The Influence of Acute Physiological Increments of Cortisol on Fuel Metabolism and Insulin Binding to Monocytes in Normal Humans *

Abstract

The role of physiological hypercortisolemia in the regulation of fuel metabolism in man was examined during a 5-h primed-continuous infusion of cortisol which raised plasma cortisol levels to 40 microgram/dl. Plasma glucose increased by 15--20 mg/dl (P less than 0.005) in spite of unchanged rates of glucose production. Glucose uptake and clearance, on the other hand, fell by 15% (P less than 0.05) and 30% (P less than 0.005), respectively, thereby accounting for cortisol-induced hyperglycemia. Total blood ketones during cortisol infusion increased 3-fold above saline control values (P less than 0.01) despite comparable FFA levels in the two groups. In addition, there was a selective 40% rise in total branched chain amino acids (P less than 0.005) during cortisol infusion. These effects of cortisol on glucose, ketone, and amino acid metabolism occurred in the absence of significant changes in the plasma insulin or glucagon concentration. Furthermore, cortisol infusion had no effect on [125I]insulin binding to circulating monocytes. Our data thus suggest that acute elevations of plasma cortisol have antiinsulin effects in man which may occur independent of alterations in insulin receptors.

Management of Diabetes and Hyperglycemia in Hospitals

“…They increase hepatic glucose production, inhibit glucose uptake into muscle, and have a complex effect on ␤-cell function (366 -368). The decrease in glucose uptake with glucocorticoids seems to be the major early defect (369,370), and thus it is not surprising that for hospitalized patients with well-controlled type 2 diabetes, postprandial hyperglycemia is the most significant problem. Although in some patients the hyperglycemia, if present, may be mild, in others the glucocorticoids may be responsible for hyperosmolar hyperglycemic syndrome (371).…”

The 10-s Maximal Sprint

“…2). Although there is some evidence that the progressive rise in cortisol levels may play a role in stabilizing glycemia due to cortisol's potential acute inhibitory effect on glucose utilization in skeletal muscle (19), it is likely that this hormone played only a minor role because the effects of cortisol on hepatic glucose production and blood glucose levels have been shown by most studies to require several hours to occur (20).…”

Functional and Molecular Aspects of Glucocorticoids in the Endocrine Pancreas and Glucose Homeostasis

“…In the latter, glucose intolerance was also a result of decreased glucose clearance; while no differences in endogenous glucose production was observed too (Schneiter & Tappy, 1998). Although the literature concerning rapid GC effects on insulin secretion in healthy individuals is scarce, it seems that insulin secretion under glucose infusion is reduced (Shamoon et al, 1980) or unaltered (Schneiter & Tappy, 1998) in response to a glucose challenge, suggesting an acute inhibitory effect of the GCs on -cells (Kalhan & Adam, 1975). It should also be mentioned that adaptive compensation to short GC exposures are transitory and usually reversible after discontinuation of steroid treatment (van Raalte et al, 2010).…”

“…The acute effects of GCs in healthy individuals, as judged by cortisol infusion (Shamoon et al, 1980) or by high doses of prednisolone (Kalhan & Adam, 1975;van Raalte et al, 2010), seem to be inhibitory for insulin secretion. This is based on the fact that circulating insulin levels during fasting state are not altered following GC treatment, despite the increase in blood glucose levels.…”

“…This is based on the fact that circulating insulin levels during fasting state are not altered following GC treatment, despite the increase in blood glucose levels. The increase in glycemia is associated with decreased glucose uptake and clearance, whereas the rates of endogenous glucose production are unchanged (Shamoon et al, 1980). Glucose intolerance is observed during an oral glucose tolerance test (oGTT) in healthy individuals receiving a single oral dose of 1 mg dexamethasone (DEX) just prior to the oGTT.…”