Highlights From the North American Society for the Study of Obesity 2004 Annual Meeting

November 14 -18, 2004; Las Vegas, Nevada

Raymond A. Plodkowski, MD


April 25, 2005

In This Article

Obesity as a Gateway Disease

The 2004 North American Association for the Study of Obesity (NAASO) Annual Scientific Meeting was, as last year, cosponsored with the American Diabetes Association. This cosponsorship acknowledges that obesity is a gateway disease that often leads to diabetes and cardiovascular disease. The discussion of this meeting will include a description of these 2 diseases and how obesity contributes to their development. The article will cover emerging knowledge with regard to adipokines (adipose cell hormones) such as adiponectin and emerging pharmacologic treatments such as cannibinoid receptor modulators. New efficacy information regarding diet composition and "low-carb diets," energy balance, behavioral modification for the treatment of obesity, and other timely topics will also be presented.

Although it may seem intuitive that obesity is a gateway disease, until recently, data from a large prospective trial had not been analyzed to determine the effect of adiposity in patients with impaired glucose tolerance (IGT), the precursor to type 2 diabetes. At the NAASO meeting, data were presented from the Diabetes Prevention Trial Body Composition Substudy to address this question.[1]

Anthropometric (body) measurements were made in 3234 patients, and the study population was monitored for the development of diabetes for approximately 2.8 years. Surprisingly, the analysis revealed that waist circumference was the best predictor of the future development of diabetes. A simple waist circumference measurement was superior to waist/height ratio, waist/hip ratio, body mass index (BMI), and weight measurements, in that order. An increase of 1 standard deviation in waist circumference increased the risk of progression to type 2 diabetes by 34% in men and 28% in women.

It should be noted that waist circumference measurements can be highly variable depending on the technique used. To make this measurement properly, use a non-stretchable tape (7-12 mm wide) and measure the waist at the top of the iliac crest while the patient is standing with the measuring tape placed in a horizontal plane around the abdomen and parallel to the floor. The tape should be snug but should not compress the skin. The measurement should be made at normal minimal respiration and recorded in centimeters.[2]

BMI is often an easier measurement to make in a busy clinical setting because it requires only a height and weight measurement by the office staff. An increase of 1 BMI unit (kg/m2) augmented the risk of developing diabetes by 29% in men and 18% in women. Thus, it is clear that as waist circumference and BMI increase, the risk of developing type 2 diabetes rises.

The link between obesity and its sequelae, diabetes and cardiovascular disease, has been a topic of frequent discussion and debate. Adipokines (adipose cell hormones) may provide a superior understanding of the link between these diseases. In the past, it was assumed that fat was simply a storage depot for energy. It is now known that adipose tissue is hormonally active and produces several products, including adiponectin, TNF-alfa, IL-6, and resistin.

Adiponectin is a large molecule that was identified approximately 8 years ago; its function has been characterized in the past few years. The basic building block of adiponectin consists of a 30-kDa protein monomer that forms tightly associated trimers. About 4-6 trimers form larger biologically active oligomers that circulate in the plasma.[3] Adiponectin appears to be a protective hormone that decreases insulin resistance and vascular inflammation. This is counter-intuitive, because one might postulate that as patients gain weight and increase their adipose cell mass, more protective adiponectin would be produced to lower insulin resistance and vascular inflammation and protect them from the dysmetabolic syndrome, type 2 diabetes, and cardiovascular disease. However, the opposite occurs. It has been shown that as people gain weight, protective adiponectin levels decrease. Thus, adiponectin may be a biological li! nk between obesity and the dysmetabolic syndrome, type 2 diabetes, and cardiovascular disease.

An oral presentation by Shadid and colleagues[4] examined the relationship between the various adipokines and insulin resistance (the cause of type 2 diabetes). The group examined whether adiponectin, resistin, and TNF-alfa affect the development of insulin resistance in research subjects with upper body obesity. Their findings confirmed earlier studies showing that adiponectin levels negatively correlate with insulin resistance. (When adiponectin levels are high, insulin resistance is low.) However, their data showed that the other adipokines (resistin, TNF-alfa, and IL-6) were not related to insulin resistance. Therefore, adiponectin appears to be the key mediator between obesity and type 2 diabetes.

Adiponectin may also have a local paracrine effect on neighboring adipose tissue. A presentation by Richelsen and colleagues[5] discussed the presence of the adiponectin receptors in adipose tissue. It is established that adipoR1 and adipoR2 receptors are found in several tissues, including muscle and liver. The group used polymerase chain reaction to quantify adipose tissue adipoR1 and adipoR2 receptors in samples from obese patients before and after weight loss (weight loss range: 10-15 lbs). They found that adipoR1 was the dominant receptor expressed, and that it was reduced in association with obesity (negative correlation with BMI (r = -0.61, P < .01). Furthermore, after diet-induced weight loss, adipoR1 expression increased. Thus these findings suggest that adiponectin may have decreased biological effects in obesity, which may further aggravate the negative metabolic effect of low levels of adiponectin in the obese state.


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