Effect of Insulin on Hepatic Bile Secretion during Normoglycaemia and Hyperglycaemia

Abstract

The roles of hyperosmolality, hyperglycaemia, and insulin in glucose-induced reduction of bile secretion were examined in anaesthetized pigs. Compared with normoglycaemia, intravenous infusion of isotonic glucose reduced bile acid-dependent bile secretion at a plasma glucose concentration of 18 mmol/l, with 34 ± 4%. Lowering of plasma glucose concentration to normoglycaemia after administration of insulin (10 U/kg body wt, low dose) increased bicarbonate-dependent bile secretion by 23 ± 3%. Induction of hyperglycaemia (plasma glucose concentration, 16 mmol/ 1) and the combined infusion of isotonic glucose and the low insulin dose decreased bile secretion by 22 ± 3%. During hyperglycaemia (plasma glucose concentration, 16 mmol/l) the combined infusion of isotonic glucose and a high dose of insulin (60 U/ kg body wt) increased bile acid-dependent bile secretion by 26 ± 3%. Hyperglycaemia reduces bile secretion without altering plasma osmolality. Endogenous production (or too rapid degradation) of insulin may be too small during intravenous glucose infusion to cope with the metabolic demands of hepatocellular glucose conversion. This may be overcome by administration of insulin in a large dose, which stimulates bile acid secretion.

Key Words:

• Bile acids
• calcium
• electrolyte transport
• glucose
• metabolism
• osmolality