Links for Keyword: Obesity

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Fat ‘remembering’ past obesity drives yo-yo diet effect

Ian Sample Science editor Losing weight can be a frustrating game: after months of successful slimming, the kilos may soon pile on again, leaving people back where they started. No one factor drives the yo-yo effect, but new research points to fatty tissue as a leading culprit. Fat “remembers” past obesity and resists attempts to lose weight, scientists found. Researchers identified the biological memory after examining fat tissue from people with obesity before and after they lost weight after bariatric surgery. The tissues were further compared with fat from healthy individuals who had never been obese. The analysis showed that fat cells were affected by obesity in a way that altered how they responded to food, potentially for years. In tests, the cells grew faster than others by absorbing nutrients more swiftly. Prof Ferdinand von Meyenn, a senior author on the study at the Federal Institute of Technology in Zurich, said: “Our study indicates that one reason maintaining body weight after initial weight loss is difficult is that the fat cells remember their prior obese state and likely aim to return to this state. “The memory seems to prepare cells to respond quicker, and maybe also in unhealthy ways, to sugars or fatty acids.” Further work on mouse cells traced the biological memory to chemical modifications on DNA or the proteins DNA is wrapped around. These epigenetic changes alter gene activity and metabolism. Writing in Nature, the scientists describe how formerly obese mice gained weight faster than others when put on a high-fat diet, suggesting a shift in metabolism that made it easier for them to gain weight. The memory of obesity in fat cells was not solely to blame, however. The scientists suspect a similar memory exists in brain cells that affects how much food animals consume and how much energy they expend. © 2024 Guardian News & Media Limited

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 29568 - Posted: 11.20.2024

Limiting sugar in infancy reduces the risk of diabetes and hypertension

By Skyler Ware The occasional sweet treat likely won’t ruin your health. But too much added sugar at a young age could increase the risk of health complications later in life. Limiting added sugars during the first 1,000 days after conception — so during pregnancy and a baby’s first two years — reduces the risk of a child developing diabetes and hypertension in adulthood, researchers report October 31 in Science. “In the first 1,000 days of life, the brain and body are gearing up to finish developing,” says Sue-Ellen Anderson-Haynes, a registered dietician in Boston and a spokesperson for the Academy of Nutrition and Dietetics. Nutrition during that timeframe is particularly important, she says, because “everything the mother eats gets transformed into nutrients for the fetus.” Current nutritional guidelines recommend that adults consume less than 40 grams of added sugars per day and that children under age 2 consume no added sugars. But by age 2, the average American child consumes about 29 grams of added sugars a day; the average adult consumes nearly 80 grams per day. To study the effects of excess added sugars early in life, economist Tadeja Gracner of the University of Southern California in Los Angeles and colleagues took advantage of a natural experiment: the end of sugar rationing in the United Kingdom after World War II. While rationing was in effect, each person was allotted about 8 ounces (about 227 grams) of sugar per week. Once sugar rationing ended in September 1953, daily sugar consumption for adults jumped to around 80 grams per day. Even though other foods were rationed during and after WWII, sugar intake increased the most after rationing was lifted. Consumption of other rationed foods, such as cheese, milk and fresh fruits remained relatively constant once rationing ended. Similarly, the end of butter rationing caused many families to switch from margarine, with its unsaturated fats, back to butter, so overall fat consumption did not increase significantly. © Society for Science & the Public 2000–2024

‘Poo milkshake’ boosts the microbiome of c-section babies

By Mariana Lenharo Feeding a baby born by caesarean section milk containing a tiny bit of their mother’s poo introduces beneficial microbes to their gut, according to a clinical trial. The approach might one day help to prevent diseases during childhood and later in life. The study — which reported early results last week during IDWeek, a meeting of infectious-disease specialists and epidemiologists in Los Angeles, California — is the first randomized controlled trial to test the ‘poo milkshake’ concept. The preliminary findings confirm researchers’ hypothesis that a small faecal-matter transplant is enough to have a positive effect on the infant’s microbiome, says Otto Helve, director of the public-health department at the Finnish Institute for Health and Welfare in Helsinki, Finland, and the study’s primary investigator. Inherited microbes Some studies show that babies born by c-section, rather than vaginal birth, have a higher risk of asthma, inflammation of the digestive system and other diseases associated with a dysfunctional immune system1. Scientists think that these differences arise because babies born by c-section aren’t exposed to and rapidly colonized by the microbes in their mothers’ vaginas and guts. Studies have even shown that c-section babies are more vulnerable to pathogens in hospitals than are babies born by vaginal birth2. Experiments have attempted to compensate for that by swabbing babies born by c-section with microbes from their mother’s vagina or giving them these microbes orally, a practice known as ‘vaginal seeding’. But this technique has had limited success, because vaginal microbes, scientists have learnt, cannot effectively colonize infants’ guts, says Yan Shao, a microbiome scientist at the Wellcome Sanger Institute in Hinxton, UK. © 2024 Springer Nature Limited

