated about two a half times; this resulted in there being more bile acids to solubilize the increased cholesterol so it didn't turn into gallstones.
"Taken together, the differences in gene expression between the exercised and sedentary mice in this study show how exercise training could simultaneously improve cholesterol levels while also inhibiting gallstone formation," he said.
Previous observational studies have suggested that people who are physically fit have fewer gallstones and lower cholesterol, but laboratory studies had not confirmed the link.
Wilund said these mice are a useful model because humans have a similar set of genes that regulate liver and bile cholesterol metabolism. He also said that human studies would be difficult to perform because of the number of years it takes for people to develop gallstones.
"We certainly found the changes in gene expression in the exercised animals very intriguing," he said. "The results add to a body of evidence that supports the importance of physical activity for good health."
Co-authors of the study are Laura A. Feeney, Emily J. Tomayko, and Hae R. Chung of the University of Illinois and Kijin Kim of Keimyung University in Daegu, Korea. Funding was provided by the University of Illinois Research Board.
Source: Phyllis Picklesimer
University of Illinois at Urbana-Champaign
четверг, 16 июня 2011 г.
Shared Facilities, Resources And Programs To Further Stem Cell Research
Research institutions across Southern California have joined forces to advance stem cell research by establishing the Southern California Stem Cell Scientific Collaboration (SC3). Members of the collaboration include the University of Southern California, Childrens Hospital Los Angeles, City of Hope, University of California, Santa Barbara, California Institute of Technology and the House Ear Institute.
"The potential applications for stem cell research in medicine are enormous," says Martin Pera, Ph.D., director of USC's Center for Stem Cell and Regenerative Medicine. "Tackling these complex problems requires scientists with diverse expertise. We are delighted to have an opportunity to work with such an outstanding collection of scientists to really accelerate the pace of discovery and translational research in regenerative medicine."
Through grants from organizations such as the California Institute for Regenerative Medicine (CIRM) and the National Institutes of Health, SC3 members have a long history of partnering on various research projects. The new agreement is a major step forward in supporting potential significant stem cell findings by allowing members to share training programs, scientific core facilities and expertise, and to team up on a wide range of research programs.
"For patients and their families, cures for cancer, HIV/AIDS and other diseases cannot come soon enough," says Michael A. Friedman, M.D., president and chief executive officer, City of Hope. "As an institution, City of Hope is working to speed advances in medical science to improve and save lives. We believe the SC3 collaboration provides a critical mass of expertise that will create new knowledge and significantly accelerate treatments for diseases that impact so many."
"Stem cell research is vibrant at Childrens Hospital Los Angeles because of the long-term, commitment of our hospital to support high quality research in general, and stem cell research in particular," says Gay M. Crooks, M.D., director of the Stem Cell Program at Childrens Hospital Los Angeles, and professor of pediatrics at the Keck School of Medicine of the University of Southern California. "We believe that such innovative research should be available to the children of California."
Each institution will appoint a faculty member to serve on a joint scientific advisory committee, which will serve as a forum to develop collaborative research ventures, facilitate access to scientific resources and provide expertise across the collaboration. Regional seminar programs and courses, such as the ongoing CIRM funded stem cell biology course between USC, Caltech and Childrens Hospital Los Angeles, will be expanded to allow additional participation. The agreement also ensures each member provides access to resources to investigators for training or to conduct short-term research projects.
"The SC3 collaboration is already engendering new ideas for collaborative projects between scientists at the participating institutions. UC Santa Barbara will benefit from shared resources and synergistic collaborations in stem cell research as part of a new proposed Center for Stem Cell Biology and Engineering," says Dennis Clegg, Chair of Molecular Biology and Director of the Stem Cell Program at UC Santa Barbara.
UC Santa Barbara has a CIRM-funded stem cell training program and a shared lab facility. Research in the proposed Center will focus on two areas of basic and discovery stem cell research: Molecular Mechanisms and Bioengineering. The long-term goal will be the application of results to the development of stem cell-based therapeutics for human disease, particularly macular degeneration.
