Effects of mammalian ACTH on potential fuels and gluconeogenic substrates in the plasma of the spiny dogfish shark (Squalus acanthias).

The effects of mammalian ACTH on plasma beta-hydroxybutyrate, glucose, alanine, and lactate levels were determined in the unfed spiny dogfish shark (Squalus acanthias). Serial blood samples were collected from a cannula implanted in the dorsal aorta. The metabolite levels were estimated by standard enzymatic procedures for 4 days before treatment and for 4 days after treatment. Plasma glucose, alanine, and lactate, but not beta-hydroxybutyrate, declined after the surgery, but the metabolites were relatively stable for at least 48 hr before treatment. ACTH (40 units/kg) or the control solution were infused via the cannula after the morning blood sample on postoperative Day 4 and again after the 12-hr blood sample. Control plasma beta-hydroxybutyrate, glucose, and lactate did not change significantly, but alanine levels increased approximately 29% by 96 hr when sampling ended. Plasma beta-hydroxybutyrate levels were not significantly changed by ACTH treatment. Plasma glucose levels increased approximately 36% by 3 hr after ACTH infusion, remained elevated following the second ACTH treatment, and then declined to approximately the initial levels by 96 hr. Plasma alanine levels increased approximately 53% by 0.75 hr after ACTH treatment, were still approximately 15% greater than the initial levels by 12 hr, rose again after the second ACTH infusion at 12 hr, and then declined to near the control levels by 96 hr. Plasma lactate levels increased approximately 107% by 1.5 hr after ACTH infusion and then decreased to approximately 22% greater than the initial levels by 12 hr. Lactate levels increased after the second ACTH infusion and remained approximately 58% greater than the initial levels when sampling ended at 96 hr. The results indicate that the pituitary-adrenocortical axis hormones do not directly influence plasma beta-hydroxybutyrate levels. However, the data support the suggestion that the hyperglycemic action of the pituitary-adrenocortical axis hormones is mediated, at least in part, by the provision of alanine and lactate substrates for gluconeogenesis.