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory and Learning
Link ID: 29525 - Posted: 10.26.2024

Eating less can lead to a longer life: massive study in mice shows why

By Elie Dolgin Cutting calorie intake can lead to a leaner body — and a longer life, an effect often chalked up to the weight loss and metabolic changes caused by consuming less food. Now, one of the biggest studies1 of dietary restrictions ever conducted in laboratory animals challenges the conventional wisdom about how dietary restriction boosts longevity. The study, involving nearly 1,000 mice fed low-calorie diets or subjected to regular bouts of fasting, found that such regimens do indeed cause weight loss and related metabolic changes. But other factors — including immune health, genetics and physiological indicators of resiliency — seem to better explain the link between cutting calories and increased lifespan. “The metabolic changes are important,” says Gary Churchill, a mouse geneticist at the Jackson Laboratory in Bar Harbor, Maine, who co-led the study. “But they don’t lead to lifespan extension.” To outside investigators, the results drive home the intricate and individualized nature of the body’s reaction to caloric restriction. “It’s revelatory about the complexity of this intervention,” says James Nelson, a biogerontologist at the University of Texas Health Science Center in San Antonio. The study was published today in Nature by Churchill and his co-authors, including scientists at Calico Life Sciences in South San Francisco, California, the anti-ageing focused biotech company that funded the study. Counting calories Scientists have long known that caloric restriction, a regimen of long-term limits on food intake, lengthens lifespan in laboratory animals2. Some studies3,4 have shown that intermittent fasting, which involves short bouts of food deprivation, can also increase longevity. © 2024 Springer Nature Limited

Should I stay (and eat) or should I go? How the brain balances hunger with competing drives

By Giorgia Guglielmi As the famed tale “Hansel and Gretel” makes clear, hunger can change behavior. The two lost and starving siblings give in to the temptation of a gingerbread cottage and ignore the danger lurking within—a wicked witch who has created the delicious house as a trap. Hunger is such a powerful driver that animals often pursue food at the expense of other survival needs, such as avoiding predators or recovering from injury. Hungry vicuñas, for example, will sometimes increase their risk of predation by pumas to get something to eat, behavioral ecologists have shown. Scientists know many of the key cells and circuits behind these competing drives—such as the hypothalamic “hunger neurons” that regulate food intake. But how the brain juggles the need to eat amidst other urges has remained mysterious, says Henning Fenselau, who leads the Synaptic Transmission in Energy Homeostasis group at the Max Planck Institute for Metabolism Research in Köln, Germany. “This is still a huge question [in neuroscience],” he says. In recent years, however, new clues about where and how hunger collides with rival motivations have come from technology to manipulate and monitor individual neurons across multiple brain regions at once. Those findings suggest that hunger neuron activity can override some brain signals, such as fear and pain. Exploring the brain’s ability to handle multiple needs simultaneously may offer insights into decision-making, anxiety and other neuropsychiatric conditions—helping to explain why people sometimes make maladaptive choices, says Nicholas Betley, associate professor of biology at the University of Pennsylvania. © 2024 Simons Foundation

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 14: Attention and Higher Cognition
Link ID: 29515 - Posted: 10.12.2024

Why do obesity drugs seem to treat so many other ailments?