"The ultimate goal of the collaborative stem cell research at the House Ear Institute is the regeneration or transplantation and successful functioning of sensory cells and other cell types in the inner ear to restore hearing," says David Lim, M.D., Executive Vice President of Research, House Ear Institute (HEI).
Scientists at HEI have discovered that sensory cell progenitors (stem cells) in the inner ear (cochlea) are supporting cells that may help manipulate hair cell regeneration to restore hearing. Future work seeks to more fully understand the biology of these two pathways, whilst at the same time examining their potential in therapeutic approaches to hair cell regeneration.
"We look forward to the establishment of this new stem cell collaboration. The shared facilities should move this important science along considerably faster," says Paul H. Patterson, professor of biological sciences and director of the stem cell training program at Caltech.
Contacts:
USC
Jon Weiner
House Ear Institute
Christa Spieth Nuber
City of Hope
Roya Alt
Childrens Hospital LA
Steve Rutledge
UC Santa Barbara
Paul Desruisseaux
Caltech
Kathy Svitil
Source: Jon Weiner
University of Southern California
"The potential applications for stem cell research in medicine are enormous," says Martin Pera, Ph.D., director of USC's Center for Stem Cell and Regenerative Medicine. "Tackling these complex problems requires scientists with diverse expertise. We are delighted to have an opportunity to work with such an outstanding collection of scientists to really accelerate the pace of discovery and translational research in regenerative medicine."
Through grants from organizations such as the California Institute for Regenerative Medicine (CIRM) and the National Institutes of Health, SC3 members have a long history of partnering on various research projects. The new agreement is a major step forward in supporting potential significant stem cell findings by allowing members to share training programs, scientific core facilities and expertise, and to team up on a wide range of research programs.
"For patients and their families, cures for cancer, HIV/AIDS and other diseases cannot come soon enough," says Michael A. Friedman, M.D., president and chief executive officer, City of Hope. "As an institution, City of Hope is working to speed advances in medical science to improve and save lives. We believe the SC3 collaboration provides a critical mass of expertise that will create new knowledge and significantly accelerate treatments for diseases that impact so many."
"Stem cell research is vibrant at Childrens Hospital Los Angeles because of the long-term, commitment of our hospital to support high quality research in general, and stem cell research in particular," says Gay M. Crooks, M.D., director of the Stem Cell Program at Childrens Hospital Los Angeles, and professor of pediatrics at the Keck School of Medicine of the University of Southern California. "We believe that such innovative research should be available to the children of California."
Each institution will appoint a faculty member to serve on a joint scientific advisory committee, which will serve as a forum to develop collaborative research ventures, facilitate access to scientific resources and provide expertise across the collaboration. Regional seminar programs and courses, such as the ongoing CIRM funded stem cell biology course between USC, Caltech and Childrens Hospital Los Angeles, will be expanded to allow additional participation. The agreement also ensures each member provides access to resources to investigators for training or to conduct short-term research projects.
"The SC3 collaboration is already engendering new ideas for collaborative projects between scientists at the participating institutions. UC Santa Barbara will benefit from shared resources and synergistic collaborations in stem cell research as part of a new proposed Center for Stem Cell Biology and Engineering," says Dennis Clegg, Chair of Molecular Biology and Director of the Stem Cell Program at UC Santa Barbara.
UC Santa Barbara has a CIRM-funded stem cell training program and a shared lab facility. Research in the proposed Center will focus on two areas of basic and discovery stem cell research: Molecular Mechanisms and Bioengineering. The long-term goal will be the application of results to the development of stem cell-based therapeutics for human disease, particularly macular degeneration.
"The ultimate goal of the collaborative stem cell research at the House Ear Institute is the regeneration or transplantation and successful functioning of sensory cells and other cell types in the inner ear to restore hearing," says David Lim, M.D., Executive Vice President of Research, House Ear Institute (HEI).
