Chapter 9. Homeostasis: Active Regulation of the Internal Environment
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By RENEE ENGELN ON Tuesday, in the wake of an online petition signed by thousands of people, Facebook announced that it was removing “feeling fat” from its list of status update emoticons. The petition argued that the offending emoticon, with its chubby cheeks and double chin, reinforced negative body images, and Facebook seemed to agree. Is it really such a big deal if you tell everyone how fat you feel? After all, a simple “I’m so fat!” can result in a chorus of empathetic voices, saying, “Me, too!” or “You’re beautiful just the way you are!” And that will help you feel better, and help others feel better, too — right? Wrong. As someone who studies this type of public body self-disparagement, known as “fat talk,” I can say that it probably will make you feel worse. And it may drag down other people with you. Conversational shaming of the body has become practically a ritual of womanhood (though men also engage in it). In a survey that a colleague and I reported in 2011 in the Psychology of Women Quarterly, we found that more than 90 percent of college women reported engaging in fat talk — despite the fact that only 9 percent were actually overweight. In another survey, which we published in December in the Journal of Health Psychology, we canvassed thousands of women ranging in age from 16 to 70. Contrary to the stereotype of fat talk as a young woman’s practice, we found that fat talk was common across all ages and all body sizes. Most important, fat talk is not a harmless social-bonding ritual. According to an analysis of several studies that my colleagues and I published in 2012 in the Psychology of Women Quarterly, fat talk was linked with body shame, body dissatisfaction and eating-disordered behavior. Fat talk does not motivate women to make healthier choices or take care of their bodies; in fact, the feelings of shame it brings about tend to encourage the opposite. © 2015 The New York Times Company
Keyword: Anorexia & Bulimia
Link ID: 20691 - Posted: 03.17.2015
|By Dina Fine Maron Obesity stems primarily from the overconsumption of food paired with insufficient exercise. But this elementary formula cannot explain how quickly the obesity epidemic has spread globally in the past several decades nor why more than one third of adults in the U.S. are now obese. Many researchers believe that a more complex mix of environmental exposures, lifestyle, genetics and the microbiome’s makeup help explain that phenomenon. And a growing body of work suggests that exposure to certain chemicals—found in nature as well as industry—may play an essential role by driving the body to produce and store surplus fat in its tissues. Evidence of that cause-and-effect relationship in humans is still limited, but in laboratory animals and in petri dishes data linking the chemicals to problematic weight gain are mounting. Moreover, the effects in animals appear to be passed on not just to immediate offspring but also grandchildren and great-grandchildren—potentially accounting for some multigenerational obesity. The murkier picture for humans may become clearer in the next five years, says Jerry Heindel, a health science administrator at the National Institute of Environmental Health Sciences. His agency is now funding 57 grants related to obesity and diabetes, he said on March 2 at a meeting of the Institute of Medicine (IOM). The studies look at how chemicals, including those that appear to alter hormone regulation (such as the plasticizer bisphenol A and the antibacterial chemical triclosan), affect weight gain or insulin resistance. Thirty-two of the ongoing studies are in humans. And 20 of those will help assess the longer-term risks to children by tracking the youngsters' chemical levels in utero or as newborns and beyond. © 2015 Scientific American
Link ID: 20660 - Posted: 03.07.2015
Dr. Lisa Sanders. On Thursday we challenged Well readers to solve the case of a middle-aged woman with arthritis who developed a wasting illness after what looked like a simple cold. Her rheumatologist was worried that the immune suppressing medications the patient took to treat her joint disease had caused the new illness. More than 300 of you took on the challenge, and 17 of you correctly identified this rarity. The correct diagnosis is … Whipple’s disease The first reader to make the diagnosis was Mike Natter, a second-year medical student at the Sidney Kimmel Medical College at Thomas Jefferson University in Philadelphia. Mike said it was an easy case for him because he had been studying for an exam the next day and had just read about the disease. He is a frequent contributor to this column and says that he got the right diagnosis twice before but this was the first time he got it in first. Well done, Mike! The Diagnosis Whipple’s was first identified in 1907 by Dr. George Whipple, who was caring for a fellow physician who had “gradual loss of weight and strength, stools consisting chiefly of neutral fat and fatty acids, indefinite abdominal signs, and a peculiar multiple arthritis.” The patient eventually died. Dr. Whipple suspected an infectious cause because he found bacteria in many of the patient’s affected tissues, but the organism itself wasn’t identified for nearly 80 years. The bug, Tropheryma whipplei, is common and found mostly in soil. And yet the infection is rare. There have been only about 1,000 reported cases of Whipple’s disease in the more than one hundred years since it was first described. Over two-thirds of those were in middle-aged white men. Many of them were farmers or others who had occupational exposure to soil. © 2015 The New York Times Company
