Chapter 9. Homeostasis: Active Regulation of the Internal Environment
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By Carey Goldberg I’d just gotten used to the idea that I’m a walking mountain of microbes. The sizzling field of research into the microbiome — our full complement of bugs — is casting new light on our role as homes to the trillions of bacteria that inhabit each of us. At least most of them are friendly, I figured. But now comes the next microbial shift in my self-image, courtesy of the new book “The Mind-Gut Connection.” My trillions of gut microbes, it seems, are in constant communication with my brain, and there’s mounting evidence that they may affect how I feel — not just physically but emotionally. Does this mean — gulp — that maybe our bugs are driving the bus? I spoke with the book’s author, Dr. Emeran Mayer, professor of medicine and psychiatry at UCLA, executive director of the Oppenheimer Center for Neurobiology of Stress and Resilience and expert in brain-gut microbiome interactions. Edited excerpts: So we’re not only packed with trillions of gut microbes but they’re in constant cross-talk with our brains — that’s the picture? First of all, you have to realize that these are invisible creatures. So even though there are 100 trillion of them living in our gut, you wouldn’t be able to see them with the naked eye. It’s not like something tangible sitting inside of you, like another organ. © Copyright WBUR 2016
Link ID: 22673 - Posted: 09.20.2016
Researchers at the National Institutes of Health have discovered a two-way link between depression and gestational diabetes. Women who reported feeling depressed during the first two trimesters of pregnancy were nearly twice as likely to develop gestational diabetes, according to an analysis of pregnancy records. Conversely, a separate analysis found that women who developed gestational diabetes were more likely to report postpartum depression six weeks after giving birth, compared to a similar group of women who did not develop gestational diabetes. The study was published online in Diabetologia. Gestational diabetes is a form of diabetes (high blood sugar level) occurring only in pregnancy, which if untreated may cause serious health problems for mother and infant. “Our data suggest that depression and gestational diabetes may occur together,” said the study’s first author, Stefanie Hinkle, Ph.D., staff scientist in the Division of Intramural Population Health Research at the NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). “Until we learn more, physicians may want to consider observing pregnant women with depressive symptoms for signs of gestational diabetes. They also may want to monitor women who have had gestational diabetes for signs of postpartum depression.” Although obesity is known to increase the risk for gestational diabetes, the likelihood of gestational diabetes was higher for non-obese women reporting depression than for obese women with depression.
Napping for more than an hour during the day could be a warning sign for type-2 diabetes, Japanese researchers suggest. They found the link after analysing observational studies involving more than 300,000 people. UK experts said people with long-term illnesses and undiagnosed diabetes often felt tired during the day. But they said there was no evidence that napping caused or increased the risk of diabetes. The large study, carried out by scientists at the University of Tokyo, is being presented at a meeting of the European Association for the Study of Diabetes in Munich. Their research found there was a link between long daytime naps of more than 60 minutes and a 45% increased risk of type-2 diabetes, compared with no daytime napping - but there was no link with naps of less than 40 minutes. The researchers said long naps could be a result of disturbed sleep at night, potentially caused by sleep apnoea. And this sleeping disorder could increase the risk of heart attacks, stroke, cardiovascular problems and other metabolic disorders, including type-2 diabetes. Sleep deprivation, caused by work or social life patterns, could also lead to increased appetite, which could increase the risk of type-2 diabetes. But it was also possible that people who were less healthy or in the early stages of diabetes were more likely to nap for longer during the day. Shorter naps, in contrast, were more likely to increase alertness and motor skills, the authors said. © 2016 BBC.