Scientists at HEI have discovered that sensory cell progenitors (stem cells) in the inner ear (cochlea) are supporting cells that may help manipulate hair cell regeneration to restore hearing. Future work seeks to more fully understand the biology of these two pathways, whilst at the same time examining their potential in therapeutic approaches to hair cell regeneration.
"We look forward to the establishment of this new stem cell collaboration. The shared facilities should move this important science along considerably faster," says Paul H. Patterson, professor of biological sciences and director of the stem cell training program at Caltech.
Contacts:
USC
Jon Weiner
House Ear Institute
Christa Spieth Nuber
City of Hope
Roya Alt
Childrens Hospital LA
Steve Rutledge
UC Santa Barbara
Paul Desruisseaux
Caltech
Kathy Svitil
Source: Jon Weiner
University of Southern California
среда, 15 июня 2011 г.
News From The American Chemical Society
Excess female to male births in Canada linked to chronic dioxin exposure
Almost 90 Canadian communities have experienced a shift in the normal 51:49 ratio of male to female births, so that more girls than boys are being born, according to two studies in ACS' Environmental Science & Technology, a semi-monthly journal. James Argo, who headed the research, attributes this so-called "inverted sex ratio" of the residents in those communities to dioxin air pollutants from oil refineries, paper mills, metal smelters and other sources.
The studies analyzed information in the Environmental Quality Database (EQDB), an inventory of pollution sources, cancer data, and other factors developed for Canadian government research on how early exposure to environmental contaminants affects the health of Canadians. Argo points out that the EQDB enables researchers to pinpoint the location of 126,000 homes relative to any of about 65 air pollution sources-types and the occurrence of cancer among residents of those homes.
Argo focused on air pollutants from those sources and the corresponding incidence of cancer among more than 20,000 residents and 5,000 controls. He identified inverted male sex ratios, sometimes as profound as 46:54 in almost all of the communities. The ratio indicated that more females than males were born, a situation that Argo attributed to chronic exposure of parents to dioxin, based on previous studies. The study "may represent one of only a few studies explicitly designed to identify the impact of carcinogens from industrial sources on residents at home," Agro stated.
"Chronic Disease and Early Exposure to Air-Borne Mixtures: 1. The Environmental Quality Database" and "Chronic Disease and Early Exposure to Air-Borne Mixtures: 2. Exposure Assessment"
CONTACT:
James Argo, Ph.D.
IntrAmericas Centre for Environment and Health
Ontario, Canada
Tiny capers pack big disease-fighting punch
Capers, used in such culinary delights as chicken piccata and smoked salmon, may be small. But they are an unexpectedly big source of natural antioxidants that show promise for fighting cancer and heart disease when added to meals, particularly meats, researchers in Italy are reporting in the current issue of ACS' Journal of Agricultural and Food Chemistry, a bi-weekly publication.
The flower buds of a small bush, capers have been used for centuries in Mediterranean cuisine, where they provide a salty tang and decorative flair to a variety of meats, salads, pastas and other foods. In the new study, Maria A. Livrea and colleagues note that other foods in the so-called Mediterranean diet have gotten plenty of attention for their health benefits. Capers, however, have been largely overlooked.
Their laboratory study involved adding caper extracts to grilled ground-turkey, and analyzing byproducts formed during simulated digestion. The scientists found that caper-extract helped prevent the formation of certain byproducts of digested meat that have been linked by others to an increased risk of cancer and heart disease. That beneficial effect occurred even with the small amounts of caper typically used to flavor food. "Caper may have beneficial health effects, especially for people whose meals are rich in fats and red meats," the study concluded.
"Bioactive Components of Caper (Capparis spinosa L.) from Sicily and Antioxidant Effects in a Red Meat Simulated Gastric Digestion"
CONTACT:
Maria A. Livrea, Ph.D.
