Chapter 13. Homeostasis: Active Regulation of the Internal Environment

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By C. Claiborne Ray Q. What keeps squirrels from gaining huge amounts of weight as they gorge on acorns and nuts each fall? A. In fact, many squirrels do achieve huge weight gain ahead of the privations of winter. Common gray squirrels may increase their weight by 25 percent in the harvest season. But not because they hibernate — they don’t. Winter foraging is hard, and gray squirrels tend to spend the winter months mostly in their nests. But they must make forays every few days to seek squirreled-away food and other nourishment. Among hibernating squirrels, much of the stored nourishment is needed to survive the cold season without foraging. A study of the Arctic ground squirrel found extreme weight gains during the active season: 42 percent among males and 63 percent among females. They slow their activity drastically before hibernating in order to maintain peak mass. While some do emerge from winter lighter, a significant share of their fat stores may remain. © 2019 The New York Times Company

Keyword: Obesity; Biological Rhythms
Link ID: 25952 - Posted: 02.12.2019

By Elizabeth Pennisi Of all the many ways the teeming ecosystem of microbes in a person’s gut and other tissues might affect health, its potential influences on the brain may be the most provocative. Now, a study of two large groups of Europeans has found several species of gut bacteria are missing in people with depression. The researchers can’t say whether the absence is a cause or an effect of the illness, but they showed that many gut bacteria could make substances that affect nerve cell function—and maybe mood. “It’s the first real stab at tracking how” a microbe’s chemicals might affect mood in humans, says John Cryan, a neuroscientist at University College Cork in Ireland who has been one of the most vocal proponents of a microbiome-brain connection. The study “really pushes the field from where it’s been” with small studies of depressed people or animal experiments. Interventions based on the gut microbiome are now under investigation: The University of Basel in Switzerland, for example, is planning a trial of fecal transplants, which can restore or alter the gut microbiome, in depressed people. Several studies in mice had indicated that gut microbes can affect behavior, and small studies of people suggested this microbial repertoire is altered in depression. To test the link in a larger group, Jeroen Raes, a microbiologist at the Catholic University of Leuven in Belgium, and his colleagues took a closer look at 1054 Belgians they had recruited to assess a “normal” microbiome. Some in the group—173 in total—had been diagnosed with depression or had done poorly on a quality of life survey, and the team compared their microbiomes with those other participants. Two kinds of microbes, Coprococcus and Dialister, were missing from the microbiomes of the depressed subjects, but not from those with a high quality of life. The finding held up when the researchers allowed for factors such as age, sex, or antidepressant use, all of which influence the microbiome, the team reports today in Nature Microbiology. They also found the depressed people had an increase in bacteria implicated in Crohn disease, suggesting inflammation may be at fault. © 2018 American Association for the Advancement of Science

Keyword: Depression
Link ID: 25932 - Posted: 02.05.2019

By Carl Zimmer In 2014 John Cryan, a professor at University College Cork in Ireland, attended a meeting in California about Alzheimer’s disease. He wasn’t an expert on dementia. Instead, he studied the microbiome, the trillions of microbes inside the healthy human body. Dr. Cryan and other scientists were beginning to find hints that these microbes could influence the brain and behavior. Perhaps, he told the scientific gathering, the microbiome has a role in the development of Alzheimer’s disease. The idea was not well received. “I’ve never given a talk to so many people who didn’t believe what I was saying,” Dr. Cryan recalled. A lot has changed since then: Research continues to turn up remarkable links between the microbiome and the brain. Scientists are finding evidence that microbiome may play a role not just in Alzheimer’s disease, but Parkinson’s disease, depression, schizophrenia, autism and other conditions. For some neuroscientists, new studies have changed the way they think about the brain. One of the skeptics at that Alzheimer’s meeting was Sangram Sisodia, a neurobiologist at the University of Chicago. He wasn’t swayed by Dr. Cryan’s talk, but later he decided to put the idea to a simple test. “It was just on a lark,” said Dr. Sisodia. “We had no idea how it would turn out.” He and his colleagues gave antibiotics to mice prone to develop a version of Alzheimer’s disease, in order to kill off much of the gut bacteria in the mice. Later, when the scientists inspected the animals’ brains, they found far fewer of the protein clumps linked to dementia. Just a little disruption of the microbiome was enough to produce this effect. Young mice given antibiotics for a week had fewer clumps in their brains when they grew old, too. © 2019 The New York Times Company

