Thanksgiving: one of those holidays of the year where gluttony is encouraged. Americans make enough food to put themselves into a calorie-induced coma for days. This happens only a few times a year, though, so why not indulge once in a while?
Lately, we have been talking about weight regulation and obesity—a relevant topic indeed close to Thanksgiving! The articles we have been reading discuss leptin, a very important hormone in the brain for feeding behavior.
What is leptin?
Leptin is a hormone that is secreted from fat cells in the body. When released, leptin suppresses appetite and tells the body to stop eating. How does this regulate body weight long-term? When more fat is being stored, leptin levels will increase; leptin is telling the brain that the person should stop eating so much. This yields in a decrease of food intake and, ideally, a decrease in weight as well. Leptin is a natural regulator of weight and food intake, in this way.
Leptin produces this effect by influencing the signaling of neurons in the hypothalamus. The hypothalamus is an area in the brain that regulates hunger and feeling full. There are many signaling pathways involved in feeding behavior that are affected by leptin. Researchers are trying to target these pathways in order to find a treatment for obesity.
What about obesity?
If leptin regulates body weight, then obesity shouldn’t be the problem we see today. However, research indicates that if a person has high levels of circulating leptin (due to long-term over-eating, poor nutrition, a high-fat diet, etc.), eventually he or she can become resistant to the appetite-suppressing effect of leptin. Leptin has tried very hard to tell the brain to decrease food intake, but over time the body becomes used to it and doesn’t even listen anymore. High levels of leptin, then, cannot decrease food intake and weight because the body is resistant to it. This is why giving leptin to treat obesity doesn’t work—obese people are probably resistant to the effects of leptin already.
Treating obesity
Leptin resistance is certainly a problem. Discovery of leptin held great potential for finding a good treatment for obesity. But leptin resistance brought much of this research to a grinding halt. So how can leptin resistance (and obesity) be treated?
Well, researchers are still working on that. But there are a few ideas out there. In 2009, Harvard University researchers found two compounds that reduced leptin resistance in mice. These substances reduce inflammation in the nerves and may simply restore natural leptin functioning. It will probably be years before this treatment is available for use.
Another option that physicians are increasingly turning to in cases of extreme and difficult-to-treat obesity is gastric bypass surgery. This should be a last option after all others have been exhausted. This involves a surgery stapling a section of the stomach to form a small pouch, the “new” stomach (see diagram below). When we eat food and our stomachs fill up, the stomach walls start to stretch. Nerves in the wall sense this stretching and send messages to the brain to stop eating. This involves the signaling of a number of chemicals and hormones, including leptin. After gastric bypass surgery, the stomach fills much faster, causing a sense of fullness rapidly as well. Additionally, leptin levels are decreased (according to recent studies in 2010 and 2011). While obese people often have chronically, stubbornly high leptin levels, gastric bypass surgery may reduce leptin resistance, allowing levels to drop and normal functioning to resume.
Medication and surgery are drastic measures to treat obesity. Exercise and careful monitoring of food intake may also affect leptin and obesity. In chronic over-eating and snacking, levels of leptin rise as the brain tries to tell the body to stop eating. If a person is always eating, however, these levels will remain high all the time. Not good. Constant advertising of food, easy access to fast food, and supersized food portions may all have contributed to the high rates of obesity in America. In the 1950s, a 12-oz can of soda was considered “king size,” big enough for two servings. Now, a 12 oz. soda at McDonald’s is considered child-size, and people regularly order their 22 and 32 oz. sizes. Do we really need all those calories? The burgeoning obesity rates in our country suggest not.
Another option is good old fashioned exercise. Leptin levels increase in the brain shortly after exercise, telling the body not to eat. In people with obesity problems, long-term exercise may eventually reduce high levels of leptin. Additionally, some research has indicated that exercise can make the body more sensitive to leptin and insulin, both essential hormones for metabolism. Increased sensitivity to these hormones makes the body more efficient in using them, and resistance is reduced. Exercise is a great natural way to help restore natural leptin functioning and beat obesity.
It’s very easy to say that you’ll exercise, but unless you set
aside a specific time, it’s also very easy for that commitment to fall by the wayside. More than 90 percent of patients with Type II Diabetes see optimistic results, sometimes with the disorder going into remission. In this procedure, the digestive tract is shortened.
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