Chapter 9. Homeostasis: Active Regulation of the Internal Environment
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By SENDHIL MULLAINATHAN Why is obesity soaring? The answer seems pretty clear. In 1955, a standard soda at McDonald’s was only seven ounces. Today, a medium is three times as large, and even a child’s-size version is 12 ounces. It’s a widely held view that obesity is a consequence of our behaviors, and that behavioral economics thus plays a central role in understanding it — with markets, preferences and choices taking center stage. As a behavioral economist, I subscribed to that view — until recently, when I began to question my thinking. For many health problems, of course, behavior plays some role but biology is often a major villain. “Biology” here is my catchall term for the myriad bodily mechanics that are only weakly connected to our choices. A few studies have led me to wonder whether the same is true with obesity. Have I been the proverbial owner of a (behavioral) hammer, looking for (behavioral) nails everywhere? Have I failed to appreciate the role of biology? A first warning sign comes from looking at other animals. Our pets have been getting fatter along with us. In 2012, some 58.3 percent of cats were, literally, fat cats. That is taken from a survey by the Association for Pet Obesity Prevention. (The very existence of this organization is telling.) Pet obesity, however, can easily be tied to human behavior: a culture that eats more probably feeds its animals more, too. And yet, a study by a group of biostatisticians in the Proceedings of the Royal Society challenges this interpretation. They collected data from animals raised in captivity: macaques, marmosets, chimpanzees, vervets, lab rats and mice. The data came from labs and centers and spanned several decades. These captive animals are also becoming fatter: weight gain for female lab mice, for example, came out to 11.8 percent a decade from 1982 to 2003. But this weight gain is harder to explain. Captive animals are fed carefully controlled diets, which the researchers argue have not changed for decades. Animal obesity cannot be explained through eating behavior alone. We must look to some other — biological — driver. © 2013 The New York Times Company
Link ID: 18905 - Posted: 11.10.2013
By NICHOLAS BAKALAR Children who do not sleep enough may be increasing their risk for obesity, according to a new study. Researchers randomly divided 37 children aged 8 to 11 into two groups. Each group increased their habitual time in bed by an hour and a half per night for one week, then decreased their time by the same amount the next week. They wore electronic devices to measure sleep time, were assessed for daily food intake three times a week, and had blood tests to measure leptin, a hormone that affects hunger, and high levels of which correlate with fat tissue accumulations. Children consumed 134 calories fewer each day during the increased sleep week than the during the week with less sleep. Fasting leptin levels were lower when the children slept more and, over all, the children’s weight averaged about a half pound less at the end of long sleep weeks than short ones. The study was published online in Pediatrics. The lead author, Chantelle N. Hart, an associate professor of public health at Temple University who was at Brown University when she did the study, cautioned that it was small, and looked only at acute changes in sleep and their effect on eating behaviors. Still, she said, “I think these findings suggest that getting a good night’s sleep in childhood could have important benefits for weight regulation through decreased food intake.” Copyright 2013 The New York Times Company
Guest post by Bruce Bower Among 16- to 22-year-old U.S. males, 7.6 percent report taking various potentially dangerous substances at least monthly to counteract what they regard as an alarming lack of muscularity. Young men whose insecurities inspire them to use growth hormones, steroids and other body-altering chemicals represent the male counterpart of females whose idealization of thinness prompts them to induce vomiting and otherwise purge their bodies of food, proposes a team led by epidemiologist Alison Field of Boston Children’s Hospital. Purging and other eating disorders occur mainly in girls and women. Boys and men so obsessed with muscles that they take substances prohibited in competitive sports are more numerous than researchers and clinicians realized, and have been overlooked, Field and her colleagues conclude November 4 in JAMA Pediatrics. The researchers examined questionnaires that each of 5,527 males completed eight times between 1999 — at ages 12 to 18 — and 2010. Most participants were white and from middle-class families. No information on sports team participation was available. © Society for Science & the Public 2000 - 2013.