Keyword: Obesity; Depression
Link ID: 25915 - Posted: 01.29.2019

Amy Lewis Cynthia Bulik began her scientific career studying childhood depression. But while she was working as a research assistant at the University of Pittsburgh in the 1980s, psychiatrist David Kupfer asked her to help write a book chapter comparing electroencephalography studies in depression and anorexia. As preparation, she shadowed a psychiatrist at a hospital inpatient unit for people with eating disorders. Bulik was intrigued by what she witnessed there. “These people were my age, my sex, and weighed half as much as I did,” she says. “They seemed very eloquent and interactive, but at the same time, in this one area of their psychology and biology, they occupied a completely different space.” Now the founding director of the Center of Excellence for Eating Disorders at the University of North Carolina at Chapel Hill, Bulik has been unraveling the biology behind eating disorders such as anorexia nervosa (AN) ever since. Characterized by extreme caloric restriction resulting in weight loss, an intense fear of gaining weight, and a distorted body image, anorexia has the highest mortality rate of any psychiatric disorder. Death can be a result of various risks associated with the condition, from suicide to heart failure. While many AN sufferers go undiagnosed, making incidence rates hard to pin down, some researchers estimate that up to 2 percent of women and 0.3 percent of men are affected globally. © 1986 - 2019 The Scientist

Keyword: Anorexia & Bulimia; Genes & Behavior
Link ID: 25914 - Posted: 01.29.2019

By Gretchen Reynolds Exercise and eating have a fraught, unsettled relationship with each other. Workouts can blunt or boost appetites. People who start an exercise program often overeat and gain weight — and yet studies and lived experience demonstrate that regular exercise is needed to avoid regaining the weight lost during a successful diet. Intrigued by these contradictory outcomes, researchers at the University of Texas Southwestern Medical Center, along with colleagues from other institutions, ran an experiment on the melanocortin circuit, a brain network in the hypothalamus known to be involved in metabolism. The resulting study, published in December in Molecular Metabolism, suggests that intense exercise might change the workings of certain neurons in ways that could have beneficial effects on appetite and metabolism. The melanocortin circuit consists mainly of two types of neurons. The neuropeptide Y (NPY) cells relay signals encouraging the body to seek food, while the pro-opiomelanocortin (POMC) neurons countermand those orders, reducing interest in food. Animals, including humans, that lack healthy POMC neurons usually become morbidly obese. The researchers focused on what exercise would do to these cells in mice, whose melanocortin circuits resemble ours. Healthy adult male mice either ran on small treadmills or, in a control group, were placed on unmoving treadmills. The exercise routine consisted of 60 minutes of fast, intense running, broken into three 20-minute blocks. Afterward, the mice were free to eat or not, as they chose. The researchers then checked neuronal activity in some of their brains by microscopically probing individual cells in living tissue to measure their electrical and biochemical signals. The tests were repeated throughout the study, which ran for as many as 10 days for some mice. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 25911 - Posted: 01.29.2019

By Jane E. Brody I had hoped to avoid ushering in the new year with yet another weight/diet column, but three circumstances prompted me to reconsider: 1) The latest data released by the Centers for Disease Control and Prevention showed that the weight of American men and women has continued its upward climb, with the average B.M.I. now almost at the cutoff for obesity; 2) The Food and Drug Administration is rolling out changes in serving sizes on packaged foods that could very well make matters worse, especially for consumers of ice cream and soda, and 3) Some good news for a change: the publication of an eminently sensible approach to weight loss, “Finally Full, Finally Slim,” written by a leading expert on portion control, Lisa R. Young, a registered dietitian and adjunct professor of nutrition at New York University. Unlike the myriad diet fads that have yet to stem the ever-increasing girth of American men and women, what Dr. Young describes is not a diet but a practical approach to food and eating that can be adapted to almost any way of life, even if most meals are eaten out or taken out. It is not prescriptive or even proscriptive. It does not cut out any category of food, like carbohydrates or fats, nor does it deprive people of their favorite foods, including sweet treats. And it works. I know, because more than half a century ago I lost 40 pounds in two years following Dr. Young’s approach, and I’ve kept the weight off ever since without dieting or deprivation. It fills me up with delicious, nutritious foods and allows me to enjoy a frequent nightcap of ice cream — half a cup (measured) at 150 calories or less. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 25907 - Posted: 01.28.2019

