Point: visceral adiposity is causally related to insulin resistance.

نویسندگان

  • Harold E Lebovitz
  • Mary Ann Banerji
چکیده

Related to Insulin Resistance The relationship between obesity and insulin resistance, while well recognized for many years, has nonetheless been confusing since not all obese individuals have insulin resistance (1) and because insulin resistance occurs in individuals who have BMIs that are within the normal or mildly overweight categories (2). Early attempts to understand the relationships between obesity, type 2 diabetes, and cardiovascular disease focused on the waist-to-hip ratio as a means of distinguishing those individuals who were at increased risk from those who were not (3,4). A high waist-to-hip ratio is a surrogate for masculine distribution of obesity (central obesity). Cross-sectional studies by Kissebah et al. (5) and Krotkiewski et al. (6) in the 1980s demonstrated that hypertension, hypertriglyceridemia, hyperinsulinemia, and glucose intolerance were increased in subjects with a high waist-to-hip ratio. Long-term longitudinal population-based studies of men (13.5 years) and women (12 years) in Gothenburg, Sweden, showed that the waist-to-hip ratio was a predictor of the future development of diabetes, myocardial infarction, angina pectoris, stroke, and death independent of BMI (3,4). Technology developed in the 1990s, including computer tomography scans and MRI, made it possible to precisely measure specific adipose tissue depots such as total body adipose tissue mass, abdominal subcutaneous adipose tissue mass, visceral adipose tissue mass, and hepatic and intramuscular triglyceride content (7,8). Utilizing those techniques, many studies have examined the relationship between total adipose tissue, abdominal subcutaneous adipose tissue, and visceral adipose tissue mass and insulin resistance, the components of the metabolic syndrome, and the development of type 2 diabetes or clinical cardiovascular events (9–21). Despite the much smaller size of the visceral adipose tissue depot compared with the total subcutaneous adipose tissue depot or total adiposity, many investigations demonstrated that the visceral adipose tissue mass and not the subcutaneous or total adipose tissue mass was significantly correlated in multivariate analyses with insulin resistance, type 2 diabetes, and cardiovascular events (9 – 11,13,14,16,19,20). The hypothesis that visceral adiposity and not total adiposity was the cause of the components and clinical consequences of the metabolic syndrome has been challenged by several studies that found either that abdominal subcutaneous adipose tissue mass and not visceral adipose tissue mass was independently correlated with insulin resistance or that they were both equally correlated (8,12,17,18,21). Studies using isotopic techniques have calculated that the majority of circulating free fatty acids are derived from peripheral adipose tissue (22) and that if free fatty acids are postulated to be responsible for the insulin resistance associated with obesity, then total adiposity rather than visceral adiposity should be responsible for insulin resistance. Several lines of evidence support the hypothesis that visceral adipose tissue and not subcutaneous adipose tissue is the major contributor in causing insulin resistance and the metabolic syndrome. They are discussed in the below sections.

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عنوان ژورنال:
  • Diabetes care

دوره 28 9  شماره 

صفحات  -

تاریخ انتشار 2005