Link ID: 20659 - Posted: 03.07.2015
|By Charles Schmidt The notion that the state of our gut governs our state of mind dates back more than 100 years. Many 19th- and early 20th-century scientists believed that accumulating wastes in the colon triggered a state of “auto-intoxication,” whereby poisons emanating from the gut produced infections that were in turn linked with depression, anxiety and psychosis. Patients were treated with colonic purges and even bowel surgeries until these practices were dismissed as quackery. The ongoing exploration of the human microbiome promises to bring the link between the gut and the brain into clearer focus. Scientists are increasingly convinced that the vast assemblage of microfauna in our intestines may have a major impact on our state of mind. The gut-brain axis seems to be bidirectional—the brain acts on gastrointestinal and immune functions that help to shape the gut's microbial makeup, and gut microbes make neuroactive compounds, including neurotransmitters and metabolites that also act on the brain. These interactions could occur in various ways: microbial compounds communicate via the vagus nerve, which connects the brain and the digestive tract, and microbially derived metabolites interact with the immune system, which maintains its own communication with the brain. Sven Pettersson, a microbiologist at the Karolinska Institute in Stockholm, has recently shown that gut microbes help to control leakage through both the intestinal lining and the blood-brain barrier, which ordinarily protects the brain from potentially harmful agents. Microbes may have their own evolutionary reasons for communicating with the brain. They need us to be social, says John Cryan, a neuroscientist at University College Cork in Ireland, so that they can spread through the human population. © 2015 Scientific American
By KATIE THOMAS The retired tennis player Monica Seles spent this month making the rounds of television talk shows, appearing on everything from “Good Morning America” to “The Dr. Oz Show” to share her personal struggle with binge eating. “It took a while until I felt comfortable talking about it,” she said in a People magazine interview, explaining that she secretly devoured food for years while she was a professional athlete. “That’s one of the reasons I decided to do this campaign: to raise awareness that binge eating is a real medical condition.” But that is not the only reason. Ms. Seles is a paid spokeswoman for Shire, which late last month won approval to market its top-selling drug, Vyvanse, to treat binge-eating disorder, a condition that once existed in the shadow of better-known disorders like anorexia and bulimia but was officially recognized as its own disorder in 2013 by the American Psychiatric Association. As Shire introduces an ambitious campaign to promote Vyvanse but also to raise awareness about the disorder, some are saying the company is going too far to market a drug, a type of amphetamine, that is classified by the federal government as having a high potential for abuse. Shire’s track record is adding to the worry: The company helped put another once-stigmatized condition — attention deficit hyperactivity disorder — on the medical map and made billions of dollars from the sale of drugs, like Vyvanse and Adderall, to treat it. In recent years, federal officials have cited the company for inappropriately marketing Vyvanse and other A.D.H.D. drugs. In addition, some drug safety experts questioned why the Food and Drug Administration so swiftly approved the drug for binge eating — seeking little outside input — despite the fact that, for decades, amphetamines, which suppress the appetite, were widely abused as a treatment for obesity. © 2015 The New York Times Company
Keyword: Anorexia & Bulimia
Link ID: 20614 - Posted: 02.25.2015
by Penny Sarchet An injection and a dash of exercise could be the secret to keeping trim. These rainbow mice, imaged in infrared to reveal how much energy they are burning while on a treadmill, are revealing how a shot can boost a muscle's ability to burn calories. Red body parts show where lots of energy is being used. The mouse on the right has a red patch on its left hind leg, which corresponds to the spot where it received an injection of a substance developed by Denice Hodgson-Zingman from the University of Iowa and colleagues. The substance is a type of morpholino, a compound that can be designed to target specific genes, in this case to alter proteins responsible for storing energy. The disruption causes muscles to burn more energy even during mild exercise, such as a gentle trot on a treadmill. In contrast, the untreated mouse on the left, which is doing the same amount of exercise, is using less energy in the same spot, as illustrated by the colder green colour. The researchers hope the injection will help people who want to burn more calories do so through routine everyday activities, eliminating the need for intense exercise. Journal reference: Molecular Therapy, DOI: 10.1038/mt.2015.2141 © Copyright Reed Business Information Ltd.
