Links for Keyword: Obesity

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By Elizabeth Pennisi The microbes that live in your body outnumber your cells 10 to one. Recent studies suggest these tiny organisms help us digest food and maintain our immune system. Now, researchers have discovered yet another way microbes keep us healthy: They are needed for closing the blood-brain barrier, a molecular fence that shuts out pathogens and molecules that could harm the brain. The findings suggest that a woman's diet or exposure to antibiotics during pregnancy may influence the development of this barrier. The work could also lead to a better understanding of multiple sclerosis, in which a leaky blood-brain barrier may set the stage for a decline in brain function. The first evidence that bacteria may help fortify the body’s biological barriers came in 2001. Researchers discovered that microbes in the gut activate genes that code for gap junction proteins, which are critical to building the gut wall. Without these proteins, gut pathogens can enter the bloodstream and cause disease. In the new study, intestinal biologist Sven Pettersson and his postdoc Viorica Braniste of the Karolinska Institute in Stockholm decided to look at the blood-brain barrier, which also has gap junction proteins. They tested how leaky the blood-brain barrier was in developing and adult mice. Some of the rodents were brought up in a sterile environment and thus were germ-free, with no detectable microbes in their bodies. Braniste then injected antibodies—which are too big to get through the blood-brain barrier—into embryos developing within either germ-free moms or moms with the typical microbes, or microbiota. © 2014 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 2: Cells and Structures: The Anatomy of the Nervous System; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 20338 - Posted: 11.20.2014

By Nicholas Bakalar Exposure to secondhand smoke and roadway traffic may be tied to increased body mass index in children and adolescents, a new study suggests. Researchers studied 3,318 children in 12 Southern California communities beginning at an average age of 10, and then followed them through age 18. They used parental questionnaires to establish exposure to smoking, and data on traffic volume and levels of nitrogen dioxide, ozone and particulates to track pollution. The study, in Environmental Health Perspectives, controlled for many other factors: sex, initial B.M.I., asthma, physical activity, insurance status, parental education and income, acres of parks and open space nearby, percentage of people living in poverty in each community. But even after accounting for these issues and more, they found that compared with children exposed to no secondhand smoke or near-roadway air pollution, B.M.I. was 0.80 higher in children exposed to pollution alone, 0.85 higher in those exposed to secondhand smoke alone, and 2.15 higher in those exposed to both. A normal B.M.I. for adults is 18.5 to 24.9. Higher than 25 is considered overweight, and above 30 obese. “It would be interesting to know more about the mechanism,” said the lead author, Dr. Rob McConnell, a professor of preventive medicine at the University of Southern California. “But the finding challenges the view that obesity is due solely to increased caloric intake and reduced physical activity. That’s not the whole story.” © 2014 The New York Times Company

Related chapters from BP7e: 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: 20322 - Posted: 11.18.2014

By Adam Brimelow Health Correspondent, BBC News A Mediterranean diet may be a better way of tackling obesity than calorie counting, leading doctors have said. Writing in the Postgraduate Medical Journal (PMJ), the doctors said a Mediterranean diet quickly reduced the risk of heart attacks and strokes. And they said it may be better than low-fat diets for sustained weight loss. Official NHS advice is to monitor calorie intake to maintain a healthy weight. Last month NHS leaders stressed the need for urgent action to tackle obesity and the health problems that often go with it. The PMJ editorial argues a focus on food intake is the best approach, but it warns crash dieting is harmful. Signatories of the piece included the chair of the Academy of Medical Royal Colleges, Prof Terence Stephenson, and Dr Mahiben Maruthappu, who has a senior role at NHS England. They criticise the weight-loss industry for focusing on calorie restriction rather than "good nutrition". And they make the case for a Mediterranean diet, including fruit and vegetables, nuts and olive oil, citing research suggesting it quickly reduces the risk of heart attacks and strokes, and may be better than low-fat diets for sustained weight loss. The lead author, cardiologist Dr Aseem Malhotra, says the scientific evidence is overwhelming. "What's more responsible is that we tell people to concentrate on eating nutritious foods. "It's going to have an impact on their health very quickly. We know the traditional Mediterranean diet, which is higher in fat, proven from randomised controlled trials, reduces the risk of heart attack and stroke even within months of implementation." The article also says adopting a Mediterranean diet after a heart attack is almost three times as effective at reducing deaths as taking cholesterol-lowering statin medication. BBC © 2014

