Abstract
This symposium concerning obesity and nutrient interactions presents a complex picture of multiple interacting variables, ranging from inherited genetic factors and basic physiological disturbances in obesity and diabetes to specific nutritional and behavioral contributors to body fat quantity and distribution. Each of the parts of this symposium focuses on an aspect of nutrition and the metabolism of body fat and energy balance, with special attention to the interactions of potentially aberrant molecular and cellular mechanisms in various forms of obesity.
An insightful analysis of the distribution of body fat and its usefulness in predicting morbidity is presented by Drs. Yuji Matsuzawa, Shigenori Fujioka, Katsuto Tokunaga, and Seiichiro Tarui. They propose that the classification of types of obesity is best carried out by including special consideration of visceral fat accumulation. They compare upper body obesity, sometimes referred to as android or central abdominal obesity, to lower body obesity, also referred to as gynoid or peripheral obesity. They present data from several obese groups, including sumo wrestlers, and obese and lean males and females of Japanese origin, and conclude that abdominal circumference alone or in association with skin folds can be deceptive in identifying the risk of abdominal obesity. Specifically, they provide evidence from computed tomography scans that the proportion of subcutaneous to visceral fat can vary widely, even in individuals with similar waist to hip ratios and body mass indices. The highest risk for metabolic disorders was suggested for the group with specifically visceral fat deposition.
Many questions are raised by these analyses. For example, why is it that the accumulation of abdominal visceral fat appears to carry with it a higher degree of risk for metabolic disorders than fat deposited in other locations? If insulin resistance is involved in the disorders of obesity and of diabetes, how does visceral abdominal fat contribute to or affect peripheral insulin resistance, as evidenced by the rate of glucose uptake by muscle in response to insulin? Is increased mobilization of free fatty acids a linking variable, and, if so, how? Do data from sumo wrestlers suggest that physical exercise and muscle mass development may prevent both visceral deposition of fat and hyperlipidemia?
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