By Smitha Mundasad Global Health Correspondent, BBC News Scientists say they have discovered the secret behind why some people are skinny while others pile on the pounds easily. Their work reveals newly discovered genetic regions linked to being very slim. The international team say this supports the idea that, for some people, being thin has more to do with inheriting a "lucky" set of genes than having a perfect diet or lifestyle. The study appears in PLOS Genetics. In the past few decades, researchers have found hundreds of genetic changes that increase the chance of a person being overweight - but there has been much less focus on the genes of people who are thin. In this investigation, scientists compared DNA samples from 1,600 healthy thin people in the UK - with a body mass index (BMI) of less than 18 - with those of 2,000 severely obese people and 10,400 people of normal weight. They also looked closely at lifestyle questionnaires - to rule out eating disorders, for example. Researchers found people who were obese were more likely to have a set of genes linked to being overweight. Meanwhile, people who were skinny not only had fewer genes linked to obesity but also had changes in gene regions newly associated with healthy thinness. Lead researcher Prof Sadaf Farooqi, from the University of Cambridge, called on people to be less judgemental about others' weight. "This research shows for the first time that healthy thin people are generally thin because they have a lower burden of genes that increase a person's chances of being overweight and not because they are morally superior, as some people like to suggest," she said. © 2019 BBC.

Keyword: Obesity; Genes & Behavior
Link ID: 25905 - Posted: 01.26.2019

Marise Parent Of course you know that eating is vital to your survival, but have you ever thought about how your brain controls how much you eat, when you eat and what you eat? This is not a trivial question, because two-thirds of Americans are either overweight or obese and overeating is a major cause of this epidemic. To date, the scientific effort to understand how the brain controls eating has focused primarily on brain areas involved in hunger, fullness and pleasure. To be better armed in the fight against obesity, neuroscientists, including me, are starting to expand our investigation to other parts of the brain associated with different functions. My lab’s recent research focuses on one that’s been relatively overlooked: memory. For many people, decisions about whether to eat now, what to eat and how much to eat are often influenced by memories of what they ate recently. For instance, in addition to my scale and tight clothes, my memory of overeating pizza yesterday played a pivotal role in my decision to eat salad for lunch today. Memories of recently eaten foods can serve as a powerful mechanism for controlling eating behavior because they provide you with a record of your recent intake that likely outlasts most of the hormonal and brain signals generated by your meal. But surprisingly, the brain regions that allow memory to control future eating behavior are largely unknown. Studies done in people support the idea that meal-related memory can control future eating behavior. © 2010–2019, The Conversation US, Inc.

Keyword: Obesity; Learning & Memory
Link ID: 25866 - Posted: 01.15.2019

Abby Olena In the never-ending search for ways to help people eat healthy, scientists have been looking into brain stimulation, specifically, sending a weak electrical current to the brain through two scalp electrodes—a technique called transcranial direct current stimulation. It has previously shown promise in limiting both food cravings and consumption in people, but in a study published yesterday (January 9) in Royal Society Open Science, researchers didn’t find any effects of tDCS on food-related behavior, indicating that the technique’s use needs another look. “The good things about the study are the large sample size and the fact that it’s fairly rigorous,” says Mark George, a psychiatrist and neurologist at the Medical University of South Carolina who did not participate in the study. “The problem [is] interpreting studies where there’s a failure to find. All you can say is that it didn’t work . . . with this group.” During tDCS, one to two milliamps of electricity—enough to feel tingles or pins and needles, but far less than the 800 or so milliamps used for electroconvulsive therapy—are delivered to the brain. Over the last two decades, scientists have reported targeting the technique to the dorsolateral prefrontal cortex, a brain area that’s been shown to be involved in food-related behavior. They’ve found it has helped people crave less and, to a lesser extent, eat fewer sweets and other tempting foods. Yet these experiments have generally included groups of 20 or fewer people, and other studies have failed to replicate their effects. © 1986 - 2019 The Scientist.