By Mariana Lenharo There’s a bar in Baltimore, Maryland, that very few people get to enter. It has a cocktail station, beer taps and shelves stacked with spirits. But only scientists or drug-trial volunteers ever visit, because this bar is actually a research laboratory. Here, in a small room at the US National Institutes of Health (NIH), scientists are harnessing the taproom ambience to study whether blockbuster anti-obesity drugs might also curb alcohol cravings. Evidence is mounting that they could. Animal studies and analyses of electronic health records suggest that the latest wave of weight-loss drugs — known as glucagon-like peptide 1 (GLP-1) receptor agonists — cut many kinds of craving or addiction, from alcohol to tobacco use. “We need randomized clinical trials as the next step,” says Lorenzo Leggio, an addiction researcher at the NIH in Baltimore. In the trial he is leading, volunteers sit at the bar and get to see, smell and hold their favourite drinks, while going through tests such as questions about their cravings; separately, participants will have their brains scanned while looking at pictures of alcohol. Some will be given the weight-loss drug semaglutide (marketed as Wegovy) and others will get a placebo. George Koob and Lorenzo Leggio pose for a photograph in a research laboratory designed as a bar inside the National Institutes of Health’s hospital. Curbing addiction isn’t the only potential extra benefit of GLP-1 drugs. Other studies have suggested they can reduce the risk of death, strokes and heart attacks for people with cardiovascular disease1 or chronic kidney ailments2, ease sleep apnoea symptoms3 and even slow the development of Parkinson’s disease4. There are now hundreds of clinical trials testing the drugs for these conditions and others as varied as fatty liver disease, Alzheimer’s disease, cognitive dysfunction and HIV complications (see ‘Diseases that obesity drugs might treat’ at the end of this article). © 2024 Springer Nature Limited

Brain goop that traps hunger neurons drives obesity

By Max Kozlov A build-up of sticky goo that traps neurons in an appetite-control centre in the brain has been implicated in worsening diabetes and obesity, according to research on mice1. The goo also prevents insulin from reaching brain neurons that control hunger. Inhibiting production of the goo led mice to lose weight, experiments found. These findings points to a new driver of metabolic disorders and could help scientists to identify targets for drugs to treat these conditions. These results were published today in Nature. Metabolic diseases such as type 2 diabetes and obesity can develop when the body’s cells become insensitive to insulin, a hormone that regulates blood-sugar levels. Scientists searching for the mechanism that causes this insulin resistance have homed in on a part of the brain called the arcuate nucleus of the hypothalamus, which senses insulin levels and, in response, adjusts energy expenditure and sensations of hunger. As the animals develop insulin resistance, a type of cellular scaffolding, called the extracellular matrix, that holds the hunger neurons in place becomes a disorganized goo. Previously, researchers had noticed that this scaffolding changes when mice are fed a high-fat diet2. The researchers wanted to see whether these brain changes might drive insulin resistance rather than merely developing alongside it. The authors fed mice a high-fat, high-sugar diet for 12 weeks and monitored the scaffolding around the hunger neurons by taking tissue samples and monitoring gene activity. © 2024 Springer Nature Limited

Research That Led to Obesity Drugs Wins Major Medical Prize

By Gina Kolata and Stephanie Nolen The Lasker Awards, a prestigious set of prizes given for advances in medicine and public health research, were given on Thursday to scientists whose research helped lead to the discovery of a new class of obesity drugs, infectious disease specialists who worked on the drivers of H.I.V. infection and how to stop it, and a scientist who discovered a way the body protects itself from infectious diseases and cancer. The Laskers are highly regarded in the fields of biomedicine and are sometimes seen as foretelling recipients of the Nobel Prizes in the sciences. This year’s Lasker-DeBakey Clinical Medical Research Award went to three scientists for their work on GLP-1, the hormone that led to drugs like Wegovy (the same compound is the basis for Ozempic), which have transformed the treatment of obesity. They are Dr. Joel Habener, Svetlana Mojsov and Lotte Bjerre Knudsen. Each of the three honorees played a role at a key moment: finding the new hormone; finding the biologically active shorter form of GLP-1; and, finally, showing that the shorter form elicits weight loss. Of course, as almost always happens in science, many others also played key roles, and the Lasker Foundation mentioned some as part of its citation. And one of the honorees, Dr. Mojsov, is receiving what many deem a long overdue recognition. The story of GLP-1 begins with Dr. Habener, an endocrinologist who arrived in the mid-1970s at Massachusetts General Hospital, where he decided to work on diabetes. Most of the focus had been on insulin, which lowers blood sugar levels. But there is another hormone, glucagon, that raises it. Dr. Habener decided to try to find the gene for glucagon, hoping it would lead to a way to squelch the hormone and so lower blood sugar. Working with anglerfish, he discovered a gene for another mysterious protein that resembles glucagon. © 2024 The New York Times Company

