Latest news with #fatcells
Forbes
6 days ago
- Health
- Forbes
An Unexpected Clue To How Metformin, The World's Top Diabetes Drug, Works
Metformin is an unassuming hero of modern medicine. For more than sixty years, this humble pill has been a mainstay of diabetes care, helping millions of people manage their blood sugar. It lowers blood sugar, improves cholesterol, modestly reduces weight, and is so safe it's prescribed to millions worldwide. And yet, for decades, scientists haven't fully understood how it works. The standard explanation has long been that metformin works in the liver, reducing how much sugar it sends into the bloodstream. It also helps muscles and fat cells respond more effectively to insulin. More recent research added other suspects: the gut, which can tweak hormones and the microbiome, and a cellular pathway called mTOR, a major regulator of metabolism and longevity. But a new study published in Science Advances suggests that part of metformin's magic might be happening somewhere unexpected: in the brain. The Blood Sugar Command Center Researchers turned their attention to a protein called Rap1, found in a small pocket of the brain known as the ventromedial hypothalamus (VMH). This area is a metabolic mission control, coordinating hunger, energy use, and glucose balance. When scientists switched off Rap1 in this brain region in mice, blood sugar levels fell, even without metformin. But when they kept Rap1 switched on, metformin lost its blood-sugar-lowering power. The results hint that, at the doses typically prescribed, metformin may partly work by silencing Rap1's activity in the brain, not just by acting on the liver or gut. Most of us think of blood sugar control as the domain of the pancreas, liver, and muscles. Yet the brain is deeply involved. The VMH works like an air traffic controller, taking in information from across the body and sending out signals to adjust glucose production and use. Metformin, it seems, may be tapping into this high-level control system. By dialing down Rap1 activity, the drug might trigger a cascade of neural instructions that ripple out to the rest of the body, improving how tissues handle sugar. Beyond Diabetes Metformin has drawn attention far beyond the diabetes world. It's being studied for its potential to slow certain aspects of aging, with researchers probing whether its effects on pathways like mTOR could help extend not just lifespan but healthspan. The discovery of the brain-Rap1 link opens new possibilities. Could this same circuit be part of metformin's longevity effects? If so, drugs that target Rap1 or its related pathways might someday offer more precise ways to improve metabolism or promote healthy aging, perhaps without some of metformin's side effects. When Old Drugs Tell New Tales This does not mean discarding what is already known about metformin's effects on the liver, muscles, and gut. Those mechanisms are still in play. But at everyday doses, the brain may have a starring role in how the drug works. At much higher doses, peripheral mechanisms can take over, but in real-world clinical use, the brain's contribution could be key. The finding is also a reminder that the brain and body are not separate actors in the story of metabolism. They are in constant conversation, adjusting and responding to keep systems in balance. And as this research shows, an old drug can reveal something entirely new about that conversation. Even after six decades, metformin still has secrets to share: secrets that may change how both the medicine itself and the intricate links between the brain, the body, and health are understood.
Fox News
28-05-2025
- Health
- Fox News
Scientists may have discovered why the pounds come back after losing weight
Many factors lead to the frustrating cycle of weight gain and weight loss — but the driving force may be fat cells keeping a memory of obesity. That's according to a recent study that was first published in the journal Nature last fall. Researchers say that fat cells influence abnormal metabolic pathways in the body long after pounds are shed, which could make it more likely for people to regain weight. The team of Swiss scientists were curious whether regaining weight after slimming down is due to "metabolic memory," where the body remembers and strives to return to its former state of obesity. They analyzed chemical markers on fat cells in mice who were fed a high-fat diet. Next, when the mice were fed only a standard meal, the researchers analyzed their fatty tissue after they had lost weight, according to the study write-up. The team then compared these samples to a lean mice group that was fed a standard meal to see if the chemical markers on the fat cells were associated with unhealthy changes in the body. The mice on the high-fat diet continued to have unhealthy changes in their metabolism after losing weight, including more difficulty in regulating sugar metabolism, more inflammation and abnormal fat storage. Mice who were previously obese gained weight faster compared to the control group after they ate a high-fat diet — suggesting a continued impairment in metabolism after losing weight, the researchers found. The study also looked at human samples, analyzing how the genes in fat cells can lead to unhealthy changes in the body as they did in mice. The researchers analyzed the fatty tissues of participants before and after they underwent bariatric surgery, comparing them to the fatty cells of lean individuals who did not have a history of obesity. "This recent research suggests that after someone loses weight, their fat cells don't fully go back to 'normal.'" In obese individuals, the genes from fat cells continued to function abnormally in the body, leading to more inflammation and metabolic problems two years after losing weight. One limitation of the study is that it only looked at one type of cell – fat cells. More research is needed to determine whether other cells or tissues in the body also keep a memory of being overweight, the researchers acknowledged. Fat cells indeed have a memory of being obese, which can make it easier to regain weight and stay in a state that promotes inflammation and metabolic issues, confirmed Gretchen Zimmermann, registered dietitian and vice president of clinical strategy at Vida Health, a virtual obesity care provider. (She was not part of the study.) "This recent research suggests that after someone loses weight, their fat cells don't fully go back to 'normal,'" Zimmermann told Fox News Digital. But while biology plays a critical role in obesity, it's not everything, she cautioned. "A complex mix of genetics, biology, environment, psychology, medications and social determinants all shape obesity," Zimmermann said. "Keep moving, eating real food and building muscle." Healthy habits can counteract the genetics that promote weight gain. Ideally, the expert said, this entails getting a combination of physical activity (including strength training), a sufficient amount of protein and fiber, and phytonutrients from plants that counter oxidative stress and chronic inflammation, according to Zimmermann. "Keep moving, eating real food and building muscle," she said. "These behaviors reduce inflammation, improve blood sugar control, contribute to a healthy microbiome and protect metabolism — even if weight doesn't drop much or stays the same." For some, however, the underlying issue may lie in epigenetics, which involves how a person's behaviors and surrounding environment influence how genes work in the body, according to the Centers for Disease Control and Prevention. "Obesity is a chronic relapsing condition that has an epigenetic cause," Dr. Caroline Apovian, professor of medicine at Harvard Medical School and co-director of the Center for Weight Management and Wellness at Brigham and Women's Hospital, told Fox News Digital. For more Health articles, visit People who are more prone to storing calories may have a harder time losing weight and keeping it off through diet and exercise, compared to those who may have an easier time, according to Apovian, who was not involved in the study. Fox News Digital reached out to the study authors for comment.