By GINA KOLATA A few years ago, Richard Kahn, the now-retired chief scientific and medical officer of the American Diabetes Association, was charged with organizing a committee to prescribe a diet plan for people with diabetes. He began by looking at the evidence for different diets, asking which, if any, best controlled diabetes. “When you look at the literature, whoa is it weak. It is so weak,” Dr. Kahn said in a recent interview. Studies tended to be short term, diets unsustainable, differences between them clinically insignificant. The only thing that really seemed to help people with diabetes was weight loss — and for weight loss there is no magic diet. But people want diet advice, Dr. Kahn reasoned, and the association really should say something about diets. So it, like the National Institutes of Health, went with the Department of Agriculture’s food pyramid. Why? “It’s a diet for all America,” Dr. Kahn said. ”It has lots of fruits and vegetables and a reasonable amount of fat.” That advice, though, recently came under attack in a New York Times commentary written by Sarah Hallberg, an osteopath at a weight loss clinic in Indiana, and Osama Hamdy, the medical director of the obesity weight loss program at the Joslin Diabetes Center at Harvard Medical School. There is a diet that helps with diabetes, the two doctors said, one that restricts — or according to Dr. Hallberg, severely restricts — — carbohydrates. “If the goal is to get patients off their medications, including insulin, and resolve rather than just control their diabetes, significant carb restriction is by far the best nutrition plan,” Dr. Hallberg said in an email. “This would include elimination of grains, potatoes and sugars and all processed foods. There is a significant and ever growing body of literature that supports this method.” She is in private practice at Indiana University Health Arnett Hospital and is medical director of a startup developing nutrition-based medical interventions. © 2016 The New York Times Company
Link ID: 22654 - Posted: 09.15.2016
By ANAHAD O’CONNOR The sugar industry paid scientists in the 1960s to play down the link between sugar and heart disease and promote saturated fat as the culprit instead, newly released historical documents show. The internal sugar industry documents, recently discovered by a researcher at the University of California, San Francisco, and published Monday in JAMA Internal Medicine, suggest that five decades of research into the role of nutrition and heart disease, including many of today’s dietary recommendations, may have been largely shaped by the sugar industry. “They were able to derail the discussion about sugar for decades,” said Stanton Glantz, a professor of medicine at U.C.S.F. and an author of the JAMA paper. The documents show that a trade group called the Sugar Research Foundation, known today as the Sugar Association, paid three Harvard scientists the equivalent of about $50,000 in today’s dollars to publish a 1967 review of research on sugar, fat and heart disease. The studies used in the review were handpicked by the sugar group, and the article, which was published in the prestigious New England Journal of Medicine, minimized the link between sugar and heart health and cast aspersions on the role of saturated fat. Even though the influence-peddling revealed in the documents dates back nearly 50 years, more recent reports show that the food industry has continued to influence nutrition science. Last year, an article in The New York Times revealed that Coca-Cola, the world’s largest producer of sugary beverages, had provided millions of dollars in funding to researchers who sought to play down the link between sugary drinks and obesity. In June, The Associated Press reported that candy makers were funding studies that claimed that children who eat candy tend to weigh less than those who do not. The Harvard scientists and the sugar executives with whom they collaborated are no longer alive. One of the scientists who was paid by the sugar industry was D. Mark Hegsted, who went on to become the head of nutrition at the United States Department of Agriculture, where in 1977 he helped draft the forerunner to the federal government’s dietary guidelines. Another was Dr. Fredrick J. Stare, the chairman of Harvard’s nutrition department. © 2016 The New York Times Company
Link ID: 22649 - Posted: 09.13.2016
