GLUCOCORTICOIDS AND TRIGLYCERIDE TRANSPORT - EFFECTS ON TRIGLYCERIDE SECRETION RATES, LIPOPROTEIN-LIPASE, AND PLASMA LIPOPROTEINS IN RAT

In order to elucidate the mechanism(s) of hyperlipidemia following glucocorticoid adminstration, dexamethasone (0.125 mg/kg) was administered daily i.m. for 2 wk to male Sprague-Dawley rats and the effects on plasma triglyceride (TG) and cholesterol (Chol), lipoprotein neutral lipids, hepatic triglyceride secretion rates (TGSR; Triton), and epididymal fat lipoprotein lipase (LPL) were determined. Special measures were taken to maintain positive caloric balance and keep the weights of control and dexamethasone-treated animals comparable. Significant increases (P < 0.001) in TG and very-low density lipoprotein (VLDL) triglyceride associated with no change in Chol and actual reduction in both triglyceride and cholesterol in low density lipoprotein (LDL) were observed in the steroid-treated animals. Dexamethasone treatment was associated with increased basal insulin and glucose levels, an insignificant increment in TGSR, and a highly significant reduction (P < 0.001) in LPL. These findings suggest that glucocorticoid treatment increases splanchnic triglyceride production rates, but the resulting hypertriglyceridemia is primarily a consequence of impaired VLDL removal due to low adipose tissue LPL activity.