Universita di Palermo
Palermo, Italy
Bacteria in the intestines can influence results of drug tests
Bacteria living in the intestines of laboratory rats -- those test tubes on four feet that stand in for humans in a wide range of research -- may influence the results of drug safety and other tests, scientists in Michigan are reporting. The findings are scheduled for the Dec. 7 issue of ACS' Chemical Research in Toxicology, a monthly journal.
Cynthia M. Rohde and colleagues note growing recognition of the hidden role of the approximately 100 trillion bacteria that thrive in the intestines of humans. Studies have shown that this so-called "gut microflora" can influence the immune system, how the body responds to foods, the action of drugs, and other functions. Researchers started the new study after noting that a genetically identical population of rats widely used in laboratory tests had developed two distinctively different metabolic types. The types involve differences in the way those animals metabolize, or breakdown, drugs and nutrients.
After detailed studies of substances in the urine of the rats, researchers concluded that the differences result from differences in the gut microbial populations between the two types. The report recommends that scientists in the future check lab rat populations for such metabolic differences due to gut microflora in order to assure accurate results, especially in experiments to evaluate the safety of new drugs.
"Metabonomic Evaluation of Schaedler Altered Microflora Rats"
CONTACT:
Cynthia M. Rohde, Ph.D.
Metabonomics Evaluation Group
Pfizer Global Research and Development
2800 Plymouth Road
Ann Arbor, Michigan 48105
Recycling of e-waste in China may expose mothers, infants to high dioxin levels
With China now the destination for 70 percent of the computers, TVs, cell phones, and other electronic waste (e-waste) recycled worldwide each year, a new study has concluded that Chinese recycling methods significantly increase dioxin levels in women and their breast-fed infants. The study is scheduled for the Nov. 15 issue of ACS' Environmental Science & Technology, a semi-monthly publication.
Ming H. Wong and colleagues did one of what they describe as "very few" studies of dioxin levels among women of child bearing age at an e-waste recycling site, and compared those levels to women in an area without e-waste recycling. They analyzed levels of dioxins -- compounds linked to cancer, developmental defects, and other health problems -- in samples of breast milk, placenta, and hair.
Samples from the e-waste site showed significantly higher levels of dioxins than those taken at the reference site. Researchers estimated that the daily intake of infants from 6 months of breast feeding at the recycling site was more than double that of the reference site. Therefore, this implies that these levels at the recycling site and the reference site were at least 25 times and 11 times higher, respectively, than the World Health Organization tolerable daily limit for adults regarding dioxins and dioxin-like PCBs. The study includes descriptions of recycling methods, which include heating scrap electronic components over coal fires in the open air.
"Body Loadings and Health Risk Assessment of Polychlorinated Dibenzo-p-dioxins and Dibenzofurans at an Intensive Electronic Waste Recycling Site in China"
CONTACT:
Ming H. Wong, Ph.D.
Hong Kong Baptist University
Kowloon Tong
Hong Kong
The American Chemical Society -- the world's largest scientific society -- is a nonprofit organization chartered by the U.S. Congress and a global leader in providing access to chemistry-related research through its multiple databases, peer-reviewed journals and scientific conferences. Its main offices are in Washington, D.C., and Columbus, Ohio.
Source: Michael Woods
American Chemical Society
Almost 90 Canadian communities have experienced a shift in the normal 51:49 ratio of male to female births, so that more girls than boys are being born, according to two studies in ACS' Environmental Science & Technology, a semi-monthly journal. James Argo, who headed the research, attributes this so-called "inverted sex ratio" of the residents in those communities to dioxin air pollutants from oil refineries, paper mills, metal smelters and other sources.
The studies analyzed information in the Environmental Quality Database (EQDB), an inventory of pollution sources, cancer data, and other factors developed for Canadian government research on how early exposure to environmental contaminants affects the health of Canadians. Argo points out that the EQDB enables researchers to pinpoint the location of 126,000 homes relative to any of about 65 air pollution sources-types and the occurrence of cancer among residents of those homes.
