Why does epinephrine increase blood glucose

Insulin levels fall, glucagon and epinephrine adrenaline levels rise and more glucose is released from the liver. At the same time, growth hormone and cortisol levels rise, which causes body tissues muscle and fat to be less sensitive to insulin. As a result, more glucose is available in the blood stream. When you have type 2 diabetes, low blood sugars from too much medication or insulin are a common cause of stress.

The hormonal response to a low blood sugar includes a rapid release of epinephrine and glucagon, followed by a slower release of cortisol and growth hormone.

These hormonal responses to the low blood sugar may last for hours — during that time the blood sugar may be difficult to control. We also thank Michael W. Schwartz, Robert S. Sherwin, and Gerald J. Taborsky for helpful comments during preparation of this manuscript. Eur J Pharmacol : — Google Scholar. Brain Res : — Ahren B Autonomic regulation of islet hormone secretion—implications for health and disease. Diabetologia 43 : — Trends Pharmacol Sci 13 : — Eur J Pharmacol 71 : 93 — Pancreatology 1 : — Ritter S , Bugarith K , Dinh TT Immunotoxic destruction of distinct catecholamine subgroups produces selective impairment of glucoregulatory responses and neuronal activation.

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Abstract Available from publisher site using DOI. A subscription may be required. Sherwin RS ,. Share this article Share with email Share with twitter Share with linkedin Share with facebook. Abstract Epinephrine causes a prompt increase in blood glucose concentration in the postabsorptive state. This effect is mediated by a transient increase in hepatic glucose production and an inhibition of glucose disposal by insulin-dependent tissues.

Epinephrine augments hepatic glucose production by stimulating glycogenolysis and gluconeogenesis. Although its effect on glycogenolysis rapidly wanes, hyperglycemia continues because the effects of epinephrine on gluconeogenesis and glucose disposal persist. Epinephrine-induced hyperglycemia is markedly accentuated by concomitant elevations of glucagon and cortisol or in patients with diabetes.

In both cases, the effect of epinephrine on hepatic glucose production is converted from a transient to a sustained response, thereby accounting for the exaggerated hyperglycemia. During glucose feeding, mild elevations of epinephrine that have little effect on fasting glucose levels cause marked glucose intolerance. This exquisite sensitivity to the diabetogenic effects of epinephrine is accounted for by its capacity to interfere with each of the components of the glucoregulatory response, i.

Our findings suggest that epinephrine is an important contributor to stress-induced hyperglycemia and the susceptibility of diabetics to the adverse metabolic effects of stress.

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