JoNel Aleccia NBC News Obesity may be a factor in early puberty in U.S. girls, a new study finds. About 17 percent of American kids ages 2 to 17 are obese, according to the CDC. There’s yet another reason to worry about the obesity epidemic among America’s kids: Extra weight may be sending U.S. girls into puberty earlier than ever. Researchers have found that girls with higher body mass index, a ratio of height and weight, may start developing breasts more than a year before their thinner friends — perhaps as early as second grade. The change is spawning a whole new market of child-sized sanitary pads — decorated with hearts and stars — and deodorants aimed at 8- to 10-year-olds, according to a new study and an editorial published Monday in the journal Pediatrics. “The girls who are obese are clearly maturing earlier,” said Dr. Frank Biro, a pediatrics professor at Cincinnati Children’s Hospital Medical Center. “BMI is, we found, the biggest single factor for the onset of puberty.” In addition, white girls are maturing about four months earlier than in a landmark 1997 study that shocked parents with the news that their daughters who played with My Little Pony could be entering puberty. Biro’s team followed more than 1,200 girls ages 6 to 8 in three cities — San Francisco, Cincinnati and New York — from 2004 to 2011, carefully documenting their BMI and their maturation process.
by Tina Hesman Saey BOSTON— Siberians may use genes to stay warm, a new study shows. As part of an effort to catalog genetic diversity in Siberia, Alexia Cardona of the University of Cambridge and collaborators sampled DNA from 200 Siberians representing 10 native groups. The team looked for genes that have more changes in Siberians than would be expected by chance — a sign that the genes evolved rapidly in the 24,000 years since people settled the frigid land. Rapid changes suggest that a gene is important for adapting to an environment. Several of the Siberians’ genes have variants that may help keep Arctic dwellers warm during the long winters, Cardona reported October 24 at the annual meeting of the American Society of Human Genetics. Among the candidates for genetic heaters are genes involved in metabolizing fats. Some Siberian groups eat mostly meat, so genes that help convert animal fat to energy are important for creating heat. Another gene with variants unique to Siberians is called PRKG1; it helps regulate body heat by controlling muscle contraction and the constriction and dilation of blood vessels. Muscle contractions are an important part of shivering, which can raise body temperature. The researchers also identified variants in genes involved in thyroid function, which plays a role in temperature regulation. A. Cardona et al. Genome-wide analysis of cold adaption in indigenous Siberian populations. American Society of Human Genetics annual meeting, Boston, October 24, 2013. © Society for Science & the Public 2000 - 2013
By James Gallagher Health and science reporter, BBC News The mocked "obesity excuse" of being born with a slow metabolism is actually true for some people, say researchers. A team at the University of Cambridge has found the first proof that mutated DNA does indeed slow metabolism. The researchers say fewer than one in 100 people are affected and are often severely obese by early childhood. The findings, published in the journal Cell, may lead to new obesity treatments even for people without the mutation. Scientists at the Institute of Metabolic Science, in Cambridge, knew that mice born without a section of DNA, a gene called KSR2, gained weight more easily. But they did not know what effect it may be having in people, so they analysed the DNA of 2,101 severely obese patients. Some had mutated versions of KSR2. It had a twin effect of increasing their appetite while their slowing metabolism. "You would be hungry and wanting to eat a lot, you would not want to move because of a slower metabolism and would probably also develop type 2 diabetes at a young age," lead researcher Prof Sadaf Farooqi told the BBC. She added: "It slows the ability to burn calories and that's important as it's a new explanation for obesity." BBC © 2013