Link ID: 20610 - Posted: 02.24.2015
By Aleksandra Sagan, CBC News Photos of emaciated women proudly displaying their protruding hips and ribs, as well as thinspirational quotes "fat-shaming" those who dare to eat, continue to thrive on social media, despite the best attempts by sites like Instagram to temper the reach of the pro-eating disorder community. Some girls gain thousands of followers posting pictures of "thigh gaps" and "bikini bridges," as well as underweight celebrities and thinspirational quotes like model Kate Moss's mantra: "nothing tastes as good as skinny feels." "It just provides a lot of positivity for them, just in a very maladaptive way," says Edward Selby, of the more visual outlet that sites like Instagram provide. An assistant professor of clinical psychology at Rutgers University in New Jersey, Selby is the director of a lab there that studies what makes people more likely to develop anorexia (self-starvation), bulimia (binge-eating and purging) and other eating disorders. About one in 20 young women in Canada has an eating disorder, according to the Toronto-based National Initiative for Eating Disorders. And people suffering from these diseases often feel good after exercising, purging, swallowing a laxative or doing other things that contribute to their illness, Selby says. They get caught in a "cyclic feedback loop," with the positive emotions pushing them to engage more in these risky behaviours. Online pro-anorexia and bulimia communities simply add to that loop by celebrating a person's unhealthy achievements, he says. "Finally under 130! Woohoo!" writes one user with a photo of her feet on a scale. "Yay congrats," reads a response. Another girl posts a screen grab from an app claiming that she's been fasting for more than a day. It receives 32 likes and a "great job" among the comments. ©2015 CBC/Radio-Canada
Keyword: Anorexia & Bulimia
Link ID: 20607 - Posted: 02.24.2015
Boer Deng Smoking marijuana may stoke a yearning for crisps, but understanding how it affects hunger is relevant not just to those who indulge in it. The drug has yielded a ripe target for scientists who seek to stimulate or suppress appetite: the receptor CB1, found in cells throughout the body. When activated by the anti-nausea drug dronabinol — which is also a component of marijuana (Cannabis sativa) — CB1 prompts the release of hunger-promoting hormones1. And suppressing its activity is thought to aid in weight loss2. But the mechanism by which the receptor kills or kindles appetite is not entirely understood. Now neuroscientist Tamas Horvath, of Yale University in New Haven, and colleagues report in Nature that nerve cells called pro-opiomelanocortin (POMC) neurons play a key role in this process3. POMC had generally been thought to promote satiation, but Horvath's team found that POMC neurons in the brain release not just a hunger-suppressing hormone, but also one that promotes appetite. Which hormone is secreted is regulated by a protein in the cells' mitochondria, structures that regulate energy levels. When the CB1 receptor is activated, this mitochondrial protein induces POMC to switch from secreting the substance that suppresses gorging to one that encourages it. The finding is intriguing, says Uberto Pagotto, a neuroscientist at the University of Bologna who has studied cannabinoids for many years. “It gives us a different starting point to look at CB1 receptors and the mitochondria,” he says. © 2015 Nature Publishing Group
Scientists have uncovered more than 90 new gene regions that could help explain why some people are more likely to put on weight than others. The team scoured DNA libraries of more than 300,000 people, constructing the largest-ever genetic map of obesity. Looking for consistent patterns they found a link with genes involved in brain processes, suggesting obesity could partly have a neurological basis. The results are published in the journal Nature. Researchers from the international Giant consortium (Genetic Investigation of Anthropometric Trait), analysed the genetics behind body mass index (a ratio of weight and height ). And in a separate Nature paper they looked specifically at how genetics influence where fat is distributed around the body. Fat around the abdomen for example can cause more health problems than fat carried around the thighs. Some 33 newly pinpointed gene regions were linked to body fat distribution - giving further clues about why some people are pear-shaped while others put on weight more around the tummy. They also identified more than 60 genetic locations that influence body mass index - tripling the number previously known. And some of these regions have links with the nervous system. © 2015 BBC
