Diabetes and obesity (part 1)

Reviews/Commentaries/ADA Statements
P E R S P E C T I V E S O N T H E N E W S

Diabetes and Obesity
Part 1
ZACHARY T. BLOOMGARDEN, MD tion that reduced adipocyte size may be related to insulin resistance), increased blood pressure, and increased triglyceride levels. Such individuals often are offspring of type 2 diabetic parents, themselves developing type 2 diabetes at relatively young ages, having history of myocardial infarction and of cholesterol cholelithiasis. Criteria for the MONW state are similar to those for metabolic syndrome (4), including hyperinsulinemic individuals with normal weight and multiple cardiovascular disease (CVD) risk factors (5). An alternative approach is to identify nonobese hypertensive individuals, recognizing this to be a group characterized by increased insulin and triglyceride levels and by decreased insulin sensitivity (6). In the U.S. National Health and Nutrition Surveys, MONW constitute a large number of at-risk individuals in the U.S. population (7). A Canadian study evaluating normal-weight individuals with features of insulin resistance showed a tripling in risk of CVD (8). Schneider asked how knowledge of the existence of this group should influence our thinking, specifically addressing the usefulness of relying on simple measures of body weight, as the MONW concept implies that a large number of normal-weight individuals would benefit from interventions now thought appropriate for obese individuals. He discussed the usefulness of measures of adipose tissue other than that of total fat mass and the question of whether measures of insulin resistance and hyperinsulinemia would be useful in ascertainment of these abnormalities. Clinically, we are not readily able to assess adiposity. The 75-kg man at age 53 years typically has 7 kg more fat and less lean mass than he had at the same weight at age 25 years, without apparent difference in physiognomy. Nondiabetic, nonobese offspring of type 2 diabetic parents will be found to