Glucocorticoid Effect on Hepatic Carbohydrate Metabolism in the Endotoxin-Shocked Monkey

Schuler, James J.; Erve, Peter R.; Schumer, William

doi:10.1097/00000658-197604000-00003

Cited by 38 publications

(14 citation statements)

References 24 publications

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“…More severe infections also inhibit gluconeogenesis, thus increasing the risk that glucose production will not keep pace with glucose utilization. Bacterial endotoxins can inhibit several enzymes required for gluco neogenesis, including phosphoenolpyruvate carboxykinase, fructose-1,6-diphosphatase, and glucose-6-phosphatase [Schuler et al, 1976].…”

Section: Discussionmentioning

confidence: 99%

Hypoglycemia and Death in Anorexia nervosa

Copeland

Herzog²

1987

Psychother Psychosom

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Several deaths in patients with anorexia nervosa have been ascribed to ‘inanition’. The proximate cause of death from inanition has not been established. There are few previous reports of life-threatening hypoglycemia in anorexia nervosa. We participated in the care of two severely cachectic women with anorexia nervosa who were in coma with serum glucose levels of 8 and 14 mg/dl, respectively. Both patients became alert after administration of intravenous glucose. Both were found to have pneumonia at the time of the hypoglycemic event. While the mechanism of the hypoglycemia is unknown, it may be related to the suppression of gluconeogenesis by infection in the setting of reduced substrate, depleted fat stores and decreased catecholamine release.

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Section: Discussionmentioning

confidence: 99%

Hypoglycemia and Death in Anorexia nervosa

Copeland

Herzog²

1987

Psychother Psychosom

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“…Insulin, which stimulates the uptake of glucose and amino acids by cells and enhances glycogen synthesis, renders mice more susceptible to the lethal action of endotoxin (25). On the other hand, glucocorticoids have been reported to ameliorate the lethal effects of endotoxin in humans and animals (4,32,35).…”

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confidence: 99%

Down regulation of hepatic glucocorticoid receptors after endotoxin treatment

Stith¹,

McCallum²

1983

Infect Immun

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The mechanism by which endotoxin administration results in hypoglycemia was evaluated by characterizing [3H]dexamethasone binding and phosphoenolpyruvate carboxykinase activity in hepatic cytosol preparations from treated and control mice. Starved mice were given Escherichia coli 0111:B4 endotoxin or saline intraperitoneally on day 3 after bilateral adrenalectomy. [3H]dexamethasone binding was measured by the charcoal method after the incubation of cytosol preparations with [3H]dexamethasone in the presence or absence of unlabeled dexamethasone. Changes in [3H]dexamethasone binding were found to be time and dose dependent in treated mice. When mice given different doses of endotoxin reached the same stage of morbidity, as indicated by the average time of death, significantly lower glucocorticoid binding was measured. Scatchard analysis of binding isotherms defined a. single class of binding sites. Association and dissociation rate constants and the equilibrium dissociation constant (Kd) were not altered, but the maximum number of binding sites was depressed by endotoxin. The rank order of potency of competitors for [3H]dexamethasone binding, dexamethasone, > hydrocortisone = corticosterone > deoxycorticosterone > progesterone > testosterone = estradiol, was consistent with a glucocorticoid receptor, although the competition was not altered by endotoxin. Endotoxin treatment prevented the glucocorticoid-induced increase in hepatic phosphoenolpyruvate carboxykinase activity. We conclude that the hypoglycemia of endotoxin poisoning is effected, in part, by the inhibition of the glucocorticoid-mediated induction of phosphoenolpyruvate carboxykinase via the down regulation of hepatic glucocorticoid receptors.

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“…It has been reported (4,30,41) that the glycogen depletion and the hypoglycemia were associated with changes in activities of enzymes involved in glycogen synthesis and glucose metabolism. Many workers (15,43,44) have suggested that gluconeogenesis was impaired by the administration of endotoxin. On the other hand, Woods et al (53) showed that Salmonella endotoxin exerted a stimulatory effect on tumor glycolysis similar to the action of insulin.…”

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confidence: 99%