Involvement of insulinemia in the postprandial hypotriacylglycerolemia induced by prazosin in the rat.

ABSTRACT

The purpose of the present study was to evaluate the role of insulin as a possible mediator of the hypotriacylglycerolemic effect of alpha 1-adrenergic blockade. To this end, determinants of triacylglycerol (TG) metabolism were measured in animals having normal postprandial fluctuations in insulin levels (intact rats) and in others having invariable insulin concentrations (insulin-depleted rats infused long-term with insulin-delivering minipumps). Postprandial changes in plasma TG level, TG secretion rate (TGSR), TG elimination rate (TGER), and lipoprotein lipase (LPL) activity of white (WAT) and brown (BAT) adipose tissues, vastus lateralis muscle (VLM), and heart were measured in animals acutely injected or not with the alpha 1-antagonist prazosin 1 hour before the intake of a high-sucrose, fat-free meal. In intact rats, postprandial increases in glucose and insulin levels were potentiated by administration of prazosin before meal intake. The postmeal increase of plasma TG level was abolished by prazosin in intact animals, whereas this effect was absent in animals with invariable insulin levels. Intact animals treated with prazosin displayed both a lower TGSR (P < .01) and a higher TGER (P < .01) than their saline-injected counterparts. In animals with invariable insulin, both TGSR and TGER remained unaffected by prazosin treatment. Prazosin treatment of intact animals did not affect LPL activity in WAT, but increased enzyme activity in BAT (P < .02). In insulin-infused animals, prazosin increased LPL activity in WAT (P < .02) and BAT (P < .03). alpha 1-Adrenergic blockade had no effect on LPL in VLM and heart. These results confirm that alpha 1-adrenergic blockade prevents the postprandial increase in plasma TG level that follows the ingestion of a high-sucrose meal both by decreasing TGSR and by increasing TGER. The findings also demonstrate that these effects of prazosin are indirect and that their occurrence requires the postprandial increase in circulating insulin levels.