By Tori Rodriguez The digestive tract and the brain are crucially linked, according to mounting evidence showing that diet and gut bacteria are able to influence our behavior, thoughts and mood. Now researchers have found evidence of bacterial translocation, or “leaky gut,” among people with depression. Normally the digestive system is surrounded by an impermeable wall of cells. Certain behaviors and medical conditions can compromise this wall, allowing toxic substances and bacteria to enter the bloodstream. In a study published in the May issue of Acta Psychiatrica Scandinavica, approximately 35 percent of depressed participants showed signs of leaky gut, based on blood tests. The scientists do not yet know how leaky gut relates to depression, although earlier work offers some hints. Displaced bacteria can activate autoimmune responses and inflammation, which are known to be associated with the onset of depression, lower mood and fatigue. “Leaky gut may maintain increased inflammation in depressed patients,” which could exacerbate the symptoms of depression if not treated, says Michael Maes, a research psychiatrist with affiliations in Australia and Thailand and an author of the paper. Currently leaky gut is treated with a combination of glutamine, N-acetylcysteine and zinc—believed to have anti-inflammatory or antioxidant properties—when behavioral and dietary modifications fail. © 2013 Scientific American
Link ID: 18830 - Posted: 10.24.2013
Doug Greene, WVIT and NBC News staff NBC News Oreos are as addictive as cocaine, at least for lab rats, and just like us, they like the creamy center best. Eating the sugary treats activates more neurons in the brain’s “pleasure center” than drugs such as cocaine, the team at Connecticut College found. “Our research supports the theory that high-fat/ high-sugar foods stimulate the brain in the same way that drugs do,” neuroscience assistant professor Joseph Schroeder says. “That may be one reason people have trouble staying away from them and it may be contributing to the obesity epidemic.” Schroeder’s neuroscience students put hungry rats into a maze. On one side went rice cakes. “Just like humans, rats don’t seem to get much pleasure out of eating them,” Schroeder said. On the other side went Oreos. Then the rats got the option of hanging out where they liked. They compared the results to a different test. In that on, rats on one side if the maze got an injection of saline while those on the other side got injections of cocaine or morphine. Rats seems to like the cookies about as much as they liked the addictive drugs. When allowed to wander freely, they’d congregate on the Oreo side for about as much time as they would on the drug side. Oh, and just like most people - the rats eat the creamy center first.
By GINA KOLATA William Howard Taft, the only massively obese man ever to be president of the United States, struggled mightily to control his weight a century ago, worrying about his health and image, and endured humiliation from cartoonists who delighted in his corpulent figure. But new research has found that his weight-loss program was startlingly contemporary, and his difficulties keeping the pounds off would be familiar to many Americans today. On the advice of his doctor, a famed weight-loss guru and author of popular diet books, he went on a low-fat, low-calorie diet. He avoided snacks. He kept a careful diary of what he ate and weighed himself daily. He hired a personal trainer and rode a horse for exercise. And he wrote his doctor, Nathaniel E. Yorke-Davies, with updates on his progress, often twice a week. In a way, he was ahead of his time. Obesity became a medical issue by the middle of the 20th century, around the time the term “obesity” rather than “corpulence” came into vogue, said Abigail C. Saguy, a sociologist at the University of California, Los Angeles, who specializes in the study of obesity. Taft’s story shows that “at least in some cases, corpulence was already treated as a medical problem early in the century,” she added. Like many dieters today, Taft, 6 feet 2 inches tall, lost weight and regained it, fluctuating from more than 350 to 255 pounds. He was 48 when he first contacted Dr. Yorke-Davies, and spent the remaining 25 years of his life corresponding with the doctor and consulting other physicians in a quest to control his weight. Taft’s struggles are recounted by Deborah Levine, a medical historian at Providence College in Rhode Island. She discovered the extensive correspondence between Taft and the diet doctor, including Taft’s diet program, his food diary, and a log of his weight. Her findings were published Monday in The Annals of Internal Medicine. His story, Dr. Levine said, “sheds a lot of light on what we are going through now.” © 2013 The New York Times Company