Argo focused on air pollutants from those sources and the corresponding incidence of cancer among more than 20,000 residents and 5,000 controls. He identified inverted male sex ratios, sometimes as profound as 46:54 in almost all of the communities. The ratio indicated that more females than males were born, a situation that Argo attributed to chronic exposure of parents to dioxin, based on previous studies. The study "may represent one of only a few studies explicitly designed to identify the impact of carcinogens from industrial sources on residents at home," Agro stated.
"Chronic Disease and Early Exposure to Air-Borne Mixtures: 1. The Environmental Quality Database" and "Chronic Disease and Early Exposure to Air-Borne Mixtures: 2. Exposure Assessment"
CONTACT:
James Argo, Ph.D.
IntrAmericas Centre for Environment and Health
Ontario, Canada
Tiny capers pack big disease-fighting punch
Capers, used in such culinary delights as chicken piccata and smoked salmon, may be small. But they are an unexpectedly big source of natural antioxidants that show promise for fighting cancer and heart disease when added to meals, particularly meats, researchers in Italy are reporting in the current issue of ACS' Journal of Agricultural and Food Chemistry, a bi-weekly publication.
The flower buds of a small bush, capers have been used for centuries in Mediterranean cuisine, where they provide a salty tang and decorative flair to a variety of meats, salads, pastas and other foods. In the new study, Maria A. Livrea and colleagues note that other foods in the so-called Mediterranean diet have gotten plenty of attention for their health benefits. Capers, however, have been largely overlooked.
Their laboratory study involved adding caper extracts to grilled ground-turkey, and analyzing byproducts formed during simulated digestion. The scientists found that caper-extract helped prevent the formation of certain byproducts of digested meat that have been linked by others to an increased risk of cancer and heart disease. That beneficial effect occurred even with the small amounts of caper typically used to flavor food. "Caper may have beneficial health effects, especially for people whose meals are rich in fats and red meats," the study concluded.
"Bioactive Components of Caper (Capparis spinosa L.) from Sicily and Antioxidant Effects in a Red Meat Simulated Gastric Digestion"
CONTACT:
Maria A. Livrea, Ph.D.
Universita di Palermo
Palermo, Italy
Bacteria in the intestines can influence results of drug tests
Bacteria living in the intestines of laboratory rats -- those test tubes on four feet that stand in for humans in a wide range of research -- may influence the results of drug safety and other tests, scientists in Michigan are reporting. The findings are scheduled for the Dec. 7 issue of ACS' Chemical Research in Toxicology, a monthly journal.
Cynthia M. Rohde and colleagues note growing recognition of the hidden role of the approximately 100 trillion bacteria that thrive in the intestines of humans. Studies have shown that this so-called "gut microflora" can influence the immune system, how the body responds to foods, the action of drugs, and other functions. Researchers started the new study after noting that a genetically identical population of rats widely used in laboratory tests had developed two distinctively different metabolic types. The types involve differences in the way those animals metabolize, or breakdown, drugs and nutrients.
After detailed studies of substances in the urine of the rats, researchers concluded that the differences result from differences in the gut microbial populations between the two types. The report recommends that scientists in the future check lab rat populations for such metabolic differences due to gut microflora in order to assure accurate results, especially in experiments to evaluate the safety of new drugs.
"Metabonomic Evaluation of Schaedler Altered Microflora Rats"
CONTACT:
Cynthia M. Rohde, Ph.D.
Metabonomics Evaluation Group
Pfizer Global Research and Development
2800 Plymouth Road
Ann Arbor, Michigan 48105
Recycling of e-waste in China may expose mothers, infants to high dioxin levels
With China now the destination for 70 percent of the computers, TVs, cell phones, and other electronic waste (e-waste) recycled worldwide each year, a new study has concluded that Chinese recycling methods significantly increase dioxin levels in women and their breast-fed infants. The study is scheduled for the Nov. 15 issue of ACS' Environmental Science & Technology, a semi-monthly publication.
