Links for Keyword: Obesity

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By ANAHAD O’CONNOR Anyone who has ever been on a diet knows that the standard prescription for weight loss is to reduce the amount of calories you consume. But a new study, published Tuesday in JAMA, may turn that advice on its head. It found that people who cut back on added sugar, refined grains and highly processed foods while concentrating on eating plenty of vegetables and whole foods — without worrying about counting calories or limiting portion sizes — lost significant amounts of weight over the course of a year. The strategy worked for people whether they followed diets that were mostly low in fat or mostly low in carbohydrates. And their success did not appear to be influenced by their genetics, a finding that casts doubt on the increasingly popular idea that different diets should be recommended to people based on their DNA makeup. The research lends strong support to the notion that diet quality, not quantity, is what helps people lose and manage their weight most easily in the long run. It also suggests that health authorities should shift away from telling the public to obsess over calories and instead encourage Americans to avoid processed foods that are made with refined starches and added sugar, like bagels, white bread, refined flour and sugary snacks and beverages, said Dr. Dariush Mozaffarian, a cardiologist and dean of the Friedman School of Nutrition Science and Policy at Tufts University. “This is the road map to reducing the obesity epidemic in the United States,” said Dr. Mozaffarian, who was not involved in the new study. “It’s time for U.S. and other national policies to stop focusing on calories and calorie counting.” The new research was published in JAMA and led by Christopher D. Gardner, the director of nutrition studies at the Stanford Prevention Research Center. It was a large and expensive trial, carried out on more than 600 people with $8 million in funding from the National Institutes of Health, the Nutrition Science Initiative and other groups. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24685 - Posted: 02.21.2018

Nicola Davis While you might be tempted to wolf down a sandwich or gobble up your dinner, researchers say there may be advantages to taking your time over a meal. According to a study looking at type 2 diabetics, eating slowly could help prevent obesity, with researchers finding a link to both lower waist circumference and body mass index (BMI). “Interventions aimed at altering eating habits, such as education initiatives and programmes to reduce eating speed, may be useful in preventing obesity and reducing the risk of non-communicable diseases,” the authors write. The latest study is not the first to suggest that taking a sedate pace at the dinner table could be beneficial: various pieces of work have hinted that those who eat quickly are more likely to be overweight, have acid reflux and have metabolic syndrome. The latest study, published in the journal BMJ Open by researchers in Japan, looked at data collected though health checkups and claims from more than 59,700 individuals as part of health insurance plans, with data spanning from 2008 to mid-2013. As part of the health checkup, participants were asked seven questions about their lifestyle, including whether their eating speed was fast, normal or slow, whether they snacked after dinner three times or more a week, and whether they skipped breakfast three times or more a week. © 2018 Guardian News and Media Limited

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 14: Attention and Consciousness
Link ID: 24653 - Posted: 02.13.2018

By ANDREW JACOBS SANTIAGO, Chile — They killed Tony the Tiger. They did away with Cheetos’ Chester Cheetah. They banned Kinder Surprise, the chocolate eggs with a hidden toy. The Chilean government, facing skyrocketing rates of obesity, is waging war on unhealthy foods with a phalanx of marketing restrictions, mandatory packaging redesigns and labeling rules aimed at transforming the eating habits of 18 million people. Nutrition experts say the measures are the world’s most ambitious attempt to remake a country’s food culture, and could be a model for how to turn the tide on a global obesity epidemic that researchers say contributes to four million premature deaths a year. “It’s hard to overstate how significant Chile’s actions are — or how hard it has been to get there in the face of the usual pressures,” said Stephen Simpson, director of the Charles Perkins Centre, an organization of scholars focused on nutrition and obesity science and policy. The multibillion dollar food and soda industries have exerted those pressures to successfully stave off regulation in many other countries. Since the food law was enacted two years ago, it has forced multinational behemoths like Kellogg to remove iconic cartoon characters from sugary cereal boxes and banned the sale of candy like Kinder Surprise that use trinkets to lure young consumers. The law prohibits the sale of junk food like ice cream, chocolate and potato chips in Chilean schools and proscribes such products from being advertised during television programs or on websites aimed at young audiences. Beginning next year, such ads will be scrubbed entirely from TV, radio and movie theaters between 6 a.m. and 10 p.m. In an effort to encourage breast-feeding, a ban on marketing infant formula kicks in this spring. The linchpin of the initiative is a new labeling system that requires packaged food companies to prominently display black warning logos in the shape of a stop sign on items high in sugar, salt, calories or saturated fat. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24633 - Posted: 02.08.2018