By SARAH HALLBERG and OSAMA HAMDY Earlier this year, the Food and Drug Administration approved a new weight-loss procedure in which a thin tube, implanted in the stomach, ejects food from the body before all the calories can be absorbed. Some have called it “medically sanctioned bulimia,” and it is the latest in a desperate search for new ways to stem the rising tides of obesity and Type 2 diabetes. Roughly one-third of adult Americans are now obese; two-thirds are overweight; and diabetes afflicts some 29 million. Another 86 million Americans have a condition called pre-diabetes. None of the proposed solutions have made a dent in these epidemics. Recently, 45 international medical and scientific societies, including the American Diabetes Association, called for bariatric surgery to become a standard option for diabetes treatment. The procedure, until now seen as a last resort, involves stapling, binding or removing part of the stomach to help people shed weight. It costs $11,500 to $26,000, which many insurance plans won’t pay and which doesn’t include the costs of office visits for maintenance or postoperative complications. And up to 17 percent of patients will have complications, which can include nutrient deficiencies, infections and intestinal blockages. It is nonsensical that we’re expected to prescribe these techniques to our patients while the medical guidelines don’t include another better, safer and far cheaper method: a diet low in carbohydrates. Once a fad diet, the safety and efficacy of the low-carb diet have now been verified in more than 40 clinical trials on thousands of subjects. Given that the government projects that one in three Americans (and one in two of those of Hispanic origin) will be given a diagnosis of diabetes by 2050, it’s time to give this diet a closer look. © 2016 The New York Times Company
Link ID: 22645 - Posted: 09.12.2016
By GRETCHEN REYNOLDS A busy brain can mean a hungry body. We often seek food after focused mental activity, like preparing for an exam or poring over spreadsheets. Researchers speculate that heavy bouts of thinking drain energy from the brain, whose capacity to store fuel is very limited. So the brain, sensing that it may soon require more calories to keep going, apparently stimulates bodily hunger, and even though there has been little in the way of physical movement or caloric expenditure, we eat. This process may partly account for the weight gain so commonly seen in college students. Scientists at the University of Alabama at Birmingham and another institution recently experimented with exercise to counter such post-study food binges. Gary Hunter, an exercise physiologist at U.A.B., oversaw the study, which was published this month in the journal Medicine & Science in Sports & Exercise. Hunter notes that strenuous activity both increases the amount of blood sugar and lactate — a byproduct of intense muscle contractions — circulating in the blood and augments blood flow to the head. Because the brain uses sugar and lactate as fuel, researchers wondered if the increased flow of fuel-rich blood during exercise could feed an exhausted brain and reduce the urge to overeat. Thirty-eight healthy college students were invited to U.A.B.’s exercise lab to determine their fitness and metabolic rates — and to report what their favorite pizza was. Afterward, they sat quietly for 35 minutes before being given as much of their favorite pizza as they wanted, which established a baseline measure of self-indulgence. At a later date, the volunteers returned and spent 20 minutes tackling selections from college and graduate-school entrance exams. Hunter says this work has been used in other studies “to induce mental fatigue and hunger.” Next, half the students sat quietly for 15 minutes, before being given pizza. The rest of the volunteers spent those 15 minutes doing intervals on a treadmill: two minutes of hard running followed by about one minute of walking, repeated five times. This is the sort of brief but intensive routine, Hunter says, that should prompt the release of sugar and lactate into the bloodstream. These students were then allowed to gorge on pizza, too. But by and large, they did not overeat. © 2016 The New York Times Company
By Jessica Hamzelou As any weight-watcher knows, carb cravings can be hard to resist. Now there’s evidence that carbohydrate-rich foods may elicit a unique taste too, suggesting that “starchy” could be a flavour in its own right. It has long been thought that our tongues register a small number of primary tastes: salty, sweet, sour and bitter. Umami – the savoury taste often associated with monosodium glutamate – was added to this list seven years ago, but there’s been no change since then. However, this list misses a major component of our diets, says Juyun Lim at Oregon State University in Corvallis. “Every culture has a major source of complex carbohydrate. The idea that we can’t taste what we’re eating doesn’t make sense,” she says. Complex carbohydrates such as starch are made of chains of sugar molecules and are an important source of energy in our diets. However, food scientists have tended to ignore the idea that we might be able to specifically taste them, says Lim. Because enzymes in our saliva break starch down into shorter chains and simple sugars, many have assumed we detect starch by tasting these sweet molecules. Her team tested this by giving a range of different carbohydrate solutions to volunteers – who it turned out were able to detect a starch-like taste in solutions that contained long or shorter carbohydrate chains. “They called the taste ‘starchy’,” says Lim. “Asians would say it was rice-like, while Caucasians described it as bread-like or pasta-like. It’s like eating flour.” © Copyright Reed Business Information Ltd.