Ming H. Wong and colleagues did one of what they describe as "very few" studies of dioxin levels among women of child bearing age at an e-waste recycling site, and compared those levels to women in an area without e-waste recycling. They analyzed levels of dioxins -- compounds linked to cancer, developmental defects, and other health problems -- in samples of breast milk, placenta, and hair.
Samples from the e-waste site showed significantly higher levels of dioxins than those taken at the reference site. Researchers estimated that the daily intake of infants from 6 months of breast feeding at the recycling site was more than double that of the reference site. Therefore, this implies that these levels at the recycling site and the reference site were at least 25 times and 11 times higher, respectively, than the World Health Organization tolerable daily limit for adults regarding dioxins and dioxin-like PCBs. The study includes descriptions of recycling methods, which include heating scrap electronic components over coal fires in the open air.
"Body Loadings and Health Risk Assessment of Polychlorinated Dibenzo-p-dioxins and Dibenzofurans at an Intensive Electronic Waste Recycling Site in China"
CONTACT:
Ming H. Wong, Ph.D.
Hong Kong Baptist University
Kowloon Tong
Hong Kong
The American Chemical Society -- the world's largest scientific society -- is a nonprofit organization chartered by the U.S. Congress and a global leader in providing access to chemistry-related research through its multiple databases, peer-reviewed journals and scientific conferences. Its main offices are in Washington, D.C., and Columbus, Ohio.
Source: Michael Woods
American Chemical Society
вторник, 14 июня 2011 г.
Research In The Bolivian Rainforest Suggests Ancient, Shared Roots Of Feeding Behaviours In Monkeys And Humans
Behavioural ecologists working in Bolivia have found that wild spider monkeys control their diets in a similar way to humans, contrary to what has been thought up to now. Rather than trying to maximize their daily energy intake, the monkeys tightly regulate their daily protein intake, so that it stays at the same level regardless of seasonal variation in the availability of different foods.
Tight regulation of daily protein intake is known to play a role in the development of obesity in humans, and the findings from this research suggest that the evolutionary origins of these eating patterns in humans may be far older than suspected. Until now it was thought humans' eating patterns originated in the Palaeolithic era (between 2.4 million and 10,000 years ago).
The research, published online yesterday in the journal Behavioral Ecology [1], also provides valuable information about which trees are important for the monkeys' diet, which is relevant to conservation; in addition, it may help to improve the care of captive primates, which can be prone to obesity and related health problems due to their diet.
Dr Annika Felton, a Departmental Visitor at the Fenner School of Environment and Society, The Australian National University, Canberra, Australia, spent a year in the Bolivian rainforest (in Departmento Santa Cruz) familiarising the Peruvian spider monkeys (Ateles chamek) to her presence and then observing their feeding habits.
She followed 15 individual monkeys (7 adult males, 8 adult females), conducting continuous observations of the same animal from dawn to dusk, and following each of the monkeys for at least one whole day a month. During observations she recorded everything they did and ate and for how long. Where possible, she counted every fruit and leaf they ate, and collected samples of what they had eaten from the actual trees the monkeys had chosen. The samples were then dried and sent to the laboratory in Australia where they were analysed for their nutritional content. It is unusual for a study of feeding habits in wild primates to be conducted in this detailed way. It enabled Dr Felton and her colleagues to calculate how much an individual monkey had consumed and the nutrients involved; usually, other field studies are only able to calculate averages for a group of animals.
Dr Felton said: "We found that the pattern of nutrient intake by wild spider monkeys, which are primarily fruit eaters, was almost identical to humans, which are omnivores. What spider monkeys and humans have in common is that they tightly regulate their daily protein intake, i.e. they appear to aim for a target amount of protein each day, regardless of whether they only ate ripe fruit or mixed in other vegetable matter as well. Finding this result in spider monkeys was unexpected because, previously, ripe fruit specialists were thought to be 'energy maximisers'. In other words, they would aim to maximise their daily energy intake. Our findings show this is not the case.