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Emotions, Aggression, and Stress
Link ID: 29488 - Posted: 09.21.2024

Inflammation May Be the Root of Our Maladies

By Daniela J. Lamas In the near future, the story of drugs like Ozempic may no longer be primarily about weight loss and diabetes. We now know that these drugs can reduce heart and kidney disease. They could very well slow the progression of dementia. They might help women struggling with infertility to get pregnant. They are even tied to lower mortality from Covid. It’s easy to attribute this to the dramatic weight loss provided by Ozempic and other drugs in its class, known as GLP-1 receptor agonists. But that isn’t the whole story. Rather, the drugs’ numerous benefits are pointing to an emerging cause of so much human disease: inflammation. As a critical care doctor, I have long considered inflammation a necessary evil, the mechanism through which our bodies sound an alarm and protect us from threat. But a growing body of research complicates that understanding. Inflammation is not just a marker of underlying disease but also a driver of it. The more medicine learns about inflammation, the more we are learning about heart disease and memory loss. This should serve as a reminder of the delicate balance that exists in our bodies, of the fact that the same system that protects us can also cause harm. Inflammation is the body’s response to infection or injury. Our innate immune system — the body’s first line of defense against bacterial or viral intruders — protects us by triggering an inflammatory response, a surge of proteins and hormones that fight infection and promote healing. Without that response, we would die of infectious disease in childhood. But by the time we make it to our 50s and beyond, our innate immune system can become more of a hindrance as inflammation begins to take a toll on the body. Acute inflammation, which happens in response to an illness, for instance, is often something we can see — an infected joint is swollen and red. But chronic inflammation is usually silent. Like high blood pressure, it’s an invisible foe. Sign up for the Opinion Today newsletter Get expert analysis of the news and a guide to the big ideas shaping the world every weekday morning. Get it sent to your inbox. © 2024 The New York Times Company

Should young kids take the new anti-obesity drugs? What the research says

By Julian Nowogrodzki Millions of adults around the world take potent drugs such as Wegovy to shed pounds. Should kids do the same? That question is growing more urgent in the face of mounting evidence that children and adolescents, as well as adults, slim down if they take the latest generation of obesity drugs. Clinical trials1,2 have shown that many adolescents with obesity lose substantial amounts of weight on these drugs, which work by mimicking a natural hormone called glucagon-like peptide 1 (GLP-1). The GLP-1 mimics semaglutide, commonly sold as Ozempic and Wegovy, and liraglutide, marketed as Saxenda and Victoza, are approved in the United States and Europe to treat obesity in children as young as 12. Now a trial has produced some of the first data on anti-obesity drugs in even younger children: those aged 6 to 11. The study3 reports that children who were treated with liraglutide showed a decrease in their body mass index (BMI), a measure of obesity. The results were published on 10 September in The New England Journal of Medicine. Nature asked specialists in obesity about the costs and benefits of giving the GLP-1 mimics to youngsters who are still growing and developing. Why test powerful weight-loss drugs on kids? Most kids with obesity become teens with obesity and then adults with obesity. Many young children with severe obesity have “already developed significant health issues”, says physician Sarah Ro, who directs the University of North Carolina Physicians Network Weight Management Program and has served as a consultant to Novo Nordisk, the manufacturer of semaglutide. Her clinic in Hillsborough treats children with severe obesity who have health issues such as high blood pressure, type 2 diabetes or an advanced form of liver disease linked to excess weight. © 2024 Springer Nature Limited

Time to Say Goodbye to the B.M.I.?