Hannah Devlin Science correspondent Babies born by caesarean section are more likely to be obese as adults, according to a study that suggests the way we are born could have a lasting impact on health. Birth by caesarean was linked to a 15% higher risk of obesity in children compared with vaginal birth. The scientists involved believe that babies born by caesarean miss out on exposure to bacteria in the birth canal that colonise the baby’s gut and may ultimately change the body’s metabolic rate - and even how hungry we feel. Audrey Gaskins, an epidemiologist at Harvard University and co-author of the new study, said: “Children born via C-section harbour less diverse gut bacteria and these patterns of less diversity have been linked to increased capacity for energy harvest by the gut microbiota. You can think of it as a slower metabolism.” Previous studies have found the same link, but were less able to rule out other factors, such as the mother’s weight or health. The latest research, which included 22,068 children born to 15,271 women, suggests that the link is not simply explained by overweight women or those with pregnancy complications such as high blood pressure being more likely to deliver by caesarean. The link remained after maternal weight was taken into account, and was more striking when siblings who had different types of births were compared. Within families, children born by caesarean were 64% more likely to be obese than their siblings born by vaginal delivery. “With siblings, they have the same mother and home environment so the genetics, the feeding environment, are all controlled for,” said Dr Gaskins. © 2016 Guardian News and Media Limited
By Alison F. Takemura | In mice, severely restricting caloric intake promotes the transformation of white fat into brown fat, which contains cells that burn energy faster, according to a study published today (August 25) in Cell Metabolism. The innate immune system, researchers from the University of Geneva, Switzerland, and their colleagues reported, mediates this fat cell-transforming effect. “The paper nicely characterizes this phenomenon,” said Ajay Chawla of the University of California, San Francisco, who was not involved in the work. “And it mechanistically seems to identify a pathway that we had identified.” Whereas the present study found diet induced a “beiging” phenotype—in which white adipose tissue starts to express more energy-expending brown fat cells—Chawla and colleagues had previously shown that cold temperatures, another extreme condition, can produce the same effect. Scientists are keenly interested in learning how to generate brown fat cells. A treatment could help stem the obesity epidemic. “Finding some mechanism to activate this response—ideally, in obese or diabetic individuals—is really attractive,” said postdoctoral researcher Salvatore Fabbiano of the University of Geneva who led the present study. Several conditions are already known to make white fat tissue more brown—cold temperatures, microbe loss, and gastric bypass surgery among them. Fabbiano and colleagues hypothesized that the common feature of all these experiences was an increased expenditure of calories compared to intake. © 1986-2016 The Scientist
Link ID: 22615 - Posted: 08.31.2016
Laura Sanders Scientists have identified the “refrigerator” nerve cells that hum along in the brains of mice and keep the body cool. These cells kick on to drastically cool mice’s bodies and may prevent high fevers, scientists report online August 25 in Science. The results “are totally new and very important,” says physiologist Andrej Romanovsky of the Barrow Neurological Institute in Phoenix. "The implications are far-reaching." By illuminating how bodies stay at the right temperature, the discovery may offer insights into the relationship between body temperature and metabolism. Scientists had good reasons to think that nerve cells controlling body temperature are tucked into the hypothalamus, a small patch of neural tissue in the middle of the brain. Temperature fluctuations in a part of the hypothalamus called the preoptic area prompt the body to get back to baseline by conserving or throwing off heat. But the actual identify of the heat sensors remained mysterious. The new study reveals the cells to be those that possess a protein called TRPM2. “Overall, this is a major discovery in the field of thermoregulation,” says Shaun Morrison of Oregon Health & Science University in Portland. Jan Siemens, a neurobiologist at the University of Heidelberg in Germany, and colleagues tested an array of molecules called TRP channels, proteins that sit on cell membranes and help sense a variety of stimuli, including painful tear gas and cool menthol. In tests of nerve cells in lab dishes, one candidate, the protein TRPM2, seemed to respond to heat. |© Society for Science & the Public 2000 - 201
Keyword: Pain & Touch
