Abdominal obesity: a marker of ectopic fat accumulation (original) (raw)

As a medical student interested in science, I was fortunate to meet the late Per Björntorp in Sweden, who was at the time an established scientist in the field of obesity research. Along with Per Björntorp, Jules Hirsch and Lester Salans at The Rockefeller University were some of the early and influential investigators who were interested in adipose tissue growth and expansion and how these processes relate to the metabolic complications of obesity. They established techniques to measure adipose cell size from local tissue biopsies and combined these measurements with total body fat to estimate adipose cell numbers in obese and nonobese individuals (1, 2). Studies that used these techniques generated much information about adipose tissue expansion in men and women. Nevertheless, access to adipose tissue was limited at that time to the subcutaneous fat, making these estimates less robust. The Hirsch and Salans group and the Björntorp group also provided early evidence that adipose cells from obese individuals were insulin resistant and suggested that obesity-associated insulin resistance could be a consequence of adipose cell expansion (3).

When I became interested in adipose tissue and its metabolism, Per Björntorp and his students had already established the basic techniques and provided me with a fairly easy ride into this novel area of research. As a physician, I had the opportunity to meet patients with different diseases, including common diabetes and lipodystrophic diabetes. One interesting group of patients had the diagnosis of Werner syndrome, which is a rare disorder characterized by premature aging and partial lipodystrophy (4). Individuals with Werner syndrome frequently develop diabetes, and I had the opportunity to phenotype some of these patients and take local biopsies of the subcutaneous adipose tissue. At that time, Mario DiGirolamo, from Emory University, was on a sabbatical in Sweden and was also involved in these studies. Much to our surprise, we found that the adipose cells in the small amount of abdominal adipose tissue in these patients were the largest we had ever seen in our studies of healthy and obese diabetic individuals (5). Lipolysis in these abnormally large adipose cells was markedly elevated, and, in fact, at the time we suggested that “… a regional abdominal adiposity...may promote the metabolic events and alterations that are typically observed in generalized forms of obesity” (5). Little did we know how right this hypothesis would turn out to be, albeit in a different way than we imagined!

The concept that abdominal obesity is a particular characteristic of metabolic risk and diabetes had already been suggested in 1953 by Jean Vague in a French journal (6); however, this work was not recognized by non-francophone scientists until much later. Vague noted that android obesity was more commonly associated with diabetes and metabolic aberrations than the gynoid (female) type of obesity (6). The possibility that obesity type is indicative of metabolic risk later became a more generally recognized concept, due at least in part to the fact that different forms of obesity are fairly easy to recognize visually!