By Roni Caryn Rabin Move over, body mass index. Make room for roundness — to be precise, the body roundness index. The body mass index, or B.M.I., is a ratio of height to weight that has long been used as a medical screening tool. It is one of the most widely used health metrics but also one of the most reviled, because it is used to label people overweight, obese or extremely obese. The classifications have been questioned by athletes like the American Olympic rugby player Ilona Maher, whose B.M.I. of 30 technically puts her on the cusp of obesity. “But alas,” she said on Instagram, addressing online trolls who tried to shame her about her weight, “I’m going to the Olympics and you’re not.” Advocates for overweight individuals and people of color note that the formula was developed nearly 200 years ago and based exclusively on data from men, most of them white, and that it was never intended for medical screening. Even physicians have weighed in on the shortcomings of B.M.I. The American Medical Association warned last year that B.M.I. is an imperfect metric that doesn’t account for racial, ethnic, age, sex and gender diversity. It can’t differentiate between individuals who carry a lot of muscle and those with fat in all the wrong places. “Based on B.M.I., Arnold Schwarzenegger when he was a bodybuilder would have been categorized as obese and needing to lose weight,” said Dr. Wajahat Mehal, director of the Metabolic Health and Weight Loss Program at Yale University. “But as soon as you measured his waist, you’d see, ‘Oh, it’s 32 inches.’” So welcome a new metric: the body roundness index. B.R.I. is just what it sounds like — a measure of how round or circlelike you are, using a formula that takes into account height and waist, but not weight. © 2024 The New York Times Company

The surprising cause of fasting’s regenerative powers

By Max Kozlov A black and gold fork, knife and spoon lay on a pale blue plate over a white background in harsh sunlight Some of the health benefits of fasting kick in when food consumption resumes, animal experiments show.Credit: Getty Breaking a fast carries more health benefits than the fasting itself, a study in mice shows1. After mice had abstained from food, stem cells surged to repair damage in their intestines — but only when the mice were tucking into their chow again, the study found. But this activation of stem cells came at a price: mice were more likely to develop precancerous polyps in their intestines if they incurred a cancer-causing genetic change during the post-fasting period than if they hadn’t fasted at all. These results, published in Nature on 21 August, show that “regeneration isn’t cost-free”, says Emmanuelle Passegué, a stem-cell biologist at Columbia University Irving Medical Center in New York City, who wasn’t involved in the study. “There is a dark side that is important to consider.” Fast way to health Researchers have been investigating the potential health benefits of fasting for decades, and there is evidence that the practice can help to delay certain diseases and lengthen lifespan in rodents. But the underlying biological mechanisms behind these benefits have been a mystery. In 2018, Ömer Yilmaz, a stem-cell biologist at the Massachusetts Institute of Technology in Cambridge, and his colleagues found that stem cells are likely to be implicated. During fasting, these cells begin burning fats rather than carbohydrates as an energy source, leading to a boost in their ability to repair damage to the intestines in mice2. © 2024 Springer Nature Limited

A hunger protein reverses anorexia symptoms in mice

By Erin Garcia de Jesús An appetite-stimulating protein can reverse anorexia in mice. Mice with lack of appetite and weight loss — symptoms similar to people with anorexia — that were genetically tweaked to secrete a protein called ACBP ate more food and weighed more than anorexic animals with an ACBP deficit, researchers report August 14 in Science Translational Medicine. The finding points to a potential treatment target for people with the eating disorder. “Anorexia is a whole brain and body illness” that is difficult to treat, says psychiatrist and neuroscientist Rachel Ross, who wasn’t involved with the new work. “One of the major challenges is that the brain of a person with anorexia is directly fighting against their body.” While the body screams for food, the brain prioritizes the need to restrict weight (SN: 7/26/13). Globally, around 1 percent of women and 0.2 percent of men develop the disorder. Roughly just a third of those people fully recover. Yet, no drugs are available; treatment typically involves medical care to stabilize weight and therapy to mend patients’ relationships with food. Some cancer patients can also develop a similar disorder called cancer cachexia, which comes from an impaired metabolism, that is similarly tough to treat (SN: 7/30/24). “Anything that has the potential to provide some sort of mechanism that would be useful for creating a new therapeutic is huge,” says Ross, of Albert Einstein College of Medicine and Montefiore Health System in New York City. And although there’s no guarantee the results will apply to people, the new findings suggest that ACBP, a protein that helps turn on parts of the brain that arouse appetite, may have that potential. © Society for Science & the Public 2000–2024.

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 8: Hormones and Sex
Link ID: 29435 - Posted: 08.15.2024

Which Weight Loss Drug Should You Choose (if You Get to Choose)?