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 20316 - Posted: 11.17.2014

Sara Reardon Companies selling ‘probiotic’ foods have long claimed that cultivating the right gut bacteria can benefit mental well-being, but neuroscientists have generally been sceptical. Now there is hard evidence linking conditions such as autism and depression to the gut’s microbial residents, known as the microbiome. And neuroscientists are taking notice — not just of the clinical implications but also of what the link could mean for experimental design. “The field is going to another level of sophistication,” says Sarkis Mazmanian, a microbiologist at the California Institute of Technology in Pasadena. “Hopefully this will shift this image that there’s too much commercial interest and data from too few labs.” This year, the US National Institute of Mental Health spent more than US$1 million on a new research programme aimed at the microbiome–brain connection. And on 19 November, neuroscientists will present evidence for the link in a symposium at the annual Society for Neuroscience meeting in Washington DC called ‘Gut Microbes and the Brain: Paradigm Shift in Neuroscience’. Although correlations have been noted between the composition of the gut microbiome and behavioural conditions, especially autism1, neuroscientists are only now starting to understand how gut bacteria may influence the brain. The immune system almost certainly plays a part, Mazmanian says, as does the vagus nerve, which connects the brain to the digestive tract. Bacterial waste products can also influence the brain — for example, at least two types of intestinal bacterium produce the neurotransmitter γ-aminobutyric acid (GABA)2. © 2014 Nature Publishing Group

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 20310 - Posted: 11.13.2014

By James Gallagher Health editor, BBC News website Weight loss surgery can dramatically reduce the odds of developing type 2 diabetes, according to a major study. Doctors followed nearly 5,000 people as part of a trial to assess the health impact of the procedure. The results, published in the Lancet Diabetes and Endocrinology journal, showed an 80% reduction in type 2 diabetes in those having surgery. The UK NHS is considering offering the procedure to tens of thousands of people to prevent diabetes. Obesity and type 2 diabetes are closely tied - the bigger someone is, the greater the risk of the condition. The inability to control blood sugar levels can result in blindness, amputations and nerve damage. Around a tenth of NHS budgets are spent on managing the condition. Surgery The study followed 2,167 obese adults who had weight loss - known as bariatric - surgery. They were compared to 2,167 fellow obese people who continued as they were. There were 38 cases of diabetes after surgery compared with 177 in people left as they were - a reduction of nearly 80%. Around 3% of morbidly obese people develop type 2 each year, however, surgery reduced the figure to around 0.5%, which is the background figure for the whole population. Bariatric surgery, also known as weight loss surgery, is used as a last resort to treat people who are dangerously obese and carrying an excessive amount of body fat. This type of surgery is available on the NHS only to treat people with potentially life-threatening obesity when other treatments have not worked. Around 8,000 people a year currently receive the treatment. The two most common types of weight loss surgery are: Gastric band, where a band is used to reduce the size of the stomach so a smaller amount of food is required to make someone feel full Gastric bypass, where the digestive system is re-routed past most of the stomach so less food is digested to make someone feel full BBC © 2014