Link ID: 18788 - Posted: 10.15.2013
by Erika Engelhaupt Could I interest you in eating the partially digested stomach contents of a porcupine? No? Maybe a spot of reindeer stomach, then. Still no? Well, that’s curious. The Western aversion to these dishes is odd, because people around the world have long partaken of — even delighted in — the delicacy known to medical science as chyme. That’s what becomes of food after it’s chewed, swallowed and mushed around in the stomach for a while with a healthy dose of hydrochloric acid. And, researchers now suggest, Neandertals were no exception. Eating chyme may even explain the presence of some puzzling plant matter found in Neandertal’s tartar-crusted teeth. Neandertals didn’t have great dental care, and in the last few years anthropologists have begun to take advantage of monstrous tartar buildup on fossilized teeth to figure out what the hominids ate. Various chemical signatures, starch grains and even tiny plant fossils called phytoliths get preserved in the tartar, also known as calculus. Just what Neandertals ate has been more of a puzzle than paleo dieters might have you believe. Isotope analyses of fossilized bones and teeth suggest Neandertals ate very high on the food chain, with high-protein diets akin to those of wolves or hyenas. But wear marks on their teeth suggest the Neandertal diet consisted of more animals in colder high-latitude areas, and more of a mix of plants and animals in warmer areas. Tartar analyses support the idea that Neandertals ate their veggies, and have also suggested the presence of plants considered inedible, or at least unpalatable and non-nutritious. These include some plants like yarrow and chamomile with medicinal value, so one team suggested Neandertals self-medicated. © Society for Science & the Public 2000 - 2013
Link ID: 18776 - Posted: 10.12.2013
By ANAHAD O'CONNOR They are a mystery to researchers: people who are significantly overweight and yet show none of the usual metabolic red flags. Despite their obesity, they have normal cholesterol levels, healthy blood pressure levels and no apparent signs of impending diabetes. Researchers call them the metabolically healthy obese, and by some estimates they represent as many as a third of all obese adults. Scientists have known very little about them, but new research may shed some light on the cause of their unusual metabolic profile. A study in the journal Diabetologia has found that compared with their healthier counterparts, people who are obese but metabolically unhealthy have impaired mitochondria, the cellular powerhouses that harvest energy from food, as well as a reduced ability to generate new fat cells. Unlike fat tissue in healthy obese people, which generates new cells to help store fat as it accumulates, the fat cells of the unhealthy obese swell to their breaking point, straining the cellular machinery and ultimately dying off. This is accompanied by inflammation, and it leads to ectopic fat accumulation — the shuttling of fat into organs where it does not belong, like the liver, heart and skeletal muscle. A fatty liver frequently coincides with metabolic abnormalities, and studies suggest that it may be one of the causes of insulin resistance, the fundamental defect in Type 2 diabetes. In the healthy obese, however, the fat tends to remain in the subcutaneous padding just beneath the skin, where it appears to be fairly innocuous. “The group that doesn’t gain fat in the liver as they get obese seems to avoid inflammation and maintain their metabolic health,” said Dr. Jussi Naukkarinen, a research scientist specializing in internal medicine at the University of Helsinki. “There is a complete difference in how they react to obesity.” Copyright 2013 The New York Times Company
Link ID: 18771 - Posted: 10.10.2013
