Interactions of stress hormones on lipid and carbohydrate metabolism in man with partial insulin deficiency

Abstract

Abstract. The metabolic responses to 4‐h infusions of adrenaline (3 μ g kg‐1 h‐1) and cortisol (10 mg m‐2 h‐1 for 2 h followed by 5 mg m‐2 h‐1 for 2 h), separately and in combination, have been studied in six healthy subjects with concurrent somatostatin infusion (250 μ g h‐1). A combined infusion of adrenaline, cortisol, glucagon (180 ng kg‐1 h‐1) and somatostatin has also been studied. Somatostatin plus adrenaline and somatostatin plus cortisol resulted in hyperglycaemia (at 240 min, somatostatin plus adrenaline 11·4 ± 0·4 mmol l‐1, P < 0·001; somatostatin plus cortisol 6·7 ± 0·3 mmol l‐1, P < 0·05; somatostatin alone 4·9 ± 0·4 mmol l‐1). No synergistic effect on blood glucose was seen with adrenaline and cortisol together. When glucagon was added, blood glucose rose more rapidly than without glucagon (9·3 ± 0·4 mmol l‐1v. 7·2 ± 0·5 mmol l‐1 at 45 min, P < 0·001), but plateau values were similar. Plasma NEFA levels were raised by somatostatin plus adrenaline (0·55 ± 0·04–1·82 ± 0·11 mmol l‐1 at 60 min). Somatostatin plus cortisol had no more effect on plasma NEFA than somatostatin alone. During the combined infusion of somatostatin plus adrenaline plus cortisol, a synergistic effect on plasma NEFA was observed (2·30 ± 0·11 mmol l‐1 at 60 min, P < 0·01 v. somatostatin plus adrenaline). This occurred despite a small escape of insulin secretion. The lipolytic actions of adrenaline are potentiated by elevated circulating cortisol levels in insulin‐deficient man. Glucagon does not modify this response, but accelerates the development of hyperglycaemia.