"The consequence of tight protein regulation is the same for monkeys and humans: if the diet is poor in protein but rich in carbohydrates and fats (energy dense food) individuals will end up ingesting a great deal of energy in order to obtain their protein target, which can lead to weight gain. This 'protein leverage effect' is thought to play a significant role in the human obesity problem found in modern western societies. Our results suggest that an adjustment of the nutritional balance of diets as a means to manage human obesity might similarly be an option for mitigating obesity in captive primates.
"Our findings are also interesting from an evolutionary point of view. Similarity in the regulatory pattern of protein intake between distantly related species, such as humans and spider monkeys, possessing very different dietary habits, may indicate that the evolutionary origins of such regulatory patterns are quite old, potentially far older than the Palaeolithic era. If we are not dealing with convergent evolution here - in other words that spider monkeys and humans have evolved this trait independently - then this trait may have been shared by our common ancestor. Spider monkeys are New World primates that split from the Old World primates about 40 million years ago.
"Finally, our research shows that nutritionally-balanced food sources that are used extensively by a wild population may need special attention in terms of conservation planning, perhaps by regulating logging and selecting certain tree species for re-planting. The majority of the monkeys' nourishment was sourced from a species of fig tree, Ficus boliviana, that is currently being harvested for timber in Bolivia."
Dr Felton and her colleagues found that the monkeys ate a wide variety of fruit and vegetables - 105 different plants belonging to 63 species during the 12 months of observation. Figs were particularly popular. The monkeys rarely ate insects, which are rich in protein.
The spider monkeys did not specifically select either the most energy-rich or the most protein-rich foods that were available, and the daily amount of food they ate varied quite widely, averaging about 1 kg a day, but sometimes as much as 2.4 kg a day. However, they maintained their daily protein intake around 0.2 MJ (11 grams), whereas their intake of carbohydrates and fats varied between 0.7-6.2 MJ. The availability of sweet, ripe fruit was significantly related to the variation in their daily energy intake - the more there was, the more they ate.
"To maintain a stable intake of protein, spider monkeys consumed large amounts of carbohydrates and fats when protein content in the food was low, for instance when their diet consisted entirely of ripe fruit, and consumed far fewer carbohydrates and fats when feeding on items rich in protein," said Dr Felton.
She concluded: "What is perhaps most fascinating about our paper is not the answers we provide, but the questions that our findings raise. For example, why do these frugivores have the same pattern of nutritional intake as human omnivores? Is this due to convergent evolution or is it a remaining trait from a common ancestor?
"I am also pleased that our findings can be applied to the management of captive primates (where obesity is a problem), and possibly the management of spider monkey forest habitat.
"Also, importantly, we have shown that the combination of intensive data collection and the application of an innovative analytical framework can dramatically change our perceptions of the nutritional ecology of a species."
[1] Protein content of diets dictates the daily energy intake of a free-ranging primate.
Behavioural Ecology.
doi:10.1093/beheco/arp021
Source
Behavioural Ecology
Tight regulation of daily protein intake is known to play a role in the development of obesity in humans, and the findings from this research suggest that the evolutionary origins of these eating patterns in humans may be far older than suspected. Until now it was thought humans' eating patterns originated in the Palaeolithic era (between 2.4 million and 10,000 years ago).
The research, published online yesterday in the journal Behavioral Ecology [1], also provides valuable information about which trees are important for the monkeys' diet, which is relevant to conservation; in addition, it may help to improve the care of captive primates, which can be prone to obesity and related health problems due to their diet.
Dr Annika Felton, a Departmental Visitor at the Fenner School of Environment and Society, The Australian National University, Canberra, Australia, spent a year in the Bolivian rainforest (in Departmento Santa Cruz) familiarising the Peruvian spider monkeys (Ateles chamek) to her presence and then observing their feeding habits.