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 20269 - Posted: 11.03.2014

Daniel Duane, Men's Journal For more than half a century, the conventional wisdom among nutritionists and public health officials was that fat is dietary enemy No. 1 — the leading cause of obesity and heart disease. It appears the wisdom was off. And not just off. Almost entirely backward. According to a new study from the National Institutes of Health, a diet that reduces carbohydrates in favor of fat — including the saturated fat in meat and butter — improves nearly every health measurement, from reducing our waistlines to keeping our arteries clear, more than the low-fat diets that have been recommended for generations. "The medical establishment got it wrong," says cardiologist Dennis Goodman, director of Integrative Medicine at New York Medical Associates. "The belief system didn't pan out." It's not the conclusion you would expect given the NIH study's parameters. Lead researcher Lydia Bazanno, of the Tulane University School of Public Health, pitted this high-fat, low-carb diet against a fat-restricted regimen prescribed by the National Cholesterol Education Program. "We told both groups to get carbs from green, leafy vegetables, because those are high in nutrients and fiber to keep you sated," Bazanno says. "We also told everyone to stay away from trans fats." The fat-restricted group continued to eat carbs, including bread and cereals, while keeping saturated fat — common in animal products — below 7 percent of total calories. By contrast, the high-fat group cut carbs in half and did not avoid butter, meat, and cheese. Most important, both groups ate as much as they wanted — no calorie counting, no going hungry.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 20251 - Posted: 10.28.2014

Clare Pain Eating a high fat and high carb diet resulted in inflammation in the brain - at least in male mice. We'll have to wait to see if the same process applies to male humans. The detrimental impact of junk food seems to be connected to inflammation in the brains of male mice, with the brains of females protected by oestrogen, according to research published today in Cell Reports. Dr Deborah Clegg, who led the study while at University of Texas Southwestern Medical Centre, Dallas, USA, was building on existing research that links brain inflammation with obesity and heart disease in male mice. "We embarked on this research because [the link with inflammation] had been shown in male mice, so we asked ourselves, do the same processes occur in females?" explains Clegg. Previous research has shown that one cause of inflammation in the hypothalamus - the part of the brain that controls energy balance - is palmitic acid, a saturated fatty acid found in palm oil, dairy products and meat, and common in high fat food. The team looked at male and female mice, fed either their normal diet or a 'high fat' diet. Besides containing 42 per cent fat, the high fat diet was also high in carbohydrates making it a good correlate of human junk food, says Clegg. © 2014 ABC

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 8: Hormones and Sex
Link ID: 20215 - Posted: 10.18.2014

BY Bethany Brookshire In this sweet, sweet world we live in, losing weight can be a dull and flavorless experience. Lovely stove-popped popcorn drenched in butter gives way to dry microwaved half-burnt kernels covered in dusty yellow powder. The cookies and candy that help us get through the long afternoons are replaced with virtuous but boring apples and nuts. Even the sugar that livens up our coffee gets a skeptical eye: That’s an extra 23 calories per packet you shouldn’t be eating. What makes life sweet for those of us who are counting calories is artificial sweeteners. Diet soda gives a sweet carbonated fix. A packet of artificial sweetener in your coffee or tea makes it a delicious morning dose. But a new study, published September 17 in Nature, found that the artificial sweetener saccharin has an unintended side effect: It alters the bacterial composition of the gut in mice and humans. The new bacterial neighborhood brings with it higher blood glucose levels, putting the humans and the murine counterparts at risk for diabetes. Many people wondered if the study’s effects were real. We all knew that sugar was bad, but now the scientists are coming for our Splenda! It seems more than a little unfair. But this study was a long time coming. The scientific community has been studying artificial sweeteners and their potential hazards for a long time. And while the new study adds to the literature, there are other studies, currently ongoing and planned for the future, that will determine the extent and necessity of our artificially sweetened future. © Society for Science & the Public 2000 - 2014.