|By Erika Beras We know junk food can change the way bodies are shaped. Now, a study finds that those irresistible sweet and salty concoctions may also change the way brains are wired—at least in rats. Researchers divided rats into two groups—one labeled Cafeteria, the other called Chow. Both groups got a typical rat food diet, but the Cafeteria rats also got a bonus: meat pies, cakes and cookies. Both rat groups gained weight. But the Cafeteria rats gained significantly more than the Chows did—nearly half a pound more, which is a big body burden for a rat. But more important, over two weeks time the Cafeteria rats seemed to care less and less about even seeking out a balanced diet. This new behavior endured even after the rats were returned to their more healthy fare. The study is in the journal Frontiers in Psychology. [Amy C. Reichelt, Margaret J. Morris and R.F. Westbrook, Cafeteria diet impairs expression of sensory-specific satiety and stimulus-outcome learning] The researchers think junk-food diets cause lasting changes in the rewards circuits part of the brain—which plays a big role in decision-making. So if you’re a regular cookie eater and the next time you mindlessly reach for a cookie you wonder why you can’t help yourself—well, it could be because you’re not in charge, your rewired brain is. © 2015 Scientific American
/ by Tanya Lewis, LiveScience You know the feeling: the dryness in the mouth, the stickiness in the throat and the creeping salivation — thirst. But what causes feelings of thirst in the brain? In a new study, scientists used laser light to activate groups of neurons in the brains of mice. By targeting specific neuron groups, the scientists could make the animals drink even if they weren't thirsty, and stop drinking even if they were thirsty. Understanding how the brain causes feelings of thirst could help scientists learn what goes awry in disorders that make people drink too much or too little fluid, researchers say. "Thirst has attracted a lot of interest because it is such a basic function for all organisms," said Yuki Oka, a neuroscientist currently at the California Institute of Technology and co-author of the study published today (Jan. 26) in the journal Nature. Before this study, scientists knew which brain regions were activated by dehydration and hydration. "But key information was missing as to which were controlling thirst," Oka told Live Science. In the new study, Oka and a team of colleagues at Columbia University used a technique called optogenetics to pinpoint the origin of thirst impulses in the brains of mice. The researchers injected the mouse brains with a virus that made certain cells sensitive to laser light, and when scientists shone the laser on those cells, it caused them to turn nerve impulses "on" or "off." © 2015 Discovery Communications, LLC.
Link ID: 20525 - Posted: 01.28.2015
By Bruce Bower Alexithymia: An inability to find words to describe one’s own feelings Mental health workers regard alexithymia as more akin to a personality trait than to a mental disorder. Many people with psychiatric conditions such as autism spectrum disorder and panic disorder — characterized by physical symptoms with emotional causes — also display alexithymia. Researchers are finding that alexithymia has the same effect on people with and without mental disorders and that it undermines the ability to describe others’ feelings as well as one’s own. A study appearing online January 21 in Royal Society Open Science found that nine of 21 young women with eating disorders had difficulty recognizing others’ facial emotions and that this characteristic was probably related to alexithymia, not some inherent feature of anorexia or bulimia. The researchers also looked at 21 women who had alexithymia but no psychiatric disorders and found that seven had comparable problems identifying others’ expressions of happiness, fear and other emotions. Citations R. Brewer et al. Emotion recognition deficits in eating disorders are explained by co-occurring alexithymia. Royal Society Open Science. Published online January 21, 2015. doi: 10.1098/rsos.140382. © Society for Science & the Public 2000 - 2015.