She followed 15 individual monkeys (7 adult males, 8 adult females), conducting continuous observations of the same animal from dawn to dusk, and following each of the monkeys for at least one whole day a month. During observations she recorded everything they did and ate and for how long. Where possible, she counted every fruit and leaf they ate, and collected samples of what they had eaten from the actual trees the monkeys had chosen. The samples were then dried and sent to the laboratory in Australia where they were analysed for their nutritional content. It is unusual for a study of feeding habits in wild primates to be conducted in this detailed way. It enabled Dr Felton and her colleagues to calculate how much an individual monkey had consumed and the nutrients involved; usually, other field studies are only able to calculate averages for a group of animals.
Dr Felton said: "We found that the pattern of nutrient intake by wild spider monkeys, which are primarily fruit eaters, was almost identical to humans, which are omnivores. What spider monkeys and humans have in common is that they tightly regulate their daily protein intake, i.e. they appear to aim for a target amount of protein each day, regardless of whether they only ate ripe fruit or mixed in other vegetable matter as well. Finding this result in spider monkeys was unexpected because, previously, ripe fruit specialists were thought to be 'energy maximisers'. In other words, they would aim to maximise their daily energy intake. Our findings show this is not the case.
"The consequence of tight protein regulation is the same for monkeys and humans: if the diet is poor in protein but rich in carbohydrates and fats (energy dense food) individuals will end up ingesting a great deal of energy in order to obtain their protein target, which can lead to weight gain. This 'protein leverage effect' is thought to play a significant role in the human obesity problem found in modern western societies. Our results suggest that an adjustment of the nutritional balance of diets as a means to manage human obesity might similarly be an option for mitigating obesity in captive primates.
"Our findings are also interesting from an evolutionary point of view. Similarity in the regulatory pattern of protein intake between distantly related species, such as humans and spider monkeys, possessing very different dietary habits, may indicate that the evolutionary origins of such regulatory patterns are quite old, potentially far older than the Palaeolithic era. If we are not dealing with convergent evolution here - in other words that spider monkeys and humans have evolved this trait independently - then this trait may have been shared by our common ancestor. Spider monkeys are New World primates that split from the Old World primates about 40 million years ago.
"Finally, our research shows that nutritionally-balanced food sources that are used extensively by a wild population may need special attention in terms of conservation planning, perhaps by regulating logging and selecting certain tree species for re-planting. The majority of the monkeys' nourishment was sourced from a species of fig tree, Ficus boliviana, that is currently being harvested for timber in Bolivia."
Dr Felton and her colleagues found that the monkeys ate a wide variety of fruit and vegetables - 105 different plants belonging to 63 species during the 12 months of observation. Figs were particularly popular. The monkeys rarely ate insects, which are rich in protein.
The spider monkeys did not specifically select either the most energy-rich or the most protein-rich foods that were available, and the daily amount of food they ate varied quite widely, averaging about 1 kg a day, but sometimes as much as 2.4 kg a day. However, they maintained their daily protein intake around 0.2 MJ (11 grams), whereas their intake of carbohydrates and fats varied between 0.7-6.2 MJ. The availability of sweet, ripe fruit was significantly related to the variation in their daily energy intake - the more there was, the more they ate.
"To maintain a stable intake of protein, spider monkeys consumed large amounts of carbohydrates and fats when protein content in the food was low, for instance when their diet consisted entirely of ripe fruit, and consumed far fewer carbohydrates and fats when feeding on items rich in protein," said Dr Felton.
She concluded: "What is perhaps most fascinating about our paper is not the answers we provide, but the questions that our findings raise. For example, why do these frugivores have the same pattern of nutritional intake as human omnivores? Is this due to convergent evolution or is it a remaining trait from a common ancestor?
"I am also pleased that our findings can be applied to the management of captive primates (where obesity is a problem), and possibly the management of spider monkey forest habitat.
"Also, importantly, we have shown that the combination of intensive data collection and the application of an innovative analytical framework can dramatically change our perceptions of the nutritional ecology of a species."
[1] Protein content of diets dictates the daily energy intake of a free-ranging primate.
Behavioural Ecology.
doi:10.1093/beheco/arp021
Source
Behavioural Ecology
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