Related chapters from BP7e: 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: 20153 - Posted: 10.02.2014

By Nicholas Bakalar Average waist circumference — but not body mass index— increased significantly in the United States between 1999 and 2012, a new study reports. Abdominal obesity — a “beer belly” or “beer gut” — is caused by fat around the internal organs. It is one of the indicators of metabolic syndrome, a group of five conditions that raises the risk for heart disease and diabetes. After adjusting for age, the overall mean waist circumference increased to 38.7 inches in 2012 from 37.5 in 1999. The increases were significant for men, women, non-Hispanic whites, non-Hispanic blacks and Mexican-Americans. They were greatest among non-Hispanic whites in their 40s, and non-Hispanic black men in their 30s. “I would encourage people to keep track of their waists,” said the lead author of the study, Dr. Earl S. Ford, a medical officer with the Centers for Disease Control and Prevention. “Standing on the scale every day is all good and well, but you can have a steady weight and still have an expanding waist. And that should be a signal for people to start looking at their diet and physical activity.” In 2012, 54.2 percent of Americans had abdominal obesity (defined as an age-adjusted waist circumference of more than 40 inches for men and more than 34.6 for women) compared with 46.4 percent in 1999. The study was published in JAMA. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 20103 - Posted: 09.23.2014

by Rachel Ehrenberg Eating artificial sweeteners may spur the very health problems that dieters try to avoid. A new multipronged study of mice and a small number of people finds that saccharin meddles with the gut’s microbial community, setting in motion metabolic changes that are associated with obesity and diabetes. Other zero-calorie sweeteners may cause the same problems, researchers say September 17 in Nature. Though the finding is preliminary, four of seven human volunteers eating a diet high in saccharin developed impaired glucose metabolism, a warning sign for type 2 diabetes. “This is very interesting and scary if it really does hold for humans,” says Robert Margolskee of the Monell Chemical Senses Center in Philadelphia, who was not involved with the work. “There could be unintended consequences of these artificial sweeteners.” Until recently, most sugar substitutes were thought to pass through the gut undigested, exerting little to no effect on intestinal cells. As ingredients in diet soda, sugar-free desserts and a panoply of other foods, the sweeteners are touted as a way for people with diabetes and weight problems to enjoy a varied diet. But the new study, led by computational biologist Eran Segal and immunologist Eran Elinav of the Weizmann Institute of Science in Rehovot, Israel, suggests that rather than helping people, the sweeteners may promote problems. © Society for Science & the Public 2000 - 2014.

Related chapters from BP7e: 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: 20093 - Posted: 09.18.2014

by Bethany Brookshire Most of us wish we ate better. I know I certainly do. But when hunger strikes, and you’re standing in line at the grab-and-go food joint, that salad seems really lackluster sitting next to that tasty-looking cookie. I can’t help but think that my diet — and my waistline — would look a lot better if I just craved lettuce a little more. Now a new study shows that although we may never cease to love cookies, we might be able to make that carrot a little more appealing. In overweight people, a behavioral intervention was associated with changes in how their brains responded to high- and low-calorie foods. The small pilot study is intriguing, but with just 13 participants, a larger study is needed before scientists will know if training the brain can make us abstain. “Everyone responds more strongly to high-calorie foods than low-calorie foods. It’s just normal,” says study coauthor Susan Roberts, a behavioral nutrition scientist from Tufts University in Medford, Mass. While most people prefer brownies over beets, people who are overweight or obese have a harder time avoiding high-calorie foods, she says. “When someone becomes overweight, there’s a dampening effect on a number of brain structures, including the reward system,” she says. “It’s harder to enjoy food generally, and so when someone becomes overweight, they really want to eat those high-calorie foods, because those are the foods that activate reward systems to the biggest extent.” Craving is a particular issue. Craving is distinct from hunger and focuses on a particular food, often foods that are high calorie. Other studies show that people who are obese have more cravings than those who are not. © Society for Science & the Public 2000 - 2014

Related chapters from BP7e: 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: 20086 - Posted: 09.17.2014

