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

Abstract

The metabolic responses to 4-h infusions of adrenaline (3 micrograms 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 micrograms 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 less than 0.001; somatostatin plus cortisol 6.7 +/- 0.3 mmol l-1, P less than 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-1 v. 7.2 +/- 0.5 mmol l-1 at 45 min, P less than 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 less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute physiological effects of glucocorticoids on fuel metabolism in humans are permissive but not direct

“…Over and above prevailing glucocorticoid concentrations, a further critical confounder is the effect of other hormones regulating lipolysis, notably insulin and adrenaline . In vivo , the effect of interactions between cortisol and either adrenaline or insulin has been examined only once in humans, although systemic rates of lipolysis were not measured as the appropriate tracers were not infused. We hypothesized that the effects of glucocorticoids on lipolysis in humans are indirect and dependent on the prevailing insulin and/or adrenaline concentrations, with glucocorticoids augmenting the pro‐lipolytic effects of adrenaline and antagonizing the suppressive effects of insulin.…”

Glucocorticoids and fatty acid metabolism in humans: fuelling fat redistribution in the metabolic syndrome

“…Studies without tracer infusion have demonstrated that adrenaline and cortisol have synergistic effects on NEFA concentrations during somatostatin administration (Pernet et al 1986), but have no effect on the anti-lipolytic effect of insulin during hyperinsulinaemia (20 mU/m 2 per min; Clerc et al 1986). Both GH and glucocorticoids may influence sensitivity to adrenaline by reducing anti-lipolytic a 2 -adrenoreceptor availability (Yip & Goodman 1999, Djurhuus et al 2004), but acute in vivo studies have demonstrated additive independent effects of GH and cortisol on lipolysis during a pancreatic clamp, suggesting separate mechanisms of action (Djurhuus et al 2004).…”