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The Insulin Problem

How It Can Make You Fat

By David Mendosa

Last Update: January 16, 2001

"It's hard enough to deal with diabetes without blaming yourself for a disease that you didn't cause," says William Polonsky, Ph.D. He is Assistant Clinical Professor in the Department of Psychiatry at the University of California, San Diego, and author of the recent book Diabetes Burnout.

Doesn't overeating cause type 2 diabetes? Lot of people believe that because of the strong correlation between obesity and type 2 diabetes. Indeed, perhaps 80 percent of people with type 2 diabetes are obese.

This strong correlation is why you will often see type 2 diabetes listed as a "lifestyle disease." It implies that the disease results from a choice, just as other lifestyle choices like cigarette smoking and heavy alcohol consumption lead to other diseases. It blames the victim.

The experts, however, are unanimous that obesity has not been shown to cause diabetes. Type 2 diabetes generally results from the combination of impaired beta cell function and insulin resistance acting on susceptible genes. Why then is there such a large overlap between obesity and type 2 diabetes?

The answer is slowly coming out of research led by three scientists who worked together for years in Seattle. Endocrinologists Daniel Porte Jr., M.D., who is now associated with the VA San Diego Health Care System, and Michael W. Schwartz of the VA Puget Sound Health Care System. They work with psychologist Stephen Woods, now of the department of psychiatry, University of Cincinnati Medical Center.

"It's complicated," Porte told us, "because everybody who is obese doesn't have diabetes, and everybody who has diabetes is not obese. So we have been looking at why they tend to overlap."

The answer, they found, is the beta cells of the pancreas that make and secrete insulin. "If the beta cells are not functioning properly this will tend to lead to diabetes," he says. "And this will also tend toward an increase in body weight."

Insulin stores fat—and supresses your eating.

Insulin has two apparently contradictory impacts on your body, Porte says. "One is that it tends to store fat. When you eat a meal, the calories will be stored so that you will be able to survive between meals. But the insulin also goes to your brain to suppress your eating—so you won't overeat."

Obesity too has "a bunch of causes," Porte says. "Diabetes and obesity occurs together more than you would expect by chance, so this gets confusing."

If you have other factors in your genes or your environment that would cause obesity, then you would probably become obese, he says, and your diabetes, if any, would be very mild. But if you have other factors that tend to damage the beta cells or to produce insulin resistance, then you would get more severe diabetes. "So you can get varying amounts of diabetes and obesity," he says, "but they will tend to occur together because of fact that insulin tends to store fat and tells the brain how fat you are, preventing overstorage."

It has taken Porte and his colleagues years to work out all the details of this complex system. They cite many of their papers in an 1998 review article, "Obesity, Diabetes and the Central Nervous System" in Diabetologia.

Scientists at the Joslin Diabetes Center in Boston published a study in the September 22 issue of Science supporting the idea that insulin signals the brain to control food intake. The article, "Role of Brain Insulin Receptor in Control of Body Weight and Reproduction," showed that mice lacking insulin receptors in the brain have increased body fat content. This demonstrated that insulin signaling in the brain is essential for normal weight regulation.

The researchers, led by Dr. C. Ronald Kahn, Joslin's president, created bioengineered mice whose brain cells lacked insulin receptors, the structures that insulin molecules normally bind to. With the receptors knocked out, the researchers knew that insulin wouldn't have any activity in the brain, but they didn't know what would happen.

"Most people thought that if insulin and the insulin receptors in the brain had any function at all, it would be in the development of the brain," Kahn says. But to the researchers' surprise, the brains of these mice developed normally—but they gained weight. The females ate more and got fatter even on a normal diet. Both males and females gained weight on a high-fat diet.

"We found evidence of a decrease in the ability of insulin to lower blood glucose levels, increased appetite, obesity, and increased infertility in the mice in which the insulin receptor in the brain had been genetically knocked out," Kahn says. "This forces us to open our minds to the idea that insulin action and resistance in the brain contribute in some way to the development of diabetes."

Does this mean that Porte would not call diabetes or obesity a lifestyle disease? "In our view obesity is not very often a behavioral disorder," he replied. "It is a biological disorder, but it is complicated because it is an interaction between the biology and the environment."

"While obesity is a biological disorder," he continues, "it is sometime amenable to behavioral intervention. But the difficulty occurs when you intervene behaviorally, because that behavior is fighting the biology. That is one of the reasons why it is so hard to regulate your weight. So we need to come up with ways to help people achieve those goals."

"We shouldn't be blaming patients."

After reading about these studies, Polonsky says he "was chagrined by what we ask our patients to do. Weight management is an enormously difficult battle and we shouldn't be blaming patients."

At the same time, he worries that people will think that they are helpless. He's afraid that they will think there is nothing they can do because with the insulin receptors in the brain their actions don't matter.

"We don't want to give people that message," he concludes. "We know that people's actions do matter and that people can lose weight. But it's really tough." 


This article originally appeared in Diabetes Wellness Letter, January 2001, pp. 1, 7.


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