By Gina Kolata People with obesity now have a choice between two powerful drugs to help them lose weight. One is semaglutide, sold by Novo Nordisk as Wegovy for obesity treatment and as Ozempic for diabetes. The second, tirzepatide, is sold by Eli Lilly as Zepbound for obesity and as Mounjaro for diabetes. Many with neither obesity or diabetes take the drugs to get thinner. A recent study suggested that people lost more weight taking Mounjaro than they did taking Ozempic, and it may leave you wondering: Which should I take? And if I’m already taking one of them, should I switch? The answers, obesity medicine experts say, are not so simple. Here are some factors that can help sort out hype from realistic hope. Is one weight loss drug really better than the other? For now, it’s hard to say. All of the information available comes from “highly flawed studies,” said Dr. Diana Thiara, medical director of the weight loss clinic at the University of California, San Francisco. That includes the recent study comparing Mounjaro and Ozempic. Using electronic health records, the researchers reported that those taking Mounjaro lost an average of 15.3 percent of their weight after a year. Those taking Ozempic lost an average of 8.3 percent. While that sounds impressive, Dr. Susan Z. Yanovski, co-director of the Office of Obesity Research at the National Institute of Diabetes and Digestive and Kidney Diseases, said, “I wouldn’t make any decisions on my medical care based solely on a study like this.” There’s an inherent difficulty in using electronic health records, she noted, because it is not known why the patients were taking the drugs — the study was underway before Zepbound was approved for treating obesity. The investigators looked at prescriptions for Ozempic and Mounjaro, which were approved to treat diabetes. Yet many in the study did not have diabetes. © 2024 The New York Times Company

Weight loss drugs without the nausea? Mouse study suggests it may be possible

By Mitch Leslie Millions of people have taken glucagon-like peptide-1 (GLP-1) agonist drugs such as Ozempic to lose weight, despite the fact that the drugs can cause severe nausea and vomiting. But a new mouse study shows distinct groups of neurons in the brain diminish appetite and trigger nausea, a finding that could lead to less stomach-turning treatments that activate one set of cells and not the other. “It’s a very solid paper,” says neuroscientist Chuchu Zhang of the University of California, Los Angeles, who wasn’t connected to the study. “It shows us something new” about the activity of GLP-1 agonists. Scientists haven’t pinned down exactly how GLP-1 agonist drugs work, and previous studies have produced conflicting results on where they exert their effects. Some research suggests the drugs curb appetite by targeting the hypothalamus, a control center for physiological functions such as thirst and hunger that is located in the center of the brain. Other findings point to the rear portion of the brain, known as the hindbrain, and still others implicate the vagus nerve, which carries messages to and from organs such as the stomach and heart. All of these locations contain cells bearing GLP-1 receptors, to which the drugs bind. Another key question is whether the drugs cause weight loss primarily because people feel full or because they feel nauseated—a side effect suffered by more than half of individuals who take the drugs. “Do we need the nausea and aversion [to food] to see the appetite suppression and weight loss?” asks neuroscientist Amber Alhadeff of the Monell Chemical Senses Center. To answer that question, she and her colleagues first tried to pinpoint where GLP-1 agonists act. Using a genetically modified virus containing genes for either of two cell-killing molecules, they selectively eliminated cells bearing GLP-1 receptors in the hypothalamus, the hindbrain, or the vagus nerve. Only destroying the hindbrain cells prevented weight loss when mice received a GLP-1 agonist, suggesting this region curtails appetite. In a follow-up experiment, the researchers stimulated cells in the hindbrain and found that even slender mice lost weight. © 2024 American Association for the Advancement of Science.

Ozempic Quiets Food Noise in the Brain—But How?