By RONI CARYN RABIN Most dieters know the hard truth: Sticking to a weight loss regimen gets more difficult as the day wears on. But while those who give in to food cravings and binge at night may blame flagging willpower, a new study suggests the problem could lie in the complex orchestra of hormones that drive hunger and signal feelings of satiety, or fullness. The small study of 32 obese men and women, half of whom had a habit of binge eating, suggests that satiety hormones may be lower during the evening hours, while hunger hormones rise toward nightfall and may be stoked even higher by stressful situations. Overweight binge eaters may be particularly susceptible to the influence of fluctuations in these appetite-regulating hormones, the researchers found. “There’s more opportunity to eat in the evening, but this study is showing that hormonal responses are setting them up to do this,” said Susan Carnell, an assistant professor of psychiatry and behavioral sciences at Johns Hopkins University School of Medicine who was a first author of the study along with Charlotte Grillot of Florida State University. It’s not clear whether these hormonal patterns precede and cause the binge eating behaviors or are conditioned by an individual’s eating habits, Dr. Carnell said. But either way, “you can get stuck in the cycle.” The study is an important reminder that myriad factors contribute to weight gain, and that shaming and blaming people for their weight problems is inappropriate, said Kelly Costello Allison, director of the Center for Weight and Eating Disorders at the University of Pennsylvania, who was not involved in the new research. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 8: Hormones and Sex
Link ID: 24591 - Posted: 01.31.2018

By JANE E. BRODY The media love contrarian man-bites-dog stories that purport to debunk long-established beliefs and advice. Among the most popular on the health front are reports that saturated fats do not cause heart disease and that the vegetable oils we’ve been encouraged to use instead may actually promote it. But the best-established facts on dietary fats say otherwise. How well polyunsaturated vegetable oils hold up health-wise when matched against saturated fats like butter, beef fat, lard and even coconut oil depends on the quality, size and length of the studies and what foods are eaten when fewer saturated fats are consumed. So before you succumb to wishful thinking that you can eat well-marbled steaks, pork ribs and full-fat dairy products with abandon, you’d be wise to consider the findings of what is probably the most comprehensive, commercially untainted review of the dietary fat literature yet published. They are found in a 26-page advisory prepared for the American Heart Association and published last June by a team of experts led by Dr. Frank M. Sacks, professor of cardiovascular disease prevention at the Harvard T.H. Chan School of Public Health. The report helps to explain why the decades-long campaign to curb cardiovascular disease by steering the American diet away from animal fats has been less successful than it might have been and how it inadvertently promoted expanding waistlines and an epidemic of Type 2 diabetes. When people cut back on a particular nutrient, they usually replace it with something else to maintain their needed caloric input. Unfortunately, in too many cases, saturated fats — and fats in general — gave way to refined carbohydrates and sugars, the so-called SnackWell phenomenon that prompted fat-wary eaters to overindulge in high-calorie, low-nutrient foods. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24585 - Posted: 01.30.2018