People who are obese may be more susceptible to environmental food cues than their lean counterparts due to differences in brain chemistry that make eating more habitual and less rewarding, according to a National Institutes of Health study published in Molecular Psychiatry External Web Site Policy. Researchers at the NIH Clinical Center found that, when examining 43 men and women with varying amounts of body fat, obese participants tended to have greater dopamine activity in the habit-forming region of the brain than lean counterparts, and less activity in the region controlling reward. Those differences could potentially make the obese people more drawn to overeat in response to food triggers and simultaneously making food less rewarding to them. A chemical messenger in the brain, dopamine influences reward, motivation and habit formation. “While we cannot say whether obesity is a cause or an effect of these patterns of dopamine activity, eating based on unconscious habits rather than conscious choices could make it harder to achieve and maintain a healthy weight, especially when appetizing food cues are practically everywhere,” said Kevin D. Hall, Ph.D., lead author and a senior investigator at National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of NIH. “This means that triggers such as the smell of popcorn at a movie theater or a commercial for a favorite food may have a stronger pull for an obese person — and a stronger reaction from their brain chemistry — than for a lean person exposed to the same trigger.” Study participants followed the same eating, sleeping and activity schedule. Tendency to overeat in response to triggers in the environment was determined from a detailed questionnaire. Positron emission tomography (PET) scans evaluated the sites in the brain where dopamine was able to act.

Related chapters from BP7e: 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: 20054 - Posted: 09.10.2014

by Laura Beil The obesity crisis has given prehistoric dining a stardom not known since Fred Flintstone introduced the Bronto Burger. Last year, “Paleo diet” topped the list of most-Googled weight loss searches, as modern Stone Age dieters sought the advice of bestsellers like The Paleo Solution or The Primal Blueprint, which encourages followers to “honor your primal genes.” The assumption is that America has a weight problem because human metabolism runs on ancient genes that are ill equipped for contemporary eating habits. In this line of thinking, a diet true to the hunter-gatherers we once were — heavy on protein, light on carbs — will make us skinny again. While the fad has attracted skepticism from those who don’t buy the idea whole hog, there’s still plenty of acceptance for one common premise about the evolution of obesity: Our bodies want to stockpile fat. For most of human history, the theory goes, hunter-gatherers ate heartily when they managed to slay a fleeing mastodon. Otherwise, prehistoric life meant prolonged stretches of near starvation, surviving only on inner reserves of adipose. Today, modern humans mostly hunt and gather at the drive-thru, but our Pleistocene genes haven’t stopped fretting over the coming famine. The idea that evolution favored calorie-hoarding genes has long shaped popular and scientific thinking. Called the “thrifty gene” hypothesis, it has arguably been the dominant theory for evolutionary origins of obesity, and by extension diabetes. (Insulin resistance and diabetes so commonly accompany obesity that doctors have coined the term “diabesity.”) However, it’s not that difficult to find scientists who call the rise of the thrifty gene theory a feat of enthusiasm over evidence. Greg Gibson, director of the Center for Integrative Genomics at Georgia Tech in Atlanta, calls the data “somewhere between scant and nonexistent — a great example of crowd mentality in science.” © Society for Science & the Public 2000 - 2014

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 20042 - Posted: 09.06.2014

By ANAHAD O’CONNOR People who avoid carbohydrates and eat more fat, even saturated fat, lose more body fat and have fewer cardiovascular risks than people who follow the low-fat diet that health authorities have favored for decades, a major new study shows. The findings are unlikely to be the final salvo in what has been a long and often contentious debate about what foods are best to eat for weight loss and overall health. The notion that dietary fat is harmful, particularly saturated fat, arose decades ago from comparisons of disease rates among large national populations. But more recent clinical studies in which individuals and their diets were assessed over time have produced a more complex picture. Some have provided strong evidence that people can sharply reduce their heart disease risk by eating fewer carbohydrates and more dietary fat, with the exception of trans fats. The new findings suggest that this strategy more effectively reduces body fat and also lowers overall weight. The new study was financed by the National Institutes of Health and published in the Annals of Internal Medicine. It included a racially diverse group of 150 men and women — a rarity in clinical nutrition studies — who were assigned to follow diets for one year that limited either the amount of carbs or fat that they could eat, but not overall calories. “To my knowledge, this is one of the first long-term trials that’s given these diets without calorie restrictions,” said Dariush Mozaffarian, the dean of the Friedman School of Nutrition Science and Policy at Tufts University, who was not involved in the new study. “It shows that in a free-living setting, cutting your carbs helps you lose weight without focusing on calories. And that’s really important because someone can change what they eat more easily than trying to cut down on their calories.” © 2014 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 20018 - Posted: 09.02.2014

