By Michelle Cotroneo, Ph.D., Scientific Advisor

Type 2 diabetes is a disorder of inadequate production of, or resistance to insulin, a hormone produced by the pancreas. A key function of insulin is to move glucose from the blood into the cells, where it is used as energy.  Without sufficient insulin function, glucose accumulates in the blood, leading to complications.  Some of the disorders that can occur as a result of type 2 diabetes include: hypertension, blindness, stroke, nephropathy (kidney disease), neuropathy (nerve damage), and skin infections.

It is estimated that there are 17.9 million diagnosed cases of diabetes in the United States and 57 million people with pre-diabetes. Risk for diabetes is increased in those with a family history of the disease, in certain ethnic groups, and in overweight or obese individuals. Aging also increases the risk for developing diabetes, affecting 23.1% of Americans over 60 (statistics from the National Diabetes Fact Sheet, American Diabetes Association). It is also estimated that by 2025, two thirds of diabetic individuals worldwide will be age 60 or older (1).

Why is aging associated with increased diabetes risk?

It is thought that the increased chance of developing type 2 diabetes as a person ages is related to increasing insulin resistance. In an interesting study comparing insulin sensitivity between different groups of individuals (2), no difference was identified in insulin sensitivity between old and young athletes, between older and younger normal weight individuals, or between older and younger obese subjects. The athletes demonstrated the highest insulin sensitivity, followed by the normal weight individuals, with obese subjects having the lowest sensitivity to insulin.  The authors concluded that aging alone cannot account for insulin resistance, but that the decreased physical activity and obesity that can occur with aging can be responsible for age-related insulin insensitivity.

An increasing amount of research has been devoted to studying the relationship between physical activity, obesity and diabetes. It is now generally accepted that the presence of abdominal fat increases the risk for diabetes and cardiovascular disease. Although abdominal fat increases during aging, it may not result in a noticeable increase in weight, as fat distribution also changes as a consequence of aging. Fat deposition in the arms, legs and hips decreases, while it increases in the abdominal area. Subcutaneous fat is under the skin, and is not associated directly with increased disease risk. On the other hand, visceral fat located deeper in the body collecting around the organs is associated with the risk for diabetes and cardiovascular disease.

How can fat increase diabetes risk?

Adipose (fat) tissue is a complex endocrine organ that produces hormones and adipocytokines that are involved in the regulation of glucose and fat metabolism. Expansion of this tissue is accompanied by the infiltration of macrophages (inflammatory cells). Abdominal obesity can result in adipocyte dysfunction, resulting in altered production of hormones and adipocytokines.  Perturbations in the balance of these factors and the presence of macrophages results in altered insulin sensitivity, glucose utilization, pancreatic cell function, fat deposition and inflammation (3,4).

Can you get rid of visceral fat?

It is a well known fact that risk for diabetes in overweight or obese individuals can be decreased by exercise and weight loss. But do these measures result in a decrease in visceral fat? A comprehensive review of scientific studies in this area has shed important light on these questions (5). These authors concluded that moderate weight loss resulted in preferential loss of visceral fat over subcutaneous fat, but that greater weight loss reduced this effect. They also found that there was no evidence that any type of weight loss strategy was more effective than another in preferentially reducing visceral adipose tissue.  Taken together, the current research underscores the importance of maintaining a healthy weight and continuing to exercise as we age.

1. King H, Aubert RE, Herman WH. Diabetes Care 1998; 21(9): 1414-31.

2. Amati F, Dubé JJ, Coen PM, Stefanovic-Racic M, Frederico G. Diabetes Care 2009; 32(8): 1547-9.

3. Ioannidis, I. Angiology 2008; 59 (39S): 39-43.

4. Hajer GR, van Haeften TW, Visseren FLJ. European Heart Journal 2008; 29: 2959–71.

5. Chaston TB, Dixon JB. International Journal of Obesity 2008; 32: 619–28.