Laura Sanders Nerve cells in the brain make elaborate connections and exchange lightning-quick messages that captivate scientists. But these cells also sport simpler, hairlike protrusions called cilia. Long overlooked, the little stubs may actually have big jobs in the brain. Researchers are turning up roles for nerve cell cilia in a variety of brain functions. In a region of the brain linked to appetite, for example, cilia appear to play a role in preventing obesity, researchers report January 8 in three studies in Nature Genetics. Cilia perched on nerve cells may also contribute to brain development, nerve cell communication and possibly even learning and memory, other research suggests. “Perhaps every neuron in the brain possesses cilia, and most neuroscientists don’t know they’re there,” says Kirk Mykytyn, a cell biologist at Ohio State University College of Medicine in Columbus. “There’s a big disconnect there.” Most cells in the body — including those in the brain — possess what’s called a primary cilium, made up of lipid molecules and proteins. The functions these appendages perform in parts of the body are starting to come into focus (SN: 11/3/12, p. 16). Cilia in the nose, for example, detect smell molecules, and cilia on rod and cone cells in the eye help with vision. But cilia in the brain are more mysterious. © Society for Science & the Public 2000 - 2017.

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 24546 - Posted: 01.20.2018

By GRETCHEN REYNOLDS Our skeletons may help to keep our weight stable, according to a fascinating new study with animals. The study suggests that bones could be much more intimately involved in tracking weight and controlling appetite than scientists realized. It also raises interesting questions about whether a sedentary lifestyle could cause us to pack on pounds in part by discombobulating our sensitive bones. There is no question that our bodies like to maintain whatever weight they have sustained for any period of time. This is in large part because of our biological predilection for homeostasis, or physiological stability, which prompts our bodies to regain any weight that we lose and, in theory, lose any weight that we gain. To achieve this stability, however, our bodies have to be able to sense how much we weigh, note when that weight changes, and respond accordingly, as if we contained an internal bathroom scale. It has not been clear how our bodies manage this trick. Some years ago, scientists did discover one of the likely mechanisms, which involves leptin, a hormone released by fat cells. In broad terms, when people add fat, they produce more leptin, which then jump-starts processes in the brain that reduce appetite and should cause their bodies to drop that new weight. But obviously this system is not perfect or no one would hold on to added pounds. So for the new study, which was published this month in Proceedings of the National Academy of Sciences, an international group of researchers began to wonder whether there might be other processes at work. To find out, they first gathered groups of mice and rats. They chose both species, hoping that, if any results were common to each, this might indicate that they also could occur in other mammals, including, potentially, us. Then the scientists implanted tiny capsules into each rodent’s abdomen. Some contained weights equaling about 15 percent of each animal’s body mass. Others were empty. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24534 - Posted: 01.17.2018

Nicola Davis Obese patients undergoing stomach-shrinking surgery have half the risk of death in the years that follow compared with those tackling their weight through diet and behaviour alone, new research suggests. Experts say obesity surgery is cost-effective, leads to substantial weight loss and can help tackle type 2 diabetes. But surgeons say not enough of the stomach-shrinking surgeries are carried out in the UK, with figures currently lagging behind other European countries, including France and Belgium – despite the latter having a smaller population. “We don’t think this [new study] alone is sufficient to conclude that obese patients should push for bariatric surgery, but this additional information certainly seems to provide additional support,” said Philip Greenland, co-author of the latest study from Northwestern University. In the new study, one of several on obesity surgery published in the Journal of the American Medical Association, researchers sought to explore whether stomach-shrinking operations, known as bariatric surgery, had a long-term impact on the risk of death among obese individuals, compared with non-surgical approaches to weight loss. In total, more than 33,500 participants were involved in the study – 8,385 of whom had one of three types of bariatric surgery between 2005 and 2014. The majority of participants had a BMI greater than 35; obesity is defined as a BMI of 30 or higher. © 2018 Guardian News and Media Limited

