Chapter 9. Homeostasis: Active Regulation of the Internal Environment

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

Keyword: Obesity
Link ID: 24534 - Posted: 01.17.2018

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

Keyword: Obesity
Link ID: 24533 - Posted: 01.17.2018

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

Keyword: Obesity
Link ID: 24521 - Posted: 01.12.2018

By LISA FOGARTY The last time I tasted my birthday cake was the spring I turned 13, a few months before I discovered the elimination game. The game went like this: first, stop eating sweets. Second, blot sauces, oils and dressings with paper towels while no one was looking. Third, count grams of fat, reject any food with over 3 grams, and keep a calorie tally in the back of your math notebook (where, if someone found it, they’d assume it was just math). The elimination game also involved adding. Add the toilet bowl and the sewer down the street to the list of places you could discard food. Add candy bar wrappers and empty full-fat yogurt containers to your bedroom nightstand as evidence that you’re not sick. Finally, add up the pounds you’ve lost that week that signify victory. So easy. Repeat. At 38, I am a former anorexic in recovery. Over the years, I’ve discovered my strengths — making my two children feel loved, encouraging sources to open up for stories I write as a magazine reporter — but I’ve never been as good at anything as I was at the elimination game. Growing up in leafy suburban Queens, N.Y., I became obsessed with made-for-TV movies from the ’80s and ’90s about anorexia. All of my early eating disorder role models — a nightmarish choice of words, but when you’re in the grip of this mental disorder, that’s what they are — were scared, sad and relatable. They were also all very, very young. My stars were Karen Carpenter, Tracy Gold and my favorite, Jennifer Jason Leigh, who, in the 1981 movie “The Best Little Girl in the World,” appeared appealingly helpless in high-waisted jeans. With one exception, these movies wrapped up anorexia in tidy boxes where therapy, feeding tubes, weight gain, finding release from a controlling mother’s grip and discovering the joys of food led to a happy ending. I was a kid who no longer ate dessert when I watched Ms. Leigh’s character jovially lick an ice cream cone beside her therapist. But even I knew then that ice cream was neither the problem nor the solution. © 2018 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 24515 - Posted: 01.11.2018

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

Keyword: Obesity
Link ID: 24511 - Posted: 01.10.2018

Want to eat better? Sleep more. Increasing the amount of sleep a person gets has been linked to eating fewer sugary foods, and making better nutritional choices. Wendy Hall, at King’s College London, and her team enlisted 42 volunteers to help them investigate the link between sleep and diet. Half the participants were given advice on how to get more sleep – such as avoiding caffeine before bed, establishing a relaxing routine, and trying not to go to bed too full or hungry. This advice was intended to help them boost the amount of sleep they each got by 90 minutes a night. The remaining 21 volunteers received no such advice. The team found that, of those who were given the advice, 86 per cent spent more time in bed, and around half slept for longer than they used to. These extended sleep patterns were associated with an average reduction in the intake of free sugars of 10 grams a day. People who were getting more sleep also ate fewer carbohydrates. There were no significant changes in diet in the control group. Free sugars include those that are added to foods by manufacturers or during cooking at home, as well as sugars in honey, syrups and fruit juice. “The fact that extending sleep led to a reduction in intake of free sugars suggests that a simple change in lifestyle may really help people to consume healthier diets,” says Hall. © Copyright New Scientist Ltd.

Keyword: Sleep; Obesity
Link ID: 24510 - Posted: 01.10.2018

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

Keyword: Obesity; Neuroimmunology
Link ID: 24473 - Posted: 12.30.2017

By JOANNA KLEIN Most rodents are just rodents. And the ones with exceptional abilities are usually cartoon rats or mice. But here in the real world of flesh, bones, brains and nerves that we mammals use each second to survive, some woodland rodents really do have a superpower that helps them tolerate cold and endure harsh winters. In grasslands from central Canada to Texas, a species known as thirteen-lined ground squirrels can adjust their body temperature to match the air around them. This is especially important during hibernation: They don’t have to fatten up like bears or find warm hide-outs like conventional mice and rats. They slumber, surviving in bodies just above freezing. Another species, the Syrian hamster, does it too. “They combine warm and cold blooded animals in one,” said Elena Gracheva, a neurophysiologist at Yale University. This uncanny ability to withstand prolonged cold (and even hypothermia) results in part from an adaptation these rodents have developed in molecules they share with other mammals, including us, Dr. Gracheva and her colleagues found in a study published last week in the journal Cell Reports. Unique properties of TRPM8, a cold-sensing protein found in their peripheral nervous systems, shields these rodents from harsh weather. It’s really important because if they’re too cold, they can’t hibernate — just like if you’re too cold, you might have trouble sleeping. The new research brings scientists closer to understanding enigmas of hibernation and solving a mystery of how this molecular sensor works. The work also may lead to therapies for allodynia, a nerve condition that causes some people to misperceive something normally not-so-cold as painful. © 2017 The New York Times Company

