Effect of dexamethasone on adipose tissue and liver pyruvate dehydrogenase and its stimulation by insulin-generated chemical mediator

• Published in: Endocrinology (Philadelphia) Vol. 114; no. 1; p. 99
• Main Authors: Begum, N, Tepperman, H M, Tepperman, J
• Format: Journal Article
• Language: English
• Published: United States 01.01.1984
• Subjects: Adipose Tissue - drug effects; Adipose Tissue - enzymology; Animals; Blood Glucose - metabolism; Dexamethasone - pharmacology; Enzyme Activation; Glycolysis - drug effects; Insulin - pharmacology; Insulin Resistance; Kinetics; Liver - drug effects; Liver - enzymology; Male; Mitochondria - metabolism; Organ Size - drug effects; Proteins - metabolism; Pyruvate Dehydrogenase Complex - metabolism; Pyruvate Dehydrogenase Complex - physiology; Rats; Rats, Inbred Strains
• ISSN: 0013-7227
• DOI: 10.1210/endo-114-1-99

Rats were treated with dexamethasone (50 micrograms/day, sc) for 4 days. Total pyruvate dehydrogenase (PDH) and insulin-stimulated PDHa activities were decreased in fat pads from dexamethasone-treated rats compared to control values. Coincubation experiments with adipocyte mitochondria, plasma membrane, and insulin demonstrated decreased stimulation of PDH in preparations from dexamethasone-treated rats. The responsiveness of the mitochondrial PDH system to insulin and control rat plasma membranes was not different in glucocorticoid-treated adipocyte preparations compared to controls. Liver mitochondria from dexamethasone-treated rats demonstrated decreased basal enzyme activity and a decreased percentage of stimulation of PDH when supernatants from insulin-exposed liver particulate fractions were tested. These experiments suggest that insulin resistance produced by glucocorticoid treatment, like that resulting from fat feeding, is accompanied by a decrease in the capacity of adipocyte and liver plasma membranes to generate PDH activator in response to insulin.