By CARL ZIMMER Your body is home to about 100 trillion bacteria and other microbes, collectively known as your microbiome. Naturalists first became aware of our invisible lodgers in the 1600s, but it wasn’t until the past few years that we’ve become really familiar with them. This recent research has given the microbiome a cuddly kind of fame. We’ve come to appreciate how beneficial our microbes are — breaking down our food, fighting off infections and nurturing our immune system. It’s a lovely, invisible garden we should be tending for our own well-being. But in the journal Bioessays, a team of scientists has raised a creepier possibility. Perhaps our menagerie of germs is also influencing our behavior in order to advance its own evolutionary success — giving us cravings for certain foods, for example. “One of the ways we started thinking about this was in a crime-novel perspective,” said Carlo C. Maley, an evolutionary biologist at the University of California, San Francisco, and a co-author of the new paper. “What are the means, motives and opportunity for the microbes to manipulate us? They have all three.” The idea that a simple organism could control a complex animal may sound like science fiction. In fact, there are many well-documented examples of parasites controlling their hosts. Some species of fungi, for example, infiltrate the brains of ants and coax them to climb plants and clamp onto the underside of leaves. The fungi then sprout out of the ants and send spores showering onto uninfected ants below. How parasites control their hosts remains mysterious. But it looks as if they release molecules that directly or indirectly can influence their brains. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 19981 - Posted: 08.20.2014

|By Melinda Wenner Moyer For most people, “fat,” particularly the kind that bulges under the skin, is a four-letter word. It makes our thighs jiggle; it lingers despite our torturous attempts to eliminate it. Too much of it increases our risk for heart disease and type 2 diabetes (the most common form of the condition). For decades researchers have looked for ways to reduce our collective stores of fat because they seemed to do more harm than good. But biology is rarely that simple. In the late 2000s several research groups independently discovered something that shattered the consensus about the absolute dangers of body fat. Scientists had long known that humans produce at least two types of fat tissue—white and brown. Each white fat cell stores energy in the form of a single large, oily droplet but is otherwise relatively inert. In contrast, brown fat cells contain many smaller droplets, as well as chestnut-colored molecular machines known as mitochondria. These organelles in turn burn up the droplets to generate heat. Babies, who have not yet developed the ability to shiver to maintain their body temperature, rely on thermogenic deposits of brown fat in the neck and around the shoulders to stay warm. Yet investigators assumed that all brown fat disappears during childhood. The new findings revealed otherwise. Adults have brown fat, too. Suddenly, people started throwing around terms like holy grail to describe the promise of brown fat to combat obesity. The idea was appealingly simple: if researchers could figure out how to incite the body to produce extra brown fat or somehow rev up existing brown fat, a larger number of calories would be converted into heat, reducing deposits of white fat in the process. © 2014 Scientific American

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 19953 - Posted: 08.13.2014

James Gorman Deep in the mouse brain, scientists recently found that a very small network of cells, a few thousand at most, turns appetite on and off. They used the most sophisticated of modern techniques, but as has often happened in science — witness penicillin, Velcro and Viagra — the researchers discovered something they weren’t looking for. “This was an accidental discovery,” said David Anderson, of the California Institute of Technology, the senior scientist on the team that reported the finding, in Nature Neuroscience. The discovery may eventually lead to a better understanding and treatment of eating disorders. The surprise and drama of the finding are immediately clear, however, in lab videos. A mouse busily munches lab chow until a light signal is sent to its brain, and the mouse wanders off, no longer interested in food. His lab had previously studied this small group of neurons, in a part of the brain called the amygdala. That earlier research was on fear, an emotion strongly associated with the amygdala in both mice and humans. As a technique called optogenetics became more and more refined, he said, it seemed worth revisiting the neurons with this new tool. Optogenetics requires genetic manipulation of specific cells to make them sensitive to light in a certain wavelength, in this case blue light. Then fiber-optic cables are inserted into the brain, and when the light is turned on, neurons can be activated or turned off. Researchers in Dr. Anderson’s lab, including Haijiang Cai, a postdoctoral researcher and a co-author of the report, prepared the mice and conducted the experiment with the entirely unexpected result. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 19945 - Posted: 08.12.2014