Keyword: Pain & Touch
Link ID: 24464 - Posted: 12.28.2017

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

Keyword: Obesity
Link ID: 24450 - Posted: 12.22.2017

Laurel Hamers The hardy souls who manage to push shorts season into December might feel some kinship with the thirteen-lined ground squirrel. The critter hibernates all winter, but even when awake, it’s less sensitive to cold than its nonhibernating relatives, a new study finds. That cold tolerance is linked to changes in a specific cold-sensing protein in the sensory nerve cells of the ground squirrels and another hibernator, the Syrian hamster, researchers report in the Dec. 19 Cell Reports. The altered protein may be an adaptation that helps the animals drift into hibernation. In experiments, mice, which don’t hibernate, strongly preferred to hang out on a hot plate that was 30° Celsius versus one that was cooler. Syrian hamsters (Mesocricetus auratus) and the ground squirrels (Ictidomys tridecemlineatus), however, didn’t seem to notice the chill until plate temperatures dipped below 10° Celsius, notes study coauthor Elena Gracheva, a neurophysiologist at Yale University. Further work revealed that a cold-sensing protein called TRPM8 wasn’t as easily activated by cold in the squirrels and hamsters as in rats. Found in the sensory nerve cells of vertebrates, TRPM8 typically sends a sensation of cold to the brain when activated by low temperatures. It’s what makes your fingertips feel chilly when you’re holding a glass of ice water. It’s also responsible for the cooling sensation in your mouth after you chew gum made with menthol. |© Society for Science & the Public 2000 - 2017

Keyword: Miscellaneous
Link ID: 24445 - Posted: 12.20.2017

By Simon Makin The brain's reward system learns the actions that produce positive outcomes, such as obtaining food or sex. It then reinforces the desire to initiate those behaviors by inducing pleasure in anticipation of the relevant action. But in some circumstances this system can become oversensitized to pleasurable but harmful behaviors, producing pathological impulses like drug addiction, binge eating and compulsive gambling. But what if we could spot impulsive urges in the brain and intervene to prevent the act? This is the promise of a new study published December 18 in Proceedings of the National Academy of Sciences, led by neurosurgeon Casey Halpern, of Stanford University. His team identified a “signature” of impulsive urges in part of the brain's reward-learning circuitry, the nucleus accumbens. Delivering electrical pulses to this region on detecting this activity reduced binge-eating behavior in mice. They also observed the same signature in a human brain, suggesting the technique has potential for treating a range of conditions involving compulsive behaviors. “We've identified a brain biomarker of loss of control,” Halpern says. “If we can use that to prevent any of these potentially dangerous actions, we can help a lot of people.” Researchers used a variation on deep-brain stimulation (DBS) in their experiments, a well-established treatment to diminish the shaking present in Parkinson's disease that is also showing promise in other conditions including depression and obsessive-compulsive disorder. Exactly how DBS has beneficial effects is still being debated, but there can be side effects. When treating movement disorders, patients may experience tingling and muscle contraction, says neurosurgeon Tipu Aziz of the University of Oxford. The long-term consequences in other regions are unknown but could include seizures, or effects on cognition, he says. © 2017 Scientific American,

Keyword: Drug Abuse; Obesity
Link ID: 24441 - Posted: 12.20.2017

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

Keyword: Obesity; Drug Abuse
Link ID: 24440 - Posted: 12.19.2017

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

Keyword: Obesity; Emotions
Link ID: 24420 - Posted: 12.14.2017

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

Keyword: Obesity; Hormones & Behavior
Link ID: 24407 - Posted: 12.08.2017

By CLYDE HABERMAN This is a season of gustatory excess, when families gather at ample tables, offices hold lavish parties, and people eat and drink till they are beyond sated. Not everyone, though. There is a grimmer corner of America. It is populated by men and, more commonly, women who shun food not because they are too poor to afford it, but because they are too troubled to desire it. The country’s obesity epidemic deservedly draws constant attention, but many have a diametrically opposite problem: They are obsessively, and perilously, thin. Some experts estimate that 30 million Americans are plagued at some point in their lives by disorders like anorexia nervosa, binge-eating and bulimia. About one-third of them are men, belying broadly held assumptions that this is almost exclusively a female concern. Many are blacks, Latinos and Asians, countering another routine belief that this is a whites-only issue. Some get better, and stay that way. Others cycle through periods of recovery and relapse. And some, roughly a third of them, remain chronically ill or die. The National Eating Disorders Association describes anorexia as having “the highest mortality rate of any psychiatric illness.” Retro Report, a series of video documentaries exploring the continued impact of major news stories of the past, examines how public understanding of this issue has evolved since the startling death of the singer Karen Carpenter in 1983. Her illness, anorexia, had long been familiar to medical professionals. An English doctor, William Gull, gave it its name in the 1870s, but the condition had been recognized for centuries. A few women proclaimed saints by the Roman Catholic Church are believed to have been anorexic. Although the problem was always hiding in plain sight, Ms. Carpenter’s death at 32 made everyone see it clearly. She and her brother, Richard, were the hugely popular Carpenters duo, their records selling in the tens of millions with 1970s hits like “Close to You,” “We’ve Only Just Begun” and “Rainy Days and Mondays.” © 2017 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 24387 - Posted: 12.04.2017

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

Keyword: Obesity
Link ID: 24365 - Posted: 11.27.2017

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

Keyword: Obesity; Chemical Senses (Smell & Taste)
Link ID: 24352 - Posted: 11.24.2017

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

Keyword: Obesity
Link ID: 24351 - Posted: 11.24.2017

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

Keyword: Obesity
Link ID: 24350 - Posted: 11.24.2017

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

Keyword: Obesity; Attention
Link ID: 24347 - Posted: 11.22.2017