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24533 - Posted: 01.17.2018

By Asha Tomlinson, Tyana Grundig, CBC News Barb Litt, 49, decided to have gastric band surgery at a private clinic in Toronto two years ago because she'd hit a low point in her life. She was depressed, unemployed and desperate to lose weight. But rather than shedding a few pounds, the mother of two ended up gaining a $12,000 debt she can't shake and a shooting pain in her side that ultimately required a second operation in hospital to remove the silicone band around her stomach that was supposed to shrink her appetite. A new Marketplace investigation reveals Litt's painful experience is hardly unique. The clinic that performed Litt's surgery, Slimband, no longer offers the procedure. Its former chief surgeon had his licence temporarily suspended by the Ontario College of Physicians and Surgeons last April, following years of complaints from clients. But the financing company linked to the clinic, Credit Medical, is still busy collecting money from clients like Litt, who took out high-interest loans to pay for the procedure. Because of the many complications with gastric bands, including erosion, bleeding, slippage and blockages, 2,363 of the devices have had to be surgically removed in public hospitals across Canada, excluding Quebec, since 2010, according to the Canadian Institute for Health Information. Each removal costs between $3,000 and $14,000, meaning taxpayers are on the hook for up to $33 million. ©2018 CBC/Radio-Canada.

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24521 - Posted: 01.12.2018

By Abby Olena Most mammalian cells have a primary cilium, an antenna-like, immobile surface projection that senses the surrounding environment. Researchers report in Nature Genetics today (January 8) that proteins localized to the cilia of neurons in the hypothalamus control food intake in mice. Furthermore, two human genetics studies published in Nature Genetics today tie variants of a neuronal ciliary gene, adenylyl cyclase 3 (ADCY3), identified in people from Pakistan, Greenland, and the United States, to an increased risk of obesity and diabetes. “This [mouse] paper contributes nicely to a consensus that cilia are important in the brain for energy homeostasis and feeding behaviors,” says Nick Berbari, a biologist at Indiana University–Purdue University Indianapolis who did not participate in the study. “It’s interesting to think about how cilia function could be important for the general population, [not] just in rare instances of ciliopathies,” he adds. Ciliopathies—rare diseases caused by mutations in genes that affect the primary cilia—can produce a variety of symptoms, including extra fingers or toes, retinal degeneration, and obesity, coauthor Christian Vaisse, a geneticist at the University of California, San Francisco, tells The Scientist. “Relatively recently, it was found that the obesity in ciliopathies was linked to a role of the primary cilium in neurons because the genetic removal of primary cilia from all neurons in an adult mouse leads to obesity,” he explains. © 1986-2018 The Scientist

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24511 - Posted: 01.10.2018

By Jessica Hamzelou Did you pile on the pounds this Christmas? At least you can take some comfort in the fact that not all fat is bad. Evidence in mice and monkeys suggests it is important for storing important immune cells and may even make them more effective at fighting infection. Yasmine Belkaid at the US National Institutes of Health and her team have found that a type of immune cell – called a memory T-cell – seems to be stored in the body fat of mice. These cells learn to fight infection. Once exposed to a pathogen, they mount a stronger response the next time they encounter it. When the researchers infected mice with parasites or bacteria, they found that memory T-cells clustered densely in the animals’ body fat. Tests showed that these cells seemed to be more effective than those stored in other organs, being better at replicating and at releasing infection-fighting chemicals, for example. After exposing the mice to the same pathogens again, the memory T-cells stored in their fat were the fastest to respond. Belkaid’s team found that monkeys also have plenty of memory T-cells in their body fat, and that these cells worked better than those from other organs. “It means that fat tissue is not only a reservoir for memory cells, but those memory cells have enhanced function,” says Belkaid. “The tissue is like a magic potion that can optimally activate the T-cells.” © Copyright New Scientist Ltd.

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Emotions, Aggression, and Stress
Link ID: 24473 - Posted: 12.30.2017