Link ID: 22605 - Posted: 08.27.2016
Laura Sanders Fractions of a second after food hits the mouth, a specialized group of energizing nerve cells in mice shuts down. After the eating stops, the nerve cells spring back into action, scientists report August 18 in Current Biology. This quick response to eating offers researchers new clues about how the brain drives appetite and may also provide insight into narcolepsy. These nerve cells have intrigued scientists for years. They produce a molecule called orexin (also known as hypocretin), thought to have a role in appetite. But their bigger claim to fame came when scientists found that these cells were largely missing from the brains of people with narcolepsy. People with narcolepsy are more likely to be overweight than other people, and this new study may help explain why, says neuroscientist Jerome Siegel of UCLA. These cells may have more subtle roles in regulating food intake in people without narcolepsy, he adds. Results from earlier studies hinted that orexin-producing nerve cells are appetite stimulators. But the new results suggest the opposite. These cells actually work to keep extra weight off. “Orexin cells are a natural obesity defense mechanism,” says study coauthor Denis Burdakov of the Francis Crick Institute in London. “If they are lost, animals and humans gain weight.” Mice were allowed to eat normally while researchers eavesdropped on the behavior of their orexin nerve cells. Within milliseconds of eating, orexin nerve cells shut down and stopped sending signals. |© Society for Science & the Public 2000 - 2016
Link ID: 22583 - Posted: 08.22.2016
By KATHERINE KINZLER You may not be surprised to learn that food preference is a social matter. What we choose to eat depends on more than just what tastes good or is healthful. People in different cultures eat different things, and within a culture, what you eat can signal something about who you are. More surprising is that the sociality of food selection, it turns out, runs deep in human nature. In research published this month in the Proceedings of the National Academy of Sciences, my colleagues and I showed that even 1-year-old babies understand that people’s food preferences depend on their social or cultural group. Interestingly, we found that babies’ thinking about food preferences isn’t really about food per se. It’s more about the people eating foods, and the relationship between food choice and social groups. While it’s hard to know what babies think before they can talk, developmental psychologists have long capitalized on the fact that babies’ visual gaze is guided by their interest. Babies tend to look longer at something that is novel or surprising. Do something bizarre the next time you meet a baby, and you’ll notice her looking intently. Using this method, the psychologists Zoe Liberman, Amanda Woodward, Kathleen Sullivan and I conducted a series of studies. Led by Professor Liberman, we brought more than 200 1-year-olds (and their parents) into a developmental psychology lab, and showed them videos of people visibly expressing like or dislike of foods. For instance, one group of babies saw a video of a person who ate a food and expressed that she loved it. Next they saw a video of a second person who tried the same food and also loved it. This second event was not terribly surprising to the babies: The two people agreed, after all. Accordingly, the babies did not look for very long at this second video; it was what they expected. © 2016 The New York Times Company
By Diana Kwon When glial cells were discovered in the 1800s, they were thought to be passive, supporting structures—the “glue”—as their Greek name implies—that holds neurons together in the brain and throughout the nervous system. In recent years, however, neuroscientists have discovered that far from being passive, these small cells play an astonishing variety of roles in both the development and functioning of the brain. Some of the latest discoveries suggest that glia play complex roles in regulating appetite and metabolism, making them a possible target for treating obesity. Signs that glia might play such roles were first identified in the 1980s. Neuroscientist Pierre Magistretti and his colleagues found evidence that neurotransmitters could promote the release of glucose reserves stored in astrocytes, a star-shaped type of glial cell. Other studies revealed that obesity leads to increased activation of glial cells in the hypothalamus—the key area of the brain for controlling metabolic processes. This was despite the fact that, for a long time, “neurons were considered the only players in the control of energy metabolism,” says Cristina García-Cáceres, a neurobiologist at the Helmholtz Diabetes Center in Germany. Two recent studies add new evidence that glia play a key role in metabolism. In one study, published last week in Cell, García-Cáceres, together with Matthias Tschöp, the director of the Helmholtz Diabetes Center and colleagues, reported that insulin acts on astrocytes to regulate sugar intake in the brain. © 2016 Scientific American,
