Epinephrine binding and the selective restoration of adenylate cyclase activity in fat-fed rats

• Published in: Journal of lipid research Vol. 14; no. 3; pp. 279 - 285
• Main Authors: Gorman, R R, Tepperman, H M, Tepperman, J
• Format: Journal Article
• Language: English
• Published: United States Elsevier 01.05.1973
• Subjects: Adenylyl Cyclases - metabolism; Adipocytes - metabolism; Animals; Cell Membrane - metabolism; Cell Size; cyclic 3′,5′-AMP; Dietary Carbohydrates - administration & dosage; Dietary Fats - administration & dosage; Epididymis - cytology; Epididymis - metabolism; Epinephrine - metabolism; glucagon; hormone receptors; hormone-stimulated adenylate cyclase; Male; Rats
• ISSN: 0022-2275
• DOI: 10.1016/S0022-2275(20)36885-1

Fat feeding results in a progressive loss of epineph-rine- and glucagon-stimulated adenylate cyclase activity in adipocyte plasma membrane sacs (ghosts). Basal and NaF-stimulated adenylate cyclase activities in fat-fed animals are not significantly different from those in preparations obtained from chow-fed rats. The high fat diet increases the mean adipocyte diameter rapidly, but increased cell size, at least in the case of epinephrine stimulation, is not responsible for the decreased hormone-stimulated adenylate cyclase activity. Diet shifts to high carbohydrate or high protein regimens result in the restoration of the epinephrine-stimulated, but not the glucagon-stimulated, activity without a significant reduction in mean cell diameter. Both hormone-resistant adipocyte ghosts from fat-fed animals and ghosts obtained from hormone-sensitive adipocytes bind the same amount of [(3)H]epinephrine per milligram of membrane protein. These data indicate that the fat diet inhibits epinephrine-stimulated adenylate cyclase activity at a point between the hormone receptor and the catalytic unit of adenylate cyclase.