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Effect of Stress on Glucoregulation in Physiology and Diabetes

  • Chapter
Fuel Homeostasis and the Nervous System

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 291))

Abstract

To examine the glucoregulatory responses to stress and their impact on diabetes, we used the following models of stress: A) Hypoglycemia; B) Epinephrine infusion; C) Intracerebroventricular (ICV) injection of carbachol, an analog of acetylcholine.

  1. A)

    Hypoglycemia induces release of all counterregulatory hormones. During acute hypoglycemia, glucose production increases initially mainly due to glucagon release but eventually also due to a very large increment in catecholamines. In newborn dogs, neither epinephrine nor glucagon respond to a decrease in plasma glucose. This lack of a safeguard against hypoglycemia may indicate that the brain in pups is less dependent on a normal supply of glucose as a fuel, than in adult dogs. Counterregulation is enhanced when the effects of endogenous opiates are blocked by naloxone, indicating that endogenous opiates play a regulatory role during hypoglycemia. However, beta-endorphins which can be released with epinephrine during various stress situations, potentiate the peripheral effect of epinephrine. Glucoregulatory responses, even to slight changes in plasma glucose, are greatly enhanced during glucocorticoid treatment. This apparently reflects the greater sensitivity of the liver to glucagon. In diabetic dogs, similar to human diabetics, the glucagon response is abolished and the response of the catecholamines is partially decreased. On the basis of histological studies, we proposed that the deficient glucagon response in diabetes could be related to an increase in the somatostatin-glucagon ratio in the diabetic pancreas. This ratio is further augmented when normoglycemia is maintained with insulin. In response to a decrease in plasma glucose, there is a biphasic increment in glucose production in normal dogs, which is missing in diabetes. When normoglycemia is restored in diabetic dogs with phlorizin treatment, the second but not the first increment in glucose production is restored. We postulated, therefore, that the toxic effect of hyperglycemia, in addition to the lack of glucagon response, is the main reason why in diabetes, glucose production cannot respond promptly to a decrease in plasma glucose. The low rate of metabolic clearance of glucose seen in diabetes in the post-absorptive state, also reflects, at least in part, the toxic effect of glucose, because with acute normalization of glucose with phlorizin, metabolic glucose clearance substantially improves. Hyperglycemia is the main reason for the decreased number of glucose transporters in diabetic muscle.

  2. B)

    Epinephrine infusion in normal dogs mimics some effects of stress, in that it increases glucose production, inhibits metabolic glucose clearance and increases lipolysis. These metabolic effects of epinephrine are independent of glucagon release. In diabetes, however, epinephrine-induced hyperglycemia is exaggerated which is mainly due to glucagon. This occurs both because of excessive glucagon release, and increased hepatic sensitivity to the effects of glucagon related to hypoinsulinemia.

  3. C)

    ICV injection of a small amount of carbachol induces a release of all counterregulatory hormones. Interestingly, insulin secretion is not affected, possibly because the alpha- and beta-adrenergic pancreatic inputs are balanced. Surprisingly, this release of counterregulatory hormones induces only a marginal change in plasma glucose, since increased glucose production is matched by a similar increase in glucose uptake. In contrast, in hyperglycemic diabetic dogs, the same carbachol injection induces a much larger increment in plasma glucose. This occurred because the metabolic clearance rate of glucose did not increase. We therefore postulated a neural mechanism which controls peripheral glucose uptake and requires a permissive effect of insulin. Somatostatin, injected ICV before carbachol, abolishes most counterregulatory responses as well as the increment in glucose turnover. Lipolysis is also decreased but FFA re-esterification is abolished, reflecting a decrease in glucose uptake in the adipocyte.

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Authors and Affiliations

  1. Departments of Physiology, Medicine and Surgery, University of Toronto, and Women’s College Hospital, Toronto, Canada

    M. Vranic & L. Lickley

  2. Department of Physiology, University of Ottawa, Canada

    G. Hetenyi Jr.

  3. Yamagata University School of Medicine, Japan

    K. Yamatani

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  1. M. Vranic
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  1. University of Toronto, Toronto, Ontario, Canada

    Mladen Vranic

  2. Karolinska Hospital, Stockholm, Sweden

    Suad Efendic

  3. Banting and Best Diabetes Centre, University of Toronto, Toronto, Ontario, Canada

    Charles H. Hollenberg

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Vranic, M. et al. (1991). Effect of Stress on Glucoregulation in Physiology and Diabetes. In: Vranic, M., Efendic, S., Hollenberg, C.H. (eds) Fuel Homeostasis and the Nervous System. Advances in Experimental Medicine and Biology, vol 291. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5931-9_13

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