Chapter 9. Homeostasis: Active Regulation of the Internal Environment
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BY Ashley Yeager A protein made by gut bacteria may trigger a chain of interactions in the body that contribute to eating disorders such as anorexia and bulimia. When the protein is produced, the body makes antibodies to bind to it, but the antibodies also attach to a hormone that controls fullness. In tests, mice given bacteria that produce the protein changed how much they ate compared with mice given bacteria that did not make the protein, a new study shows. Researchers also found that the antibodies to the protein were higher in patients with anorexia and bulimia. The results, which appear October 7 in Translational Psychiatry, seem to be some of the earliest to link gut bacteria to eating disorders. © Society for Science & the Public 2000 - 2014.
Keyword: Anorexia & Bulimia
Link ID: 20188 - Posted: 10.11.2014
|By Bret Stetka Multiple sclerosis (MS) is an electrical disorder, or rather one of impaired myelin, a fatty, insulating substance that better allows electric current to bolt down our neurons and release the neurotransmitters that help run our bodies and brains. Researchers have speculated for some time that the myelin degradation seen in MS is due, at least in part, to autoimmune activity against the nervous system. Recent work presented at the MS Boston 2014 Meeting suggests that this aberrant immune response begins in the gut. Eighty percent of the human immune system resides in the gastrointestinal tract. Alongside it are the trillions of symbiotic bacteria, fungi and other single-celled organisms that make up our guts’ microbiomes. Normally everyone wins: The microorganisms benefit from a home and a steady food supply; we enjoy the essential assistance they provide in various metabolic and digestive functions. Our microbiomes also help calibrate our immune systems, so our bodies recognize which co-inhabitants should be there and which should not. Yet mounting evidence suggests that when our resident biota are out of balance, they contribute to numerous diseases, including diabetes, rheumatoid arthritis, autism and, it appears, MS by inciting rogue immune activity that can spread throughout the body and brain. One study presented at the conference, out of Brigham and Women’s Hospital (BWH), reported a single-celled organism called methanobrevibacteriaceae that activates the immune system is enriched in the gastrointestinal tracts of MS patients whereas bacteria that suppress immune activity are depleted. Other work, which resulted from a collaboration among 10 academic researcher centers across the U.S. and Canada, reported significantly altered gut flora in pediatric MS patients while a group of Japanese researchers found that yeast consumption reduced the chances of mice developing an MS-like disease by altering gut flora. © 2014 Scientific American
Keyword: Multiple Sclerosis
Link ID: 20186 - Posted: 10.09.2014
by Laura Starecheski From the self-affirmations of Stuart Smalley on Saturday Night Live to countless videos on YouTube, saying nice things to your reflection in the mirror is a self-help trope that's been around for decades, and seems most often aimed at women. The practice, we're told, can help us like ourselves and our bodies more, and even make us more successful — allow us to chase our dreams! Impressed, but skeptical, I took this self-talk idea to one of the country's leading researchers on body image to see if it's actually part of clinical practice. David Sarwer is a psychologist and clinical director at the Center for Weight and Eating Disorders at the University of Pennsylvania. He says that, in fact, a mirror is one of the first tools he uses with some new patients. He stands them in front of a mirror and coaches them to use gentler, more neutral language as they evaluate their bodies. "Instead of saying, 'My abdomen is disgusting and grotesque,' " Sarwer explains, he'll prompt a patient to say, " 'My abdomen is round, my abdomen is big; it's bigger than I'd like it to be.' " The goal, he says, is to remove "negative and pejorative terms" from the patient's self-talk. The underlying notion is that it's not enough for a patient to lose physical weight — or gain it, as some women need to — if she doesn't also change the way her body looks in her mind's eye. This may sound weird. You're either a size 4 or a size 8, right? Not mentally, apparently. In a 2013 study from the Netherlands, scientists watched women with anorexia walk through doorways in a lab. The women, they noticed, turned their shoulders and squeezed sideways, even when they had plenty of room. © 2014 NPR
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.
|By Melinda Wenner Moyer Autism is primarily a disorder of the brain, but research suggests that as many as nine out of 10 individuals with the condition also suffer from gastrointestinal problems such as inflammatory bowel disease and “leaky gut.” The latter condition occurs when the intestines become excessively permeable and leak their contents into the bloodstream. Scientists have long wondered whether the composition of bacteria in the intestines, known as the gut microbiome, might be abnormal in people with autism and drive some of these symptoms. Now a spate of new studies supports this notion and suggests that restoring proper microbial balance could alleviate some of the disorder's behavioral symptoms. At the annual meeting of the American Society for Microbiology held in May in Boston, researchers at Arizona State University reported the results of an experiment in which they measured the levels of various microbial by-products in the feces of children with autism and compared them with those found in healthy children. The levels of 50 of these substances, they found, significantly differed between the two groups. And in a 2013 study published in PLOS ONE, Italian researchers reported that, compared with healthy kids, those with autism had altered levels of several intestinal bacterial species, including fewer Bifidobacterium, a group known to promote good intestinal health. One open question is whether these microbial differences drive the development of the condition or are instead a consequence of it. A study published in December 2013 in Cell supports the former idea. When researchers at the California Institute of Technology incited autismlike symptoms in mice using an established paradigm that involved infecting their mothers with a viruslike molecule during pregnancy, they found that after birth, the mice had altered gut bacteria compared with healthy mice. © 2014 Scientific American,
Link ID: 20104 - Posted: 09.23.2014
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
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.
