Abstract
Publisher Summary Clinical studies in patients with hypertension, diabetes mellitus, and in females receiving oral contraceptives have shown a significant relationship between serum triglyceride (TG) concentration and the activity of γ-glutamyl transferase (GGT). Serum-GGT activity is a marker of hepatic microsomal enzyme induction in humans, and the steps in the acylation of sn–glycerol–3–phosphate (G–3–P) leading to TG synthesis occur in the endoplasmic reticulum. It has been postulated that hepatic microsomal enzyme induction may be a cause of hypertriglyceridemia. Experiments were undertaken to test this hypothesis in the rat. Hepatic microsomal enzyme induction by phenobarbital (PB) in the rat was accompanied by significant increase of liver TG content. This occurred whether the animals were sacrificed without fasting or after an 18-hr fast. Five days after withdrawal of the drug, indices of enzyme induction approached the level of the controls, and the TG contents of the liver in the two groups were similar. However, the serum TG concentration in the PB-treated rats was below that of the controls during PB-treatment, and this difference persisted for further five days following withdrawal of the drug. These findings suggest that there are at least two mechanisms involved: (1) an enzyme induction-associated increase in hepatic TG content and (2) an enzyme induction-independent fall in serum TG concentration.
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