Keyword: Obesity
Link ID: 25861 - Posted: 01.14.2019

By Emily Willingham For centuries, some indigenous groups in South America have relied on a brew made from the parts of a local vine and a shrub. The effects of this drink, called ayahuasca, would begin with severe vomiting and diarrhea, but the real reason for drinking the tea was the hallucinating that followed. These visions were thought to uncover the secrets of the drinker’s poor health and point the way to a cure. Modern techniques have revealed that one of the compounds underlying these mystic experiences is the psychoactive drug harmine. What these first users of ayahuasca couldn’t have known was that, one day, this ingredient in their enlightening brew would be positioned as a key to treating diabetes. Such a cure is a long way off, but researchers took another step toward it when they combined naturally occurring harmine with a compound synthesized from scratch in a lab. Together, the pair can coax the insulin-producing pancreatic cells, called beta cells, into replicating at the fastest rates ever reported, according to findings published December 20 in Molecular Cell. Type 1 diabetes arises when the body turns on these cells and destroys them. Type 2 diabetes develops when these same cells wear out and can no longer make insulin. Either effect is a point of no return because the beta cells we make in early life are the only ones we’ll ever have. © 2018 Scientific American

Keyword: Drug Abuse; Obesity
Link ID: 25810 - Posted: 12.21.2018

Nicola Davis Having even one night without sleep leads people to view junk food more favourably, research suggests. Scientists attribute the effect to the way food rewards are processed by the brain. Previous studies have found that a lack of shuteye is linked to expanding waistlines, with some suggesting disrupted sleep might affect hormone levels, resulting in changes in how hungry or full people feel. But the latest study suggests that with hormones may have little to do with the phenomenon, and that the cause could be changes in the activity within and between regions of the brain involved in reward and regulation. . “Our data brings us a little closer to understanding the mechanism behind how sleep deprivation changes food valuation,” said Prof Jan Peters, a co-author of the research from the University of Cologne. Writing in the Journal of Neuroscience, Peters and colleagues describe how they recruited 32 healthy men aged between 19 and 33 and gave all of them the same dinner of pasta and veal, an apple and a strawberry yoghurt. Participants were then either sent home to bed wearing a sleep-tracking device, or kept awake in the laboratory all night with activities including parlour games. All returned the next morning to have their hunger and appetite rated, while 29 of the men had their levels of blood sugar measured, as well as levels of certain hormones linked to stress and appetite. Participants also took part in a game in which they were presented with pictures of 24 snack food items, such as chocolate bars, and 24 inedible items, including hats or mugs, and were first asked to rate how much they would be willing to pay for them on a scale of €0-€3. © 2018 Guardian News and Media Limited

Keyword: Sleep; Obesity
Link ID: 25797 - Posted: 12.18.2018

By Robert F. Service BOSTON—Implanted electronics can steady hearts, calm tremors, and heal wounds—but at a cost. These machines are often large, obtrusive contraptions with batteries and wires, which require surgery to implant and sometimes need replacement. That's changing. At a meeting of the Materials Research Society here last month, biomedical engineers unveiled bioelectronics that can do more in less space, require no batteries, and can even dissolve when no longer needed. "Huge leaps in technology [are] being made in this field," says Shervanthi Homer-Vanniasinkam, a biomedical engineer at University College London. By making bioelectronics easier to live with, these advances could expand their use. "If you can tap into this, you can bring a new approach to medicine beyond pharmaceuticals," says Bernhard Wolfrum, a neuroelectronics expert at the Technical University of Munich in Germany. "There are a lot of people moving in this direction." One is John Rogers, a materials scientist at Northwestern University in Evanston, Illinois, who is trying to improve on an existing device that surgeons use to stimulate healing of damaged peripheral nerves in trauma patients. During surgery, doctors suture severed nerves back together and then provide gentle electrical stimulation by placing electrodes on either side of the repair. But because surgeons close wounds as soon as possible to prevent infection, they typically provide this stimulation for an hour or less. © 2018 American Association for the Advancement of Science