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
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.
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
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
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
|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
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
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.
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
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
Link ID: 19887 - Posted: 07.28.2014
Obese women may have a "food learning impairment" that could explain their attitude to food, research from Yale School of Medicine suggests. Tests on groups of obese and healthy-weight people found that the obese women performed worst when asked to remember a sequence of food picture cards. Writing in Current Biology, Yale researchers tested 135 men and women. The findings could lead to new ways to tackle obesity, the study says. Study author Ifat Levy, assistant professor at Yale School of Medicine, said the difference in the performance of the obese women compared with the other groups was "really striking" and "significant". The tests looked at an individual's ability to learn and predict the appearance of pictures of food or money on coloured cards. The participants were told they would be given whatever appeared on these "reward" cards. In the first phase, the reward cards always followed a particular coloured card in a sequence. Later, the order was changed and the reward cards appeared following a different coloured card. During this time, participants were asked to predict the likelihood of a reward card appearing as the cards were shown one by one. The results showed that obese women performed worst because they overestimated how often the pictures of food, including pretzels or chocolate, appeared. Even after researchers had accounted for other factors, there was still a large difference in their learning performance. Prof Levy said: "This is not a general learning impairment, as obese women had no problem learning when the reward was money rather than food. BBC © 2014
By GRETCHEN REYNOLDS Sleep is essential for good health, as we all know. But a new study hints that there may be an easy but unrealized way to augment its virtues: lower the thermostat. Cooler bedrooms could subtly transform a person’s stores of brown fat — what has lately come to be thought of as “good fat” — and consequently alter energy expenditure and metabolic health, even into daylight hours. Until recently, most scientists thought that adults had no brown fat. But in the past few years, scanty deposits — teaspoonfuls, really — of the tissue have been detected in the necks and upper backs in many adults. This is important because brown fat, unlike the more common white stuff, is metabolically active. Experiments with mice have shown that it takes sugar out of the bloodstream to burn calories and maintain core temperature. A similar process seems to take place in humans. For the new study, published in June in Diabetes, researchers affiliated with the National Institutes of Health persuaded five healthy young male volunteers to sleep in climate-controlled chambers at the N.I.H. for four months. The men went about their normal lives during the days, then returned at 8 every evening. All meals, including lunch, were provided, to keep their caloric intakes constant. They slept in hospital scrubs under light sheets. For the first month, the researchers kept the bedrooms at 75 degrees, considered a neutral temperature that would not prompt moderating responses from the body. The next month, the bedrooms were cooled to 66 degrees, a temperature that the researchers expected might stimulate brown-fat activity (but not shivering, which usually begins at more frigid temperatures). The following month, the bedrooms were reset to 75 degrees, to undo any effects from the chillier room, and for the last month, the sleeping temperature was a balmy 81 degrees. Throughout, the subjects’ blood-sugar and insulin levels and daily caloric expenditures were tracked; after each month, the amount of brown fat was measured. © 2014 The New York Times Company
Link ID: 19844 - Posted: 07.17.2014
by Azeen Ghorayshi Food could be a new weapon in shaking off the effects of jet lag after research in mice showed that the insulin released as a result of eating can be a key factor in restoring a disrupted body clock. Miho Sato and her colleagues at The Research Institute for Time Studies at Yamaguchi University in Japan did experiments in mice and tissue cultures to show, for the first time, that increases in insulin affect circadian rhythms. These daily rhythms affect alertness, sleep patterns, and mediate many other physiological processes. Your biological clock is regulated by two broad factors: first, the central rhythm is reset daily by light, as sensory input from the eyes is processed by a small part of the brain called the suprachiasmatic nucleus. The rise and fall of hormones linked to sleep, for example, match this rhythm. But circadian rhythms are also present in peripheral "clocks" in a wide range of cell types in the body. Some of these can be influenced by food. Sato demonstrated the role of insulin by shifting the peripheral body clock in the livers of mice by feeding them only at night. They then split the mice into two groups, supressed insulin levels in one group, and returned all the mice to daytime feeding. Four days later, the livers of the non-supressed mice had readjusted to a normal daily rhythm, as revealed by the daily rise and fall of liver-gene expression. The livers of the insulin-suppressed mice had still not returned to normal. © Copyright Reed Business Information Ltd.
Keyword: Biological Rhythms
Link ID: 19830 - Posted: 07.15.2014