By Catherine Offord Jerrold Olefsky has spent much of the last decade trying to decipher the connection between obesity and the risk for type 2 diabetes. It’s now known that “in obesity, the adipose tissue becomes highly inflamed and fills up with macrophages and other immune cells,” Olefsky, an endocrinologist at the University of California, San Diego, explains. “This inflammation is very important for causing insulin resistance,” in which cells fail to respond to hormonal signals to take up glucose. But a crucial piece of the puzzle has been missing. “Insulin resistance is a systemic thing,” Olefsky says. For inflamed fat tissue to trigger it, “somehow, all the tissues must talk to each other. We just didn’t know how.” Research has not supported a major role for early suspects such as cytokines. But reading a paper a few years ago on the role of tiny vesicles called exosomes in intercellular communication in cancer, Olefsky was struck by the fact that, “Well, gee, all these cells make exosomes.” Known to carry microRNAs (miRNAs)—small nucleic acids that influence gene expression—exosomes seemed like plausible candidates for an inter-tissue communication system in obesity. Olefsky’s group isolated macrophages from adipose tissue in obese and lean mice and harvested exosomes produced by the cells in vitro. Then, the researchers added these vesicles to cultured muscle, liver, and fat cells—major insulin targets in the body. While lean-type exosomes made recipient cells “super insulin-sensitive,” Olefsky says, obese-type exosomes induced insulin resistance. In vivo work showed a similar effect: lean mice injected with obese-type exosomes became insulin resistant without gaining weight, while obese mice treated with lean-type exosomes stayed obese, but developed normalized insulin sensitivity. © 1986-2017 The Scientist

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24450 - Posted: 12.22.2017

Esther Landhuis Picture this: While reaching for the cookie jar — or cigarette or bottle of booze or other temptation — a sudden slap denies your outstretched hand. When the urge returns, out comes another slap. Now imagine those "slaps" occurring inside the brain, protecting you in moments of weakness. In a report published Monday in the Proceedings of the National Academy of Sciences, Stanford neuroscientists say they've achieved this sort of mind-reading in binge-eating mice. They found a telltale pattern of brain activity that comes up seconds before the animals start to pig out — and delivering a quick zap to that part of the brain kept the mice from overindulging. Whether this strategy could block harmful impulses in people remains unclear. For now the path seems promising. The current study used a brain stimulation device already approved for hard-to-treat epilepsy. And based on the new findings, a clinical trial testing this off-the-shelf system for some forms of obesity could start as early as next summer, says Casey Halpern, the study's leader and an assistant professor of neurosurgery at Stanford. He thinks the approach could also work for eating disorders and a range of other addictive or potentially life-threatening urges. As a physician-researcher, Halpern specializes in deep brain stimulation (DBS), a surgical treatment in which battery-powered implants send electrical pulses to brain areas where signals go awry. © 2017 npr

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 24440 - Posted: 12.19.2017

Eating is prompted, in part, by brain regions that help to maintain the body’s energy levels. But hunger pangs are not the only motivation for a trip to the snack bar. In an effort to understand how the brain’s emotional and cognitive machinery influences appetite, Yunlei Yang and his colleagues at the State University of New York Upstate Medical University in Syracuse examined the medial septal complex, a group of brain cells that has a role in emotion. Some of the complex’s cells produce a signalling chemical called glutamate. When the scientists turned on these glutamate-producing cells in mice, the animals ate less than half as much as control mice. That makes the region a good starting point for studies of emotionally triggered eating, the team says. Proc. Natl Acad. Sci. USA (2017)

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Emotions, Aggression, and Stress
Link ID: 24420 - Posted: 12.14.2017

By Mitch Leslie Scientists once had high hopes that inhibiting a hormone named ghrelin would be the key to preventing obesity. Ghrelin didn’t turn out to be a weight loss panacea. But now, the discovery of the first molecule naturally made by the body that blocks ghrelin’s effects may open up new avenues for treating other conditions, including diabetes and anorexia. The finding may also explain some of the benefits of bariatric surgery, which shrinks or reroutes the stomach to control weight. “It’s a very impressive piece of research,” says bariatric physician Carel le Roux of University College Dublin, who wasn’t connected to the study. “I think it will have significant clinical impact.” When researchers discovered ghrelin about 20 years ago, they dubbed it the “hunger hormone” because early results suggested it ramped up our appetite. But studies soon found that thwarting the molecule didn’t curtail food consumption or promote weight loss in mice. Still, the hormone induces a variety of other positive changes in our metabolism. For example, ghrelin may bolster muscle strength, spurring scientists to test whether drugs that mimic the hormone can counteract the muscle deterioration and weakness often suffered by cancer patients. The new study didn’t start as a hunt for ghrelin-blocking compounds. Instead, a team headed by researchers at NGM Biopharmaceuticals in South San Francisco, California, was investigating how bariatric surgery overhauls metabolism. The scientists operated on obese mice, performing a type of bariatric surgery called vertical sleeve gastrectomy that involves removing most of the stomach. They then examined which genes became more or less active after the procedure. As they report online today in Cell Metabolism, the rodents’ downsized stomachs produced 52 times more of a protein named LEAP2 than normal. © 2017 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 8: Hormones and Sex
Link ID: 24407 - Posted: 12.08.2017