Keyword: Obesity; Robotics
Link ID: 25786 - Posted: 12.13.2018

By Gina Kolata You’d think that scientists at an international conference on obesity would know by now which diet is best, and why. As it turns out, even the experts still have widely divergent opinions. At a recent meeting of the Obesity Society, organizers held a symposium during which two leading scientists presented the somewhat contradictory findings of two high-profile diet studies. A moderator tried to sort things out. In one study, by Christopher Gardner, a professor of medicine at Stanford, patients were given low-fat or low-carb diets with the same amount of calories. After a year, weight loss was the same in each group, Dr. Gardner reported. Another study, by Dr. David Ludwig of Boston Children’s Hospital, reported that a low-carbohydrate diet was better than a high-carbohydrate diet in helping subjects keep weight off after they had dieted and lost. The low-carbohydrate diet, he found, enabled participants to burn about 200 extra calories a day. So does a low-carbohydrate diet help people burn more calories? Or is the composition of the diet irrelevant if the calories are the same? Does it matter if the question is how to lose weight or how to keep it off? There was no consensus at the end of the session. But here are a few certainties about dieting amid the sea of unknowns. What we know People vary — a lot — in how they respond to dieting. Some people thrive on low-fat diets, others do best on low-carb diets. Still others succeed with gluten-free diets or Paleo diets or periodic fasts or ketogenic diets or other options on the seemingly endless menu of weight-loss plans. Most studies comparing diets have produced results like Dr. Gardner’s: no difference © 2018 The New York Times Company

Keyword: Obesity
Link ID: 25775 - Posted: 12.11.2018

Laura Beil Martha Carlin married the love of her life in 1995. She and John Carlin had dated briefly in college in Kentucky, then lost touch until a chance meeting years later at a Dallas pub. They wed soon after and had two children. John worked as an entrepreneur and stay-at-home dad. In his free time, he ran marathons. Almost eight years into their marriage, the pinky finger on John’s right hand began to quiver. So did his tongue. Most disturbing for Martha was how he looked at her. For as long as she’d known him, he’d had a joy in his eyes. But then, she says, he had a stony stare, “like he was looking through me.” In November 2002, a doctor diagnosed John with Parkinson’s disease. He was 44 years old. Carlin made it her mission to understand how her seemingly fit husband had developed such a debilitating disease. “The minute we got home from the neurologist, I was on the internet looking for answers,” she recalls. She began consuming all of the medical literature she could find. With her training in accounting and corporate consulting, Carlin was used to thinking about how the many parts of large companies came together as a whole. That kind of wide-angle perspective made her skeptical that Parkinson’s, which affects half a million people in the United States, was just a malfunction in the brain. “I had an initial hunch that food and food quality was part of the issue,” she says. If something in the environment triggered Parkinson’s, as some theories suggest, it made sense to her that the disease would involve the digestive system. Every time we eat and drink, our insides encounter the outside world. |© Society for Science & the Public 2000 - 2018.

Keyword: Parkinsons; Neuroimmunology
Link ID: 25765 - Posted: 12.08.2018

By Jonathan D. Grinstein It is well known that a high salt diet leads to high blood pressure, a risk factor for an array of health problems, including heart disease and stroke. But over the last decade, studies across human populations have reported the association between salt intake and stroke irrespective of high blood pressure and risk of heart disease, suggesting a missing link between salt intake and brain health. Interestingly, there is a growing body of work showing that there is communication between the gut and brain, now commonly dubbed the gut–brain axis. The disruption of the gut–brain axis contributes to a diverse range of diseases, including Parkinson’s disease and irritable bowel syndrome. Consequently, the developing field of gut–brain axis research is rapidly growing and evolving. Five years ago, a couple of studies showed that high salt intake leads to profound immune changes in the gut, resulting in increased vulnerability of the brain to autoimmunity—when the immune system attacks its own healthy cells and tissues by mistake, suggesting that perhaps the gut can communicate with the brain via immune signaling. Now, new research shows another connection: immune signals sent from the gut can compromise the brain’s blood vessels, leading to deteriorated brain heath and cognitive impairment. Surprisingly, the research unveils a previously undescribed gut–brain connection mediated by the immune system and indicates that excessive salt might negatively impact brain health in humans through impairing the brain’s blood vessels regardless of its effect on blood pressure. © 2018 Scientific American