By ABBY ELLIN When binge eating disorder gained legitimacy as a full-fledged mental condition in the latest edition of the Diagnostic and Statistical Manual of Mental Disorders in May, many people in the eating disorders and obesity communities wondered: Will this inspire us to finally get along? It was a good question, since historically, the two groups have been at odds. Unlike people with anorexia or bulimia, who tend to be excessively thin, many binge eaters are overweight or obese. And much of the focus of anti-obesity efforts — listing calories at restaurants, banning cupcakes in schools, sending students home with body mass index “report cards” — are decried by eating disorder activists, who say such measures can encourage anorexia or bulimia. Anti-obesity activists, in turn, worry that the eating disorder community minimizes the medical risks of obesity, which the American Medical Association classified as a disease in June, and plays down the discrimination many obese people face. “They come out of different traditions,” said Kelly Brownell, dean of the Sanford School of Public Policy at Duke University. “Obesity was mainly dealt with in medical professions, and eating disorders were dealt with more in psychology professions.” But binge eating disorder, symptoms of which include consuming enormous amounts of food in a two-hour window without purging at least once a week for three months, could bridge the gap between the two worlds, while also reducing the stereotype that only thin people suffer from eating disorders. Copyright 2013 The New York Times Company
Keyword: Anorexia & Bulimia
Link ID: 18770 - Posted: 10.10.2013
by Linda Geddes They are identical in almost every way, except one twin is fat and the other is thin. Now a study of this rare group is shedding light on a medical mystery: how some people can be obese and perfectly healthy. Obesity usually goes hand in hand with metabolic syndrome – high blood pressure, high cholesterol and type 2 diabetes – but a minority of obese people escape this fate. To probe the fit fat phenomenon, Jussi Naukkarinen at the University of Helsinki in Finland and his colleagues turned to a registry of identical twins, picking 16 pairs whose body weight differed by 17 kilograms on average. They are a perfect model for studying such differences because they are genetically identical and have usually been raised in very similar environments. Naukkarinen's team started by looking at the siblings' body fat distribution and quickly saw that the fat twins fell into two groups: those that tended to accumulate fat within their livers, and those whose liver fat resembled that of their thin twin. Suppressed activity Next, they looked at other markers of ill-health, including insulin resistance, cholesterol, inflammation and blood pressure. These measures also divided the group. "Basically all the hallmarks of the metabolic syndrome were lacking in the group where there was no liver fat," Naukkarinen says. Researchers also compared samples of the twins' abdominal fat, or adipose tissue. In unhealthy obese twins, genes involved in inflammation were activated – genes that were not activated in their thin twin. The activity of cellular powerhouses called mitochondria seemed to be suppressed as well. But in healthy obese twins, gene expression was similar to that of the thin twin. © Copyright Reed Business Information Ltd.
by Ed Yong I’ve just arrived home from 14 hours of flying. The clocks on my phone and laptop have been ticking away the whole time, and it takes a few seconds to reset them to British time. The clocks in my body are more difficult. We run on a daily 24-hour body clock, which controls everything from our blood pressure to our temperature to how hungry we feel. It runs on proteins rather than gears. Once they’re built, these proteins stop their own manufacture after a slight delay, meaning that their levels rise and fall with a regular rhythm. These timers tick away inside almost all of our cells, and they’re synchronised by a tiny collection of 10,000 neurons at the bottom of our brain. It’s called the suprachiasmatic nucleus (SCN). It’s the master clock. It’s the conductor that keeps the orchestra in sync. The SCN is also sensitive to light. It gets signals from our eyes, which allows it to synchronise its ticking with the 24-hour cycle of day and night outside. The SCN is what connects the rhythms of our bodies with those of the planet. But when we travel far and fast, and suddenly land in a new time zone, the SCN becomes misaligned with the environment. It takes time to re-adjust, typically one day for every time zone crossed. In the meantime, our sleep is disrupted and our physiology goes weird. In other words: jet lag. But at Kyoto University, Yoshiaki Yamaguchi and Toru Suzuki have engineered mice that break this rule. They are, with apologies for the awful word, unjetlaggable. If you change the light in their cages to mimic an 8-hour time difference, they readjust almost immediately. Put them on a red-eye flight from San Francisco to London and they’d be fine.