By Melissa Healy A pill may help those whose out-of-control eating is a cause of extreme distress An ADHD drug may offer hope for a different psychiatric disorder Binge eating disorder, a newly recognized condition in which bouts of voracious eating lead to guilt, shame and often obesity, may yield to lisdexamfetamine (marketed as Vyvanse), a medication that has been used for several years to treat attention deficit and hyperactivity disorder in children and adults. In an 11-week clinical trial that tested a range of Vyvanse dosages, researchers found that, compared to those taking a placebo pill, subjects diagnosed with binge eating disorder who took a daily 50 or 70 mg dose of the ADHD drug had fewer binge eating episodes, were more likely to cease binge eating for a four-week period, reported greater improvement in their functioning, and lost substantially more weight. The findings, published online early in the journal JAMA Psychiatry on Wednesday, offer early evidence that patients whose consumption patterns are punctuated by episodes of out-of-control eating may be helped by some medication. The disorder, which has in recent years won wider recognition by the psychiatric establishment, has traditionally been treated with psychotherapy. It has proved a difficult condition to treat. Among those getting lisdexamfetamine, side effects were similar to those experienced by adults who take the medication to treat symptoms of ADHD, including dry mouth, difficulty falling asleep, increased heart rate and headaches. Adverse events prompted six of 196 subjects in the active arm of treatment to withdraw from the study.
Keyword: Anorexia & Bulimia
Link ID: 20492 - Posted: 01.17.2015
By Brady Dennis The Food and Drug Administration on Wednesday approved a device aimed at helping obese people shed weight in a novel way – by targeting the nerve pathway between the brain and the stomach that controls feelings of hunger and fullness. The Maestro Rechargeable System, as it is known, consists of an electrical charge generator, wire leads and electrodes that are implanted surgically into a patient’s abdomen. It sends electrical pulses designed to interfere with the vagus nerve, which signals to the brain when the stomach is full or empty. Though researchers don't know exactly how such electrical stimulation leads to weight loss, the approach seems promising. In a year-long clinical trial involving 233 patients with a body-mass index, or BMI, of 35 or greater, those who received a working Maestro device lost 8.5 percent more weight than those without it. About half those in the experimental group lost at least 20 percent of their excess weight, and more than a third lost more than 25 percent of their excess weight. The overall figure was below the original goal of the trial, which was to show weight loss of 10 percent more excess weight in the control group than in those using the new device. Nevertheless, an FDA advisory group said the data showed sustained weight loss among participants and argued that the benefits of the device outweigh its risks for certain patients. In the clinical trial, some patients experienced nausea, vomiting, surgical complications and other side effects. The FDA is requiring the device's manufacturer, EnteroMedics, to conduct a five-year, post-approval study to gather additional data about its safety and effectiveness.