Keyword: Obesity; Neuroimmunology
Link ID: 25754 - Posted: 12.06.2018

By Abby Ellin The issue was peanut butter. No matter what form it took — creamy, crunchy, straight from the jar or smeared between two slices of bread — it caused Sunny Gold enormous anxiety. In fact, the gooey spread posed such a threat that during her first few years of recovery from binge eating disorder, between 2006 and 2007, Ms. Gold, 42, a communications specialist in Portland, Ore., couldn’t keep it around the house. It was one of her favorite foods, and she feared she would binge on it. Just knowing it was there, lurking in her cupboard, made her feel “unsafe,” as she put it. And that’s when things got really tricky. Because her boyfriend at the time, John Pavlus, didn’t think twice about peanut butter — or any food, for that matter. When Ms. Gold, the author of “Food: The Good Girl’s Drug,” told him that it would be a casualty of her getting healthy, he was taken aback. “It was a bit uncomfortable for me at first,” Mr. Pavlus, a 40-year-old writer and filmmaker, admitted. He knew that Ms. Gold had grappled with binge eating since she was a teenager, but food was something they’d bonded over. So when she decided that she needed to “cut herself off,” he felt that he was losing something, “less for the practical inconvenience than the unexpected feeling of being subtly disconnected from her,” he said. “It was strange to think of these parts of our shared reality as being so radically — to me — redefined. Is peanut butter literally dangerous now? Does that mean I have to treat it that way too? Will it be like this forever?” Mr. Pavlus’s reaction is echoed by many romantic partners of someone with an eating disorder, many of whom — though certainly not all — are women. Partners often want to help, but simply don’t know how. © 2018 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 25734 - Posted: 11.30.2018

By Roni Caryn Rabin A. A deficiency of vitamin B12 can cause neurological and psychiatric problems that “can progress if left untreated, and can lead to irreversible damage,” said Dr. Donald Hensrud, director of the Mayo Clinic’s Healthy Living Program. Fortunately, it can be reversed fairly easily with vitamin pills or injections. Vitamin B12 is required for proper red blood cell formation, nerve function and DNA synthesis. It is naturally present in fish, meat, eggs and dairy products, as well as some fortified breakfast cereals and nutritional yeast products. Strict vegans who avoid animal products can develop a deficiency of B12 over time if they don’t take a supplement. But two-thirds of cases occur in the elderly, who are susceptible because they may not absorb adequate amounts of B12 from foods but who are not routinely tested, Dr. Hensrud said. Consequences of B12 deficiency can cause a range of symptoms that include fatigue, weakness, constipation, loss of appetite and weight loss. Other symptoms include difficulty maintaining balance, depression, confusion, dementia, poor memory and soreness in the mouth or tongue. B12 deficiency may also result in a form of anemia called megaloblastic anemia, which can also result from a deficiency of folic acid, another B vitamin. If anemia is detected on blood tests, levels of both vitamins should be checked. Neurological symptoms can, however, occur in the absence of anemia. Early treatment is critical to avoid potentially irreversible damage. Older adults are susceptible to B12 deficiency because they may have decreased secretion of hydrochloric acid in the stomach, which makes it difficult to absorb B12. Also vulnerable to B12 deficiency are those with gastrointestinal disorders like celiac disease or Crohn’s disease; those who have had weight loss or other gastrointestinal surgery; and those who use certain acid reflux drugs or the diabetes drug metformin. Individuals with pernicious anemia, which affects up to 2 percent of older adults, are also susceptible. © 2018 The New York Times Company