By Roxanne Khamsi, What if controlling the appetite were as easy as flipping a switch? It sounds like the stuff of science fiction, but Jeffrey Friedman of Rockefeller University and his colleagues did exactly this in genetically engineered mice to try to shed light on how the brain influences appetite. Friedman and his colleagues used magnetic stimulation to switch on neurons in a region of the brain called the ventromedial hypothalamus and found that doing so increased the rodents' blood sugar levels and decreased levels of the hormone insulin. Turning on the neurons also caused the mice to eat more than their control counterparts. The ultimate confirmation came when they inhibited these neurons and saw the opposite effects: it drove blood sugar down, elevated insulin levels and suppressed the animals' urge to consume their chow. That the brain influences hunger is not an unexpected finding, but scientists have recently narrowed in on how it has sway on what ends up in the gut—and how the gut talks to the mind. This two-way communication, defined as the 'gut–brain axis', happens not only through nerve connections between the organs, but also through biochemical signals, such as hormones, that circulate in the body. “The idea that there is bidirectional communication between the gastrointestinal tract and brain that affects metabolism traces back more than a century,” Friedman says, referring to the work of the nineteenth-century French scientist Claude Bernard, who made seminal discoveries into how the body maintains physiological equilibrium. “Our new findings that insulin-producing cells in the pancreas can be controlled by certain neurons in the brain that sense blood sugar provides further experimental evidence supporting this notion.” © 2016 Scientific American,
Link ID: 22522 - Posted: 08.06.2016
By Jonathan Webb Science reporter, BBC News Scientists have glimpsed activity deep in the mouse brain which can explain why we get thirsty when we eat, and why cold water is more thirst-quenching. A specific "thirst circuit" was rapidly activated by food and quietened by cooling down the animals' mouths. The same brain cells were already known to stimulate drinking, for example when dehydration concentrates the blood. But the new findings describe a much faster response, which predicts the body's future demand for water. The researchers went looking for this type of system because they were puzzled by the fact that drinking behaviour, in humans as well as animals, seems to be regulated very quickly. "There's this textbook model for homeostatic regulation of thirst, that's been around for almost 100 years, that's based on the blood," said the study's senior author Zachary Knight, from the University of California, San Francisco. "There are these neurons in the brain that… generate thirst when the blood becomes too salty or the blood volume falls too low. But lots of aspects of everyday drinking can't possibly be explained by that homeostatic model because they occur much too quickly." Take the "prandial thirst" that comes while we consume a big, salty meal - or the fact that we feel quenched almost as soon as we take a drink. © 2016 BBC.
Link ID: 22518 - Posted: 08.04.2016
The brains of overweight middle-aged people resemble brains that are a decade older in healthier people. A study of 473 adults has found that people who are overweight have less white matter, which connects different brain areas and enables signaling between them. The volume of white matter in the brains of overweight people at 50 were similar to that seen in the brains of lean people at 60. Human brains naturally shrink with age, but previous research has shown that this seems to happen more quickly in obese people. “As our brains age, they naturally shrink in size, but it isn’t clear why people who are overweight have a greater reduction in the amount of white matter,” says Lisa Ronan, at the University of Cambridge, a member of the research team. “We can only speculate on whether obesity might in some way cause these changes or whether obesity is a consequence of brain changes.” Intriguingly, the difference between lean and overweight people’s brains was only apparent from middle age onwards. It’s possible that this is because we are particularly vulnerable in some way at this time, says team-member Paul Fletcher, also at the University of Cambridge. However, despite this reduction in white matter, cognitive tests did not find any evidence that being overweight was linked to reduced brain function. “We don’t yet know the implications of these changes in brain structure,” says Sadaf Farooqi, at the University of Cambridge, who was also involved in the research. © Copyright Reed Business Information Ltd.
