Are You Stuck with That Spare Tire?
Scientists once thought that fat cells were just passive storage sites, but it turns out they’re dynamos. Barbara Corkey, PhD, director of the Obesity Research Center at Boston University, is one of the researchers responsible for fat’s new status. Over the past 25 years, while investigating the relationship between metabolism and obesity, her lab has studied many of fat’s metabolic functions, including the production of chemicals that coordinate the body’s energy supplies, moderate the immune response and dictate appetite and weight. We asked her to give us the lowdown on why midlife fat is harder to fight and what we can do about it.
Q: Fat cells were originally a survival mechanism. Haven’t we evolved beyond them?
A: You still need them for their energy-storing abilities. Otherwise, you’d be eating constantly, because your body wouldn’t be able to store any reserve fuel. And in the past five years, we’ve learned that fat cells produce hormones and proteins that keep the metabolism and other systems in balance. Fat is now considered an active body tissue. Some researchers say that it’s your fat that controls your brain, not the other way around.
Q: What happens to our fat cells as we age?
A: You’re born with a certain number of fat cells, and that number is probably genetically determined. But as you age, there are two opposite changes. From middle to early age, fat cells get bigger. In the last quarter of life, fat cells decrease in size and number. These changes impair communication with other cells. As a result, you’ll tend to gain weight until the last quarter of your life, when you’ll start to lose weight—even if you eat the same amount of food. That’s why you rarely see a fat 90-year-old. If you live that long, you lose weight because the body starts to regulate your metabolism differently.
Q: What causes the midlife belly?
A: Aging, stress and hormones all contribute. Women produce less estrogen as they age, so the male hormone, testosterone, starts to become more prominent. That prompts fat to migrate from other body parts, such as the hips, to the gut. Stress has a similar effect on fat distribution. When you’re under stress, the body makes cortisol, a hormone that encourages fat storage in the belly. Although they’ve not been studied, I suspect that yoga and other stress-reduction techniques lead to a better distribution of fat.
That midlife potbelly is actually composed of two types of fat. One kind, subcutaneous, is right under the skin. It’s soft and pinchable; it’s there to pad the organs and protect the body from infection if you get a cut. The other kind, inside the abdominal cavity, is visceral fat, which also helps protect organs but is hard. Visceral fat produces various chemicals; excess amounts of it are associated with heart disease and diabetes.
Q: Is that why it’s so hard to get rid of belly fat—because it’s different than other types?
A: It’s actually easier to get rid of visceral fat than fat in other places. This fat responds rapidly to dieting and exercise because it’s much more active than subcutaneous fat: It forms and breaks down and then re-forms. By contrast, it’s harder to lose thigh fat with diet and exercise because that’s only subcutaneous fat, which forms and breaks down more slowly.
Q: If you eat fat, does it go directly to your fat cells?
A: The fat you eat doesn’t have any effect on your fat cells. If you consume more calories than you need for fuel, whether they’re in the form of fat, carbohydrates or protein, they get stored as fat. Excess is what matters, not a particular nutrient. However, the type of fat you eat does matter from a health perspective.
Q: How does exercise affect fat metabolism?
A: Exercise burns fat. It also reduces the size of fat cells: A small five-year study at Wake Forest University found that walking on a treadmill for 30 to 50 minutes three times a week reduced the size of the fat cells in the bellies of obese women by about 18percent. Another group who dieted but did not exercise had no change in the size of their abdominal fat cells. That’s important because large fat cells and small ones work differently and secrete different chemicals in different amounts.
Exercise also prevents fat from being stored in the wrong places, such as the muscles, pancreas and liver. When fat cells are full, these places get the overflow of fat—and that can damage the liver, the pancreas and even the heart.
In addition, exercising after a meal—I’m talking about taking a 10-minute stroll when you get up from the table—helps regulate your insulin level: It stimulates the muscles to absorb glucose from the food you’ve eaten without requiring your pancreas to release insulin. (Usually, you need insulin to store glucose.) Ultimately, that can help prevent diabetes.
Q: How is recent research affecting the way doctors treat obesity?
A: We now recognize that the products secreted by fat cells form a communication system with the brain and the rest of the body. Knowing how the system works may possibly lead to a cure for obesity and the diseases it causes.
One of the best-known fat-cell products is leptin, which tells the body if fat cells are full or empty. Leptin levels rise with increasing amounts of fat, and large fat cells produce more of it than small ones. Subcutaneous fat cells put out more leptin than visceral fat cells. Usually, when there’s not enough leptin, the brain receives the signal to eat. The leptin signal works well in people whose weight is normal, but as you get fatter and fatter, you may become leptin resistant. That means that although your fat releases plenty of leptin, either the signal doesn’t get to the brain, its impact is lost or it doesn’t make you feel full when you should—so you just keep eating.
Another chemical, adiponectin, helps the body burn fuel more effectively and stimulates the muscles to burn fat. Adiponectin levels are higher in leaner people; as fat cells get fatter, adiponectin levels go down. So we’re studying how to stimulate adiponectin secretion to decrease weight. We know some of the players; now we just have to figure out how to manipulate them.