Pathophysiologic changes in obesity

Abstract

Obesity is the common expression of several diverse interacting genetic, familial and environmental factors. In addition to having hypertrophic fat cells because of inordinate triglyceride accumulation, many patients with childhood-onset obesity and those who are massively obese regardless of age at onset have an excessive number of adipocytes. Several endocrinologic and metabolic abnormalities are associated with obesity. Triglyceride formation in and lipid mobilization from hypertrophic adipocytes are exaggerated. The increased availability of free fatty acids to the liver contributes to the excessive synthesis of triglycerides and very-low-density lipoproteins; thus, hypertriglyceridemia is frequently associated with obesity. Hepatic synthesis and biliary excretion of cholesterol are also increased. Most of the excess cholesterol is stored in fat cells. The plasma concentrations of high-density lipoproteins are decreased. Hyperinsulinemia, which is characteristically found in the obese, leads to a decreased number of insulin receptors in target cells. The relative insulin insensitivity of the obese frequently results in glucose intolerance. The endocrinologic and metabolic abnormalities are correctable by an appropriate program of meal planning and physical activity.