Jessica Brown Sugar’s demise from childhood staple to public enemy can be seen everywhere. Chocolate bars are shrinking, sugary drinks are set to be taxed and our recommended daily sugar intake has been slashed in half. But the battle against sugar might have begun sooner if the industry hadn’t kept secrets to protect its commercial interests, according to new findings. In 1967, when scientists were arguing over the link between sugar consumption and increased risk of heart disease, researchers now claim that the International Sugar Research Foundation (ISRF) withheld findings that rats that were fed a high-sugar diet had higher levels of triglycerides (a fat found in the blood) than those fed starch. In a move researchers from the University of California at San Francisco have compared to the tobacco industry’s self-preservation tactics, the foundation stopped funding the project. Cristin Kearns, one of the researchers who analysed ISRF documents, says, “ISRF’s research was designed to cast doubt on the importance of elevated triglycerides in the blood as a heart disease risk factor. It is now commonly accepted that triglycerides are a risk factor, but this was controversial for decades. I think the scientific community would have come to consensus about elevated triglycerides being a risk factor for heart disease much sooner [if the research been published].” A year later the foundation funded Project 259, looking into the effects of sucrose consumption in the intestinal tracts of rats. It found a possible link between sugar consumption and increased risk of bladder cancer, and described the findings as “one of the first demonstrations of a biological difference between sucrose and starch fed rats”. But the ISRF terminated the project’s funding before the experiments were finished, despite the study having already lasted 27 months, and requiring only three more months. © 2017 Guardian News and Media Limited

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24365 - Posted: 11.27.2017

By Diana Kwon | Most of us are familiar with the role of smell in our dining habits—that basket of freshly baked cookies is usually much harder to resist than a plate of odorless carrot sticks, and the taste of food is strongly tied to its aroma. But animals’ sense of smell is even more intricately linked with eating and metabolism. Prior studies have shown that, in humans, fasting enhances olfactory sensitivity, while satiety reduces it. And a new study, published today (July 5) in Cell Metabolism, suggests that, at least in mice, this link may go even further—animals engineered to lack a sense of smell gained less weight and burned more fat than their unaltered counterparts. This difference in weight gain was almost entirely due to alterations in body fat composition. “The major thing was that [the mice lacking smell] weren’t gaining fat,” coauthor Andrew Dillin, a biology professor at the University of California, Berkeley, tells The Scientist. “Somehow, the olfactory system is engaging the major control circuit in the brain that controls peripheral metabolism . . . and that is turning on a program to burn fat.” Dillin says his team was interested in knowing whether simply eating fattening food led to weight gain, or if it was how the olfactory system “perceived” those calories that matters. To assess this link between olfaction and metabolism, scientists genetically engineered mice that expressed a gene for a diphtheria toxin receptor on olfactory sensory neurons. Once the animals were around seven weeks old, the researchers injected the toxin to kill off these nerve cells and found that these animals had lost their sense of smell. Control animals generated without this receptor retained all their smell neurons after receiving the toxin. © 1986-2017 The Scientist

