The morphology and metabolism of intraabdominal adipose tissue in men.
Level 4 - case-series / case-control
Cross-sectional physiological study in humans
PubMed 1435298 · doi:10.1016/0026-0495(92)90016-4
What was done
Researchers examined total, subcutaneous, visceral, and retroperitoneal adipose tissue mass, morphology, and metabolism in 16 men with varying degrees of body fat. Total and regional fat masses were quantified by CT scans. Lipid uptake was measured in vivo using orally administered labeled oleic acid in triglyceride. Isolated adipocytes were assessed for lipolytic responsiveness to catecholamines and sensitivity to insulin. Systemic glucose disposal rates (GDR) were determined using euglycemic glucose clamps alongside fasting glucose, insulin, hormone levels, blood pressure, and liver function tests.
What was found
Intraabdominal fat made up approximately 20% of total fat mass, with visceral and retroperitoneal fat comprising roughly 80% and 20% of intraabdominal fat, respectively. Enlargement of intraabdominal depots was driven exclusively by adipocyte hypertrophy. Lipid uptake was approximately 50% higher in omental versus subcutaneous fat. Omental adipocytes showed greater lipolytic sensitivity and responsiveness to catecholamines and diminished antilipolytic sensitivity to insulin. Visceral lipid uptake and lipolytic activity correlated strongly with fasting blood glucose and plasma insulin (r = 0.8 to 0.9) and correlated negatively with GDR. No such metabolic correlations occurred with lipid uptake in subcutaneous or retroperitoneal depots.
Why it matters
These findings provide direct metabolic evidence that visceral adipocytes have a higher lipid turnover rate and relative resistance to insulin compared to subcutaneous fat, explaining why visceral adiposity strongly associates with systemic insulin resistance.
Limits
The study is limited by a very small sample size of 16 participants and included only men. The cross-sectional design cannot establish causality between altered lipid turnover and insulin resistance. Exact confidence intervals and p-values were not reported in the abstract.
Cited by
- partial Unlike subcutaneous fat, visceral fat lipolysis does not shut down in response to insulin, continually releasing free fatty acids to the liver via the portal vein.