By Lauren J. Young Kimberly Chauche, a corporate secretary in Lincoln, Neb., says she’s always been overweight. When she was as young as five years old, her doctors started trying to figure out why. Since then her life has involved nutritionists and personal trainers, and eventually she sought therapists to treat her compulsive eating and weight-related anxiety. Yet answers never arrived, and solutions never lasted. At 43, Chauche was prescribed a weight-loss medication called Wegovy—one of a new class of drugs that mimic a hormone responsible for insulin production. She took her first dose in March 2024, injecting it into herself with a needle. Within a couple of months she had lost almost 20 pounds, and that felt great. But the weight loss seemed like a bonus compared with a startling change in how she reacted to food. She noticed the shift almost immediately: One day her son was eating popcorn, a snack she could never resist, and she walked right past the bowl. “All of a sudden it was like some part of my brain that was always there just went quiet,” she says. Her eating habits improved, and her anxiety eased. “It felt almost surreal to put an injector against my leg and have happen in 48 hours what decades of intervention could not accomplish,” she says. “If I had lost almost no weight, just to have my brain working the way it’s working, I would stay on this medication forever.” Chauche is hardly alone in her effusive descriptions of how Wegovy vanquished her intrusive thoughts about food—an experience increasingly referred to as the “quieting of food noise.” Researchers—some of whom ushered in the development of these blockbuster drugs—want to understand why. Among them is biochemist Svetlana Mojsov of the Rockefeller University, who has spent about 50 years investigating gut hormones that could be key to regulating blood glucose levels. In seeking potential treatments for type 2 diabetes, Mojsov ultimately focused on one hormone: glucagonlike peptide 1, or GLP-1. Her sequence of the protein in the 1980s became the initial template for drugs like Wegovy. The medications, called GLP-1 receptor agonists, use a synthetic version of the natural substance to activate the hormone’s receptors. The first ones arrived in 2005. In 2017 the U.S. Food and Drug Administration approved semaglutide—now widely known as Ozempic. © 2024 SCIENTIFIC AMERICAN,

Burning the stomach lining reduces the ‘hunger hormone’ and cuts weight

By Meghan Rosen An experimental weight loss procedure cranks up the heat to dial down hunger. Blasting a patch of patients’ stomach lining with thermal energy curbed hunger and cut pounds, researchers reported in a small pilot study to be presented at the annual Digestive Disease Week meeting on May 19 in Washington, D.C. Called gastric fundus mucosal ablation, the procedure relies on an endoscope, a thin tube that can be threaded down the throat. It takes less than an hour and doesn’t require hospitalization. “The advantage of this is that it’s a relatively straightforward procedure,” says Cleveland Clinic surgical endoscopist Matthew Kroh, who was not involved with the work. Side effects, which included mild nausea and cramping, are minimal, one study author said in a news conference on May 8. That’s a big difference from bariatric surgery, considered the gold standard treatment for obesity, which includes many techniques to restrict stomach size or affect food absorption. Patients can be hospitalized for days and take weeks to recover. Obese people often avoid these treatments because they don’t want to endure surgery, Kroh says. The new procedure could one day offer an easier option — if the results hold up in larger groups of patients. “There’s potential,” Kroh says, “but I think we have to be cautious.” The trial included 10 women, so the method is still at the proof-of-concept stage. On average, the women lost nearly 8 percent of their body weight, some 19 pounds, over six months. That’s less than patients typically see from bariatric surgery or pharmaceutical treatments like the anti-obesity drug Wegovy (SN 12/13/23). © Society for Science & the Public 2000–2024.

Experimental obesity drug packs double punch to reduce weight

By Asher Mullard With obesity drugs now helping people to slim down, researchers are working to capitalize on their popularity by bulking up the weight-loss drug pipeline. The latest contender takes a Trojan horse approach — hiding a small molecule in a gut-hormone-mimicking peptide already used in obesity drugs — to strike a double blow to the brain cells that control appetite. The new work, which demonstrated the effects of this drug candidate in mice and rats, was published today in Nature1. “It’s a strong paper,” says Daniel Drucker, an endocrinologist at Mount Sinai Hospital in Toronto, Canada, who helped to unravel the role of gut hormones such as GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic polypeptide) in obesity. The blockbuster weight-loss drugs semaglutide (Wegovy) and tirzepatide (Zepbound) act by mimicking these hormones, binding to their receptors on neurons in the brain that control hunger pangs. These drugs can help people to lose 15–20% of their body weight. And it could be possible to eke even more activity from these hormone mimics by fusing them to other drugs, the new study suggests. “Very high marks for the novelty” of the research, says Drucker, who was not involved and consults for the pharmaceutical industry. “Let’s hope that we’ll see some proof of concept in the clinic”, when the approach is tested in humans. Trojan therapeutics The drug contender takes aim at both the GLP-1 receptor and the NMDA receptor, an ion channel found on cells in the brain that was linked to obesity in 20152. At the time, small molecules that blocked the NMDA receptor seemed like a non-starter for obesity-drug developers, because this type of compound, which includes the party drug and antidepressant ketamine, is riddled with harmful side effects. But Christoffer Clemmensen, a metabolism specialist at the University of Copenhagen, saw a path forwards. He speculated that it might be possible to sidestep the safety risks by fusing an NMDA-receptor blocker to a gut-hormone mimic that acts only on the neurons that regulate appetite. © 2024 Springer Nature Limited