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 24352 - Posted: 11.24.2017

By Abby Olena Two people with a rare genetic disorder have helped shed light on the fundamental neuroscience of appetite and, scientists say, opened up a new target for potential obesity treatments. Neonatal progeroid syndrome (NPS) affects only a handful of people worldwide. The most telling features of the condition are an aged appearance due to an absence of the fat layer under the skin and extreme thinness. Researchers report in in Nature Medicine today (November 6) that a glucose-releasing hormone involved in the disease crosses the blood-brain barrier and homes in on neurons that regulate appetite in mice. The study suggests it might be possible to target the hormone, asprosin, in the treatment of diabetes and obesity. “Rare diseases with extreme phenotypes like this are very valuable to learn important things that then apply to more common diseases,” says coauthor and medical geneticist Atul Chopra of Baylor College of Medicine in Houston, Texas. Chopra and colleagues showed in a previous study that patients with NPS have mutations near the end of a gene called FBN1, which encodes profibrillin. It was already known that profibrillin is processed to form fibrillin 1, an extracellular matrix protein. The 140-amino-acid chunk cleaved from the end of profibrillin, which Chopra’s group named asprosin, is secreted by adipose tissue and functions as a hormone that causes the liver to make glucose. They determined that two individuals with NPS are heterozygous for FBN1 mutations and have greatly reduced levels of circulating asprosin. © 1986-2017 The Scientist

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24351 - Posted: 11.24.2017

By Bob Grant In 1971, a 27-year-old, 456-pound man went to the University of Dundee’s department of medicine in Scotland looking for help. Patient A.B., as doctors referred to him, needed to lose weight. His physicians recommended a short but drastic course of action: stop eating altogether. The patient responded so well to a brief stint without food that he decided to prolong the deprivation—for more than a year. “[H]is fast was continued into what is presently the longest recorded fast (Guinness Book of Records, 1971),” the clinicians wrote in a 1973 case report, claiming A.B. suffered little or no untoward effects on his health.1 And at the end of his 382-day dietary abstinence, during which he had ingested only vitamin supplements, yeast, and noncaloric fluids, A.B. had lost a remarkable 276 pounds. When doctors checked back in on A.B. five years later, their patient reported gaining back only about 15 pounds. Although aspects of this published report seem almost unbelievable, and the period of fasting is obviously extreme, the case highlights some of the metabolic dynamics that result when bodies are deprived of food. For example, when external calories stop fueling an animal’s metabolism, stores of triglycerides in fat cells are mobilized, and levels of ketones—chemicals that result from the burning of fat for fuel—rise. Decreases in body weight follow. © 1986-2017 The Scientist

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24350 - Posted: 11.24.2017

By Stephani Sutherland When we experience something painful, our brain produces natural painkillers that are chemically similar to potent drugs such as morphine. Now research suggests these endogenous opioids also play another role: helping regulate the body's energy balance. Lauri Nummenmaa, a brain-imaging scientist at the University of Turku in Finland, and his colleagues measured endogenous opioid release in the brains of 10 healthy men. The subjects were injected with a radioactive substance that binds to opioid receptors, making it possible to visualize the receptors' activity using positron-emission tomography. The study found evidence of natural painkillers in the men's brains after they ate a palatable meal of pizza. Surprisingly, their brains released even more of the endogenous opioids after they ate a far less enticing—but nutritionally similar—liquid meal of what Nummenmaa called “nutritional goo.” Although the subjects rated the pizza as tastier than the goo, opioid release did not appear to relate to their enjoyment of the meal, the researchers reported earlier this year in the Journal of Neuroscience. Advertisement “I would've expected the opposite result,” says Paul Burghardt, an investigator at Wayne State University, who was not involved in the work. After all, previous human and animal studies led researchers to believe that endogenous opioids helped to convey the pleasure of eating. Nummenmaa, too, was surprised. His group's earlier research showed that obese people's brains had fewer opioid receptors—but that receptor levels recover with weight loss. “Maybe when people overeat, endogenous opioids released in the brain constantly bombard the receptors, so they [decrease in number],” he says. © 2017 Scientific American

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 24347 - Posted: 11.22.2017