Link ID: 22512 - Posted: 08.04.2016
By James Gallagher Controlling human nerve cells with electricity could treat a range of diseases including arthritis, asthma and diabetes, a new company says. Galvani Bioelectronics hopes to bring a new treatment based on the technique before regulators within seven years. GlaxoSmithKline and Verily, formerly Google, Life Sciences, are behind it. Animal experiments have attached tiny silicone cuffs, containing electrodes, around a nerve and then used a power supply to control the nerve's messages. One set of tests suggested the approach could help treat type-2 diabetes, in which the body ignores the hormone insulin. They focused on a cluster of chemical sensors near the main artery in the neck that check levels of sugar and the hormone insulin. The sensors send their findings back to the brain, via a nerve, so the organ can coordinate the body's response to sugar in the bloodstream. GSK vice-president of bioelectronics Kris Famm told the BBC News website: "The neural signatures in the nerve increase in type 2-diabetes. "By blocking those neural signals in diabetic rats, you see the sensitivity of the body to insulin is restored." And early work suggested it could work in other diseases too. "It isn't just a one-trick-pony, it is something that if we get it right could have a new class of therapies on our hands," Mr Famm said. But he said the field was only "scratching the surface" when it came to understanding which nerve signals have what effect in the body. Both the volume and rhythm of the nerve signals could be having an effect rather than it being a simple case of turning the nerve on or off. © 2016 BBC
Link ID: 22507 - Posted: 08.03.2016
By Alice Klein Blame grandpa. A study in mice shows that the grandsons of obese males are more susceptible to the detrimental health effects of junk food, even if their fathers are lean and healthy. The finding adds to evidence that new traits can be passed down the family line without being permanently recorded in a family’s genes – a phenomenon called transgenerational epigenetics. Last year, a study found that the DNA in the sperm of obese men is modified in thousands of places, and that these sperm also contain short pieces of RNA. These are epigenetic modifications – they don’t affect the precise code of genes, but instead may affect how active particular genes are. Now Catherine Suter at Victor Chang Cardiac Research Institute in Sydney and her team have investigated the longer-term effects of paternal obesity. To do this, they mated obese male mice with lean female mice. They found that, compared with the offspring of lean males, both the sons and grandsons of the obese males were more likely to show the early signs of fatty liver disease and diabetes when given a junk food diet. The same effect wasn’t seen in daughters or granddaughters. Even when the sons of the obese males were fed a healthy diet and kept at a normal weight, their sons still had a greater tendency to develop obesity-related conditions when exposed to a junk diet. © Copyright Reed Business Information Ltd.
Tina Hesman Saey ORLANDO, Fla. — Weight gain may depend on how an individual’s genes react to certain diets, a new study in mice suggests. Four strains of mice fared differently on four different diets, William Barrington of North Carolina State University in Raleigh reported July 15 at the Allied Genetics Conference. One strain, the A/J mouse, was nearly impervious to dietary changes. Those mice didn’t gain much weight or have changes in insulin or cholesterol no matter what they ate: a fat-and-carbohydrate-laden Western diet, traditional Mediterranean or Japanese diet (usually considered healthy) or very low-carbohydrate, fat-rich fare known as the ketogenic diet. In contrast, NOD/ShiLtJ mice gained weight on all but the Japanese diet. Those mice’s blood sugar shot up — a hallmark of diabetes — on a Mediterranean diet, but decreased on the Japanese diet. FVB/NJ mice didn’t get fat on the Western diet, but became obese and developed high cholesterol and other health problems on the ketogenic diet. The opposite was true for C57BL/6J mice. They became obese and developed cholesterol and other problems linked to heart disease and diabetes in people on the Western diet, but not on the ketogenic diet. They also fattened up on the Mediterranean diet. © Society for Science & the Public 2000 - 2016.
Link ID: 22454 - Posted: 07.19.2016