Regional adiposity and morbidity.

Adipose tissue distribution and risk of metabolic disease: does thiazolidinedione-induced adipose tissue redistribution provide a clue to the answer?

“…Several large epidemiological investigations performed in Sweden and the United States in the early 1980s, using skinfold thickness, waist circumference or WHR as surrogate markers of truncal fatness, confirmed the association between abdominal (upper-body or central) obesity and the risk of cardiovascular disease and diabetes [1,2].…”

“…However, clinical studies of NEFA kinetics do not support this hypothesis [1,7]. It has been reported that, in effect, post-absorptive NEFA levels are not different between obese women with a visceral adipose tissue area of ≥65 cm 2 and those with an area of ≥65 cm 2 , as measured by CT at the level of L4-L5 [1,2]. In addition, obese men with a visceral fat area of ≥130 cm 2 have normal fasting plasma NEFA levels, and the increased postprandial NEFA concentrations in these subjects appear to be related to impaired triacylglycerol clearance [1,2].…”

“…Visceral obesity has since been reproducibly implicated as an independent risk factor for insulin resistance and glucose intolerance, which predict type 2 diabetes and cardiovascular disease in different ethnic populations [1,2]. One of the hypotheses proposed to explain the link between visceral obesity and the chronic complex metabolic diseases is the visceral/portal hypothesis, in which: (1) an increased hepatic uptake of the 'first pass' of NEFAs released from visceral fat lipolysis into the portal vein may reduce the hepatic extraction of insulin and thus impair insulin-induced suppression of hepatic gluconeogenesis, leading to increased endogenous glucose production; (2) an increased hepatic lipase activity may remove lipids from LDL and HDL, which, in combination with the decreased degradation of apolipoprotein B and the increased esterification of NEFAs, results in the increased synthesis and secretion of VLDL and smaller, denser LDL and HDL particles into the systemic circulation, distorting the circulating lipid profile; and (3) an increased systemic NEFA flux may impair insulin action in skeletal muscle and other key tissues via malonyl-CoA/acetyl-CoA carboxylase β fuel-sensing and regulation mechanisms [1,2,6].…”

“…A large epidemiological survey conducted from 1976-1980 on 11,864 men and women clearly showed that people with a BMI of 28 kg/m 2 or higher have a significantly increased risk of developing type 2 diabetes, hyperlipidaemia and hypertension [1,2]. Nevertheless, the level of risk differs among obese individuals; approximately 20% of people who meet the criteria for obesity are apparently insulin sensitive and metabolically normal, despite having large amounts of body fat.…”

Genetic and environmental influences on body fat and blood pressure in African-American adult twins

“…4 Abdominal obesity has been shown to be more closely associated with these chronic disease outcomes through its association with insulin resistance, hyperinsulinemia, hypertension, and hypertriglyceridemia. [5][6][7] The rates of hypertension among African Americans are also cause for concern with 41.6% of United States AfricanAmerican male subjects and 44.7% of African-American female subjects considered hypertensive. 2 These numbers are in comparison to 32.2% of Caucasian male subjects and 29.5% of Caucasian female subjects.…”