Keyword: Depression
Link ID: 25732 - Posted: 11.30.2018

Abby Olena Mice with faulty circadian clocks are prone to obesity and diabetes. So are mice fed a diet high in fat. Remarkably, animals that have both of these obesity-driving conditions can stay lean and metabolically healthy by simply limiting the time of day when they eat. In a study published today (August 30) in Cell Metabolism, researchers report that restricting feeding times to mice’s active hours can overcome both defective clock genes and an unhealthy diet, a finding that may have an impact in the clinic. The work corroborates previous research showing how powerful restricted feeding can be to improve clock function, says Kristin Eckel-Mahan, a circadian biologist at the University of Texas Health Science Center at Houston who did not participate in the study. Over the last 20 years, biologists have found circadian clocks keeping physiologic time in almost every organ. They have also shown that mice with disrupted clocks often develop metabolic diseases, such as obesity, and that circadian clock proteins physically bind to the promoters of many metabolic regulators and instruct them when to turn on and off. For Satchidananda Panda of the Salk Institute, these lines of evidence came together in 2009, when his group published a study showing that in mice without the clock component Cryptochrome, feeding and fasting could drive the expression of some, but not all, of the metabolic regulators throughout the body. Other groups have also confirmed that even in the absence of the clock it is still possible to drive some genetic rhythms. In this latest study, he and colleagues wanted to look more closely at how the cycling of clock and metabolic transcripts induced by time-restricted feeding, rather than normal genetic rhythms, influences the health of mice. © 1986 - 2018 The Scientist

Keyword: Obesity
Link ID: 25711 - Posted: 11.24.2018

Selene Meza-Perez, Troy D. Randall Fat is a loaded tissue. Not only is it considered unsightly, the excess flab that plagues more than two-thirds of adults in America is associated with many well-documented health problems. In fact, obesity (defined as having a body mass index of 30 or more) is a comorbidity for almost every other type of disease. But, demonized as all body fat is, deep belly fat known as visceral adipose tissue (VAT) also has a good side: it’s a critical component of the body’s immune system. VAT is home to many cells of both the innate and adaptive immune systems. These cells influence adipocyte biology and metabolism, and in turn, adipocytes regulate the functions of the immune cells and provide energy for their activities. Moreover, the adipocytes themselves produce antimicrobial peptides, proinflammatory cytokines, and adipokines that together act to combat infection, modify the function of immune cells, and maintain metabolic homeostasis. Unfortunately, obesity disrupts both the endocrine and immune functions of VAT, thereby promoting inflammation and tissue damage that can lead to diabetes or inflammatory bowel disease. As researchers continue to piece together the complex connections between immunity, gut microbes, and adipose tissues, including the large deposit of fat in the abdomen known as the omentum, they hope not only to gain an understanding of how fat and immunity are linked, but to also develop fat-targeted therapeutics that can moderate the consequences of infectious and inflammatory diseases. © 1986 - 2018 The Scientist.

Keyword: Obesity; Neuroimmunology
Link ID: 25710 - Posted: 11.24.2018

Abby Olena Anticipating something tasty can lead to a watering mouth and grumbling stomach, but these familiar responses aren’t the only ways the body prepares for nourishment. According to a study published today (November 15) in Cell, sensing food primes mice to process incoming nutrients by directions from the central nervous system to the liver. “It’s a great tour de force combining [several strategies] in one paper to then identify pathways by which food anticipation could alter hepatic metabolism,” says Christoph Buettner, a physician and researcher at Icahn School of Medicine at Mount Sinai in New York who was not involved in the study. “It’s interesting that even before your food hits your tongue or ends up in your stomach, there are changes that prepare an organism for nutrient storage.” Two types of cells in the brain’s hypothalamus have been shown in previous studies to play opposing roles in regulating how much an organism eats. AgRP neurons are turned on when energy stores are low, making an animal seek out food, while POMC neurons, activated when an animal is sated, inhibit eating. Up until a few years ago, the prevailing wisdom was that ingested food resulted in hormonal changes and subsequent neuronal activation after some lag time, says Jens Brüning, an endocrinologist and geneticist at the Max Planck Institute for Metabolism Research in Germany. But in 2015, researchers from the University of California, San Francisco, showed in mice that these neurons change their state of activation nearly instantaneously in response to the sight or smell of food. © 1986 - 2018 The Scientist

Keyword: Obesity
Link ID: 25709 - Posted: 11.24.2018