By Shelly Fan Disclaimer: First things first. Please note that I am in no way endorsing nutritional ketosis as a supplement to, or a replacement for medication. As you’ll see below, data exploring the potential neuroprotective effects of ketosis are still scarce, and we don’t yet know the side effects of a long-term ketogenic diet. This post talks about the SCIENCE behind ketosis, and is not meant in any way as medical advice. The ketogenic diet is a nutritionist’s nightmare. High in saturated fat and VERY low in carbohydrates, “keto” is adopted by a growing population to paradoxically promote weight loss and mental well-being. Drinking coffee with butter? Eating a block of cream cheese? Little to no fruit? To the uninitiated, keto defies all common sense, inviting skeptics to wave it off as an unnatural “bacon-and-steak” fad diet. Yet versions of the ketogenic diet have been used to successfully treat drug-resistant epilepsy in children since the 1920s – potentially even back in the biblical ages. Emerging evidence from animal models and clinical trials suggest keto may be therapeutically used in many other neurological disorders, including head ache, neurodegenerative diseases, sleep disorders, bipolar disorder, autism and brain cancer. With no apparent side effects. Sound too good to be true? I feel ya! Where are these neuroprotective effects coming from? What’s going on in the brain on a ketogenic diet? In essence, a ketogenic diet mimics starvation, allowing the body to go into a metabolic state called ketosis (key-tow-sis). © 2013 Scientific American
Link ID: 18732 - Posted: 10.02.2013
By Julianne Wyrick Some people are drawn to the thick smell of bacon, sizzling and crackling in the skillet on a Saturday morning. For others, it’s the aroma of freshly baked cookies on a Friday night or the smell of McDonald’s fries creeping in through the car window. At this time of year, I find the scent of freshly baked pumpkin muffins irresistible. Of course, I’d like to think I’m not a slave to my nose, at least not when I’m nice and full from dinner. If I were a fruit fly, my outlook might not be so good. Already-fed fruit fly larvae exposed to certain food-related odors ate more food than larvae that didn’t experience the smells, according to research published by scientists at the University of Georgia last spring. “They’re not hungry, but they will get an extra kick in terms of appetite, so they will eat, for example, 30 percent extra,” said Ping Shen, lead author on the study. The scents, which included the sweet odor of bananas or the sharper smell of balsamic vinegar, served as “cues” or triggers that the flies associated with food. The triggers motivated the fly larvae to eat, even when they’d already had dinner. That doesn’t bode so well for flies trying to watch their weight. For the fly to feel this urge to eat, the smell has to be transported from sensory receptors in the nose to the part of the brain that regulates appetite—the brain’s “feeding center”—via a series of neurons. Part of this signal transfer involves dopamine, a neurotransmitter associated with behavior motivated by a cue or hint of something to come, like smells associated with food. © 2013 Scientific American
By Laura Sanders By hijacking connections between neurons deep within the brain, scientists forced full mice to keep eating and hungry mice to shun food. By identifying precise groups of cells that cause eating and others that curb it, the results begin to clarify the intricate web of checks and balances in the brain that control feeding. “This is a really important missing piece of the puzzle,” says neuroscientist Seth Blackshaw of Johns Hopkins University in Baltimore. “These are cell types that weren’t even predicted to exist.” A deeper understanding of how the brain orchestrates eating behavior could lead to better treatments for disorders such as anorexia and obesity, he says. Scientists led by Joshua Jennings and Garret Stuber of the University of North Carolina at Chapel Hill genetically tweaked mice so that a small group of neurons would respond to light. When a laser shone into the brain, these cells would either fire or, in a different experiment, stay quiet. These neurons reside in a brain locale called the bed nucleus of the stria terminalis, or BNST. Some of the message-sending arms of these neurons reach into the lateral hypothalamus, a brain region known to play a big role in feeding. When a laser activated these BNST neurons, the mice became ravenous, voraciously eating their food, the researchers report in the Sept. 27 Science. “As soon as you turn it on, they start eating and they don’t stop until you turn it off,” Stuber says. The opposite behavior happened when a laser silenced BNST neurons’ messages to the lateral hypothalamus: The mice would not eat, even when hungry. © Society for Science & the Public 2000 - 2013