Link ID: 20488 - Posted: 01.15.2015
Carl Zimmer Among scientists who study how our DNA affects our weight, a gene called FTO stands out. “It’s the poster child for the genetics of obesity,” said Struan F. Grant, an associate professor of pediatrics at the University of Pennsylvania School of Medicine. In 2007, researchers discovered that people with a common variant of FTO tend to be heavier than those without it. Since then, studies have repeatedly confirmed the link. On average, one copy of the risky variant adds up to 3.5 extra pounds of weight. Two copies of the gene bring 7 extra pounds — and increase a person’s risk of becoming obese by 50 percent. But the gene doesn’t seem to have always been a problem. If scientists had studied FTO just a few decades ago, they would have found no link to weight whatsoever. A new study shows that FTO became a risk only in people born after World War II. The research, published this week in the Proceedings of the National Academy of Sciences, raises questions that extend far beyond obesity. Genes clearly influence our health in many ways, but so does our environment; often, it is the interplay between them that makes the difference in whether we develop obesity or cancer or another ailment. But the relative importance of certain genes may shift over the years, the new study suggests, as our environment changes. James Niels Rosenquist of Massachusetts General Hospital and his colleagues were inspired to conduct the study by recent research documenting how people’s experiences alter the effects of their genes. A variant of a gene called AKT1, for example, can raise the risk of psychosis — but only if the carrier smokes a lot of marijuana. If he avoids smoking, the AKT1 variant doesn’t cause a problem. © 2015 The New York Times Company
By James Gallagher Health editor, BBC News website Higher rates of obesity and ill-health have been found in shift workers than the general population. Health Survey for England data showed they were in worse health despite often being young. The lead researcher told the BBC that the rise of zero-hours contracts may be increasing the numbers doing shift work and could raise "pretty serious problems" for the nation's health. Scientists said it was "fairly clear now" that shift work was unhealthy. The report, by the Health and Social Care Information Centre, showed 33% of men and 22% of women of working age were doing shift work. They defined shifts as employment outside 0700-1900. Rachel Craig, the research director for the Health Survey for England, told the BBC: "Overall, people who are doing shift work are not quite as healthy as their counterparts doing regular working hours." The data showed 30% of shift workers were obese, compared with 24% of men and 23% of women doing normal hours. Meanwhile, 40% of men and 45% of women on shifts had long-standing health conditions such as back-pain, diabetes or chronic obstructive pulmonary disease compared with 36% and 39% of the rest of the population. Younger people Shift working is most common in the 16-24 age group with nearly half of men and a third of women having this working pattern. The rates fell with age so that fewer than a third of men and a fifth of women were working shifts after the age of 55. Ms Craig said that, overall, young people should be in better health: "You'd expect less ill-health and fewer long-standing conditions that reflect lifestyle like obesity, so it makes it an even stronger relationship [between shifts and poor health]." BBC © 2014
by Andy Coghlan It may not sound very appetising, but an edible powder made from waste excreted by bacteria in our guts may help people to avoid gaining weight. Stabilising a person's weight could have a major health impact, says Gary Frost of Imperial College London, because as people on Western diets grow older, they tend to put on between 0.3 and 0.8 kilograms per year on average. A fatty acid called propionate is released when the bacteria in our gut digest fibre. Propionate makes people feel full by activating cells in the large intestine that produce the satiety hormones GLP-1 and PYY: these tell the brain that it's time to stop eating. But to trigger a big enough dose of this appetite-suppressing signal from gut bacteria alone, people would have to eat extremely large amounts of fibre. To get around that, Frost and his team made the molecule in a concentrated form called inulin-propionate ester (IPE). "That gives you eight times the amount of someone following a typical Western diet," he says. To test its appetite-stemming properties, the team gave powdered IPE, mixed in with fruit juice or a milkshake, to a group of overweight volunteers every day for six months. A type of ordinary fibre was given to another set of people, who acted as controls. Only one of the 25 volunteers taking IPE put on more than 3 per cent of their body weight over that time, compared with six of the 24 controls. One reason for this might be that the IPE recipients ate around 9 per cent less over the six months. © Copyright Reed Business Information Ltd.