The gurgles made by a hungry belly are familiar to us all, but they are not just the side effect of an empty stomach. Brain cells not normally associated with communication send out a signal when they detect blood glucose levels are running low, and this triggers the stomach contractions. Richard Rogers of the Pennington Biomedical Research Center at Louisiana State University and colleagues used a drug called fluorocitrate to knock out the function of certain astrocytes and neurons in the brains of rats, blocking the sensation of hunger. Only when astrocyte function was restored did the gastric grumbles return, showing that it is these cells that respond to low glucose levels (Journal of Neuroscience, DOI: 10.1523/JNEUROSCI.1406-14.2014). The feeling of discomfort you get when hungry is called "hypoglycaemia awareness". "For most people this is only slightly unpleasant, but for diabetics whose glucose levels can drop significantly, [being hungry] can be dangerous," says Rogers. "It's important to understand how this mechanism works." © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 19922 - Posted: 08.07.2014

Sarah C. P. Williams Every fall, grizzly bears pack on the pounds in preparation for their winter hibernation. In humans, such extreme weight gain would likely lead to diabetes or other metabolic diseases, but the bears manage to stay healthy year after year. Their ability to remain diabetes-free, researchers have now discovered, can be chalked up to the shutting down of a protein found in fat cells. The discovery could lead to new diabetes drugs that turn off the same pathway in humans. The findings are “provocative and interesting,” says biologist Sandy Martin of the University of Colorado, Denver, who was not involved in the new work. “They found a natural solution to a problem that we haven’t been able to solve.” As people gain weight, fat, liver, and muscle cells typically become less sensitive to the hormone insulin—which normally helps control blood sugar levels—and insulin levels rise. In turn, that increased insulin prevents the breakdown of fat cells, causing a vicious cycle that can lead to full-blown insulin resistance, or diabetes. Developing new diabetes drugs has been hampered by the fact that findings from many mouse models of diabetes have not translated to humans. So Kevin Corbit, a senior scientist at Thousand Oaks, California–based drug company Amgen, decided to start looking at obesity and metabolic disease in other animals. “When I was thinking about things that are quite fat, one of the first things I thought of was bears, and what they do to prepare to go into hibernation,” he says. “But of course you don’t see bears running around with diabetes and heart disease.” © 2014 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 19919 - Posted: 08.06.2014

By Smitha Mundasad Health reporter, BBC News Scientists have discovered a central hub of brain cells that may put the brakes on a desire to eat, a study in mice shows. And switching on these neurons can stop feeding immediately, according to the Nature Neurosciences report. Researchers say the findings may one day contribute to therapies for obesity and anorexia. Experts say this sheds light on the many complex nerve circuits involved in appetite control. Scientists from the California Institute of Technology suggest the nerve cells act as a central switchboard, combining and relaying many different messages in the brain to help reduce food intake. Using laser beams they were able to stimulate the neurons - leading to a complete and immediate stop to food consumption. Prof David Anderson, lead author of the study told the BBC: "It was incredibly surprising. "It was like you could just flick a switch and prevent the animals from feeding." Researchers then used chemicals to mimic a variety of scenarios - including feelings of satiety, malaise, nausea and a bitter taste. They found the neurons were active in all situations, suggesting they may be integral in the response to many diverse stimuli. BBC © 2014

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 19887 - Posted: 07.28.2014