Link ID: 18717 - Posted: 09.28.2013
By Tara Haelle A change in the way anorexia is diagnosed may make it easier to help more teens, not just thin ones, with the illness. Previously, overweight or obese teens were more likely to fall through the cracks when they developed anorexic behaviors. Now, the release of the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) has broadened the disorder criteria by taking away the weight requirement. The change shifts the focus of the diagnosis from “being thin” to the behaviors of those with the illness. The previous criteria perpetuated the idea that anorexia is a weight disorder—rather than a psychological one. “A lot of people need help even if they don’t narrowly fit the definition of an illness,” says David Hahn, medical director of The Renfrew Center of Philadelphia. “This criteria makes clear that the behaviors, even without a very low weight, are pathologic and need to be addressed. The criteria may very much help pediatricians catch an eating disorder sooner and may teach the public and families to intervene more quickly if it’s understood that anorexia doesn’t only mean underweight.” Anorexia nervosa most often begins in adolescence and affects approximately 0.3 percent of teens. An additional 0.8 percent were found in one large study to have “subthreshold anorexia nervosa”—they showed the symptoms but did not meet all the criteria. Overall, about 6 percent of teens suffer from some kind of eating disorder, such as bulimia, binge-eating and other eating issues previously classified in the DSM-IV as “Eating Disorder—Not Otherwise Specified” (ED-NOS). © 2013 Scientific American
Keyword: Anorexia & Bulimia
Link ID: 18704 - Posted: 09.26.2013
Declan Butler Ghost writing is taking on an altogether different meaning in a mysterious case of alleged scientific fraud. The authors of a paper published in July (A. Vezyraki et al. Biochem. Biophys. Res. Commun. http://doi.org/nxb; 2013), which reported significant findings in obesity research, seem to be phantoms. They are not only unknown at the institution listed on the paper, but no trace of them as researchers can be found. The paper, published in the Elsevier journal Biochemical and Biophysical Research Communications (BBRC), is not the kind of prank that journals have encountered before, in which hoaxsters have submitted dummy papers to highlight weaknesses in the peer-review process. The paper’s reported findings — that overexpression of two novel proteins in fat cells leads to improvements in metabolic processes related to diabetes and obesity in mice — are, in fact, true. Too true, in the opinion of Bruce Spiegelman, a cell biologist at Harvard Medical School’s Dana-Farber Cancer Institute in Boston, Massachusetts. He says that he has presented similar findings at about six research meetings, and is preparing to submit them to a journal. He suspects that the BBRC paper was intended as a spoiler of his own lab’s work. Now withdrawn, the article lists five authors who are all supposedly from the School of Health Sciences at the University of Thessaly in Trikala, Greece, and is entitled ‘Identification of meteorin and metrnl as two novel pro-differentiative adipokines: Possible roles in controlling adipogenesis and insulin sensitivity’. Adipokines are proteins secreted by fat tissue that play an active part in such processes as sugar and fat metabolism, inflammation and obesity-related metabolic disorders, including insulin resistance and diabetes. © 2013 Nature Publishing Group
Link ID: 18701 - Posted: 09.25.2013
By Michelle Roberts Health editor, BBC News online People prescribed anti-depressants should be aware they could be at increased risk of type 2 diabetes, say UK researchers. The University of Southampton team looked at available medical studies and found evidence the two were linked. But there was no proof that one necessarily caused the other. It may be that people taking anti-depressants put on weight which, in turn, increases their diabetes risk, the team told Diabetes Care journal. Or the drugs themselves may interfere with blood sugar control. Their analysis of 22 studies involving thousands of patients on anti-depressants could not single out any class of drug or type of person as high risk. Prof Richard Holt and colleagues say more research is needed to investigate what factors lie behind the findings. And they say doctors should keep a closer check for early warning signs of diabetes in patients who have been prescribed these drugs. With 46 million anti-depressant prescriptions a year in the UK, this potential increased risk is worrying, they say. Prof Holt said: "Some of this may be coincidence but there's a signal that people who are being treated with anti-depressants then have an increased risk of going on to develop diabetes. BBC © 2013