Link ID: 20416 - Posted: 12.13.2014
By Dr. Mitesh Popat It’s common knowledge that eating better, exercising more, limiting alcohol intake and not smoking can lead to a healthier, longer life. For many, sustaining healthy behaviors is not easy. For diabetics, maintaining healthy behaviors is even more challenging, although it is critical. If well managed, the disease can be held in check; if not, it can be devastating, leading to kidney failure, blindness, stroke and even death. It may be a surprise that there is strong association between depression, anxiety and diabetes. Not only can depression and anxiety seriously affect the ability to manage the disease, but there also is evidence that, for some, depression plays a role in actually causing diabetes. Research indicates that depression is unrecognized and untreated in approximately two-thirds of patients with diabetes. Whether cause or effect, the medical profession needs to do more to address the psychological issues associated with the disease. As a family medicine physician, I see the association on daily basis. Some patients are so overwhelmed by the necessary daily self-care that comes with diabetes that they become highly anxious and depressed. Others who are suffering from complications or are having trouble managing their blood sugar levels may feel a loss of control and get anxious or depressed. These symptoms are often compounded in people who live in poverty, including the low-income Latinos, African Americans and seniors whom we care for at Marin Community Clinics. Diabetes has become an epidemic in these groups. Working three jobs and constantly worrying about making ends meet can trigger depression and anxiety in anyone. Add to that the need to adopt a disciplined healthy lifestyle, and it can be a real struggle.
Link ID: 20410 - Posted: 12.13.2014
By Nsikan Akpan Gut surgery is often the only option for life-threatening obesity and diabetes, but what if doctors could cut the pounds without using a knife? Scientists have engineered an antiobesity drug that rivals the dramatic benefits seen with surgery, dropping excess body weight by a third. Though the work was done only in rodents, the drug is the first to influence three obesity-related hormones in the gut at once. Bariatric surgery, including gastric bypass, typically involves limiting food intake by removing part of the stomach or intestines. Yet it does more than shrink the size of patient’s stomach or intestines. It also changes the release of multiple gut-related hormones, explains clinical endocrinologist Stephen O'Rahilly of the University of Cambridge in the United Kingdom, who wasn’t involved with the study. That’s important, because years of eating a diet high in fat and sugar can throw a person’s metabolism into disarray. Cells undergo genetic reprogramming that negatively impacts how they process sugar and store fat, locking in obesity. This pattern makes it harder and harder to lose weight, even if a person changes their diet and begins exercising. Bariatric surgery interrupts that cycle by stimulating the production of several hormones that reduce blood sugar, burn fat, and curb appetite. (It may also change the composition of the gut’s microbes.) Three of these hormones are called glucagon-like peptide-1 (GLP-1), gastric inhibitory peptide (GIP), and glucagon. Cells in your gut release GLP-1 and GIP after a meal to keep your body’s blood sugar levels in a normal range. GLP-1 also curbs appetite, signaling to your brain that you are full. In type 2 diabetes, the body stops responding to GLP-1 and GIP, which contributes to hyperglycemia, or too much blood sugar. Hyperglycemia causes the devastating hallmarks of diabetes, such as kidney injury, cardiovascular disease, and nerve damage. © 2014 American Association for the Advancement of Science.
Link ID: 20408 - Posted: 12.10.2014
by Michael Slezak The elusive link between obesity and high blood pressure has been pinned down to the action of leptin in the brain, and we might be able to block it with drugs. We've known for more than 30 years that fat and high blood pressure are linked, but finding what ties them together has been difficult. One of the favourite candidates has been leptin – a hormone produced by fat cells. Under normal circumstances, when fat cells produce leptin, the hormone sends the message that you've had enough food. But in people with obesity, the body stops responding to this message, and large levels of leptin build up. Leptin is known to activate the regulatory network called the sympathetic nervous system, and it's the activation of sympathetic nerves on the kidneys that seem to be responsible for raising blood pressure. Leptin has thus been linked to blood pressure. However, conclusive evidence has been hard to come by. Michael Cowley of Monash University in Melbourne, Australia, and his colleagues have now conducted a string of experiments that provide some evidence. Through genetic and drug experiments in mice, they have pinpointed an area in the mouse brain that increases blood pressure when it is exposed to high leptin levels. This region is called the dorsomedial hypothalamus, and is thought to be involved in controlling energy consumption. Their findings show that high levels in leptin do indeed boost blood pressure, via this brain region. © Copyright Reed Business Information Ltd.
Link ID: 20398 - Posted: 12.06.2014