A Year on Ozempic Taught Me We’re Thinking About Obesity All Wrong

By Johann Hari Ever since I was a teenager, I have dreamed of shedding a lot of weight. So when I shrank from 203 pounds to 161 in a year, I was baffled by my feelings. I was taking Ozempic, and I was haunted by the sense that I was cheating and doing something immoral. I’m not the only one. In the United States (where I now split my time), over 70 percent of people are overweight or obese, and according to one poll, 47 percent of respondents said they were willing to pay to take the new weight-loss drugs. It’s not hard to see why. They cause users to lose an average of 10 to 20 percent of their body weight, and clinical trials suggest that the next generation of drugs (probably available soon) leads to a 24 percent loss, on average. Yet as more and more people take drugs like Ozempic, Wegovy and Mounjaro, we get more confused as a culture, bombarding anyone in the public eye who takes them with brutal shaming. This is happening because we are trapped in a set of old stories about what obesity is and the morally acceptable ways to overcome it. But the fact that so many of us are turning to the new weight-loss drugs can be an opportunity to find a way out of that trap of shame and stigma — and to a more truthful story. In my lifetime, obesity has exploded, from being rare to almost being the norm. I was born in 1979, and by the time I was 21, obesity rates in the United States had more than doubled. They have skyrocketed since. The obvious question is, why? And how do these new weight-loss drugs work? The answer to both lies in one word: satiety. It’s a concept that we don’t use much in everyday life but that we’ve all experienced at some point. It describes the sensation of having had enough and not wanting any more. The primary reason we have gained weight at a pace unprecedented in human history is that our diets have radically changed in ways that have deeply undermined our ability to feel sated. My father grew up in a village in the Swiss mountains, where he ate fresh, whole foods that had been cooked from scratch and prepared on the day they were eaten. But in the 30 years between his childhood and mine, in the suburbs of London, the nature of food transformed across the Western world. He was horrified to see that almost everything I ate was reheated and heavily processed. The evidence is clear that the kind of food my father grew up eating quickly makes you feel full. But the kind of food I grew up eating, much of which is made in factories, often with artificial chemicals, left me feeling empty and as if I had a hole in my stomach. In a recent study of what American children eat, ultraprocessed food was found to make up 67 percent of their daily diet. This kind of food makes you want to eat more and more. Satiety comes late, if at all. © 2024 The New York Times Company

Why queasiness kills hunger: brain circuit identified

By Gillian Dohrn No one wants to eat when they have an upset stomach. To pinpoint exactly where in the brain this distaste for eating originates, scientists studied nauseated mice. The work, published in Cell Reports on 27 March1, describes a previously uncharacterized cluster of brain cells that fire when a mouse is made to feel nauseous, but don’t fire when the mouse is simply full. This suggests that responses to satiety and nausea are governed by separate brain circuits. “With artificial activation of this neuron, the mouse just doesn’t eat, even if it is super hungry,” says Wenyu Ding at the Max Planck Institute for Biological Intelligence in Martinsried, Germany, who led the study. Ding and colleagues suspected that this group of neurons was involved in processing negative experiences, such as feeling queasy, so they injected the mice with a chemical that induces nausea and then scanned the animals’ brains. This confirmed that the neurons are active when mice feel nauseous. Using a light-based technique called optogenetics, the team artificially activated the neurons of mice that had been deprived of food in the hours before the experiment. When the neurons were ‘off’, the mice ate. When the researchers turned them on, the mice walked away mid-chow. These brain cells could influence how fast you eat — and when you stop Researchers also blocked the activity of these neurons in nauseated mice that were hungry and found that the mice overcame their nausea to eat. © 2024 Springer Nature Limited

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 9: Hearing, Balance, Taste, and Smell
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 29263 - Posted: 04.20.2024

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