Binding and action of glucagon in isolated adipocytes from cortisol-treated rats |
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| Authors: | C Calle P Sanchez-Casas M A Simón P Mayor |
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| Institution: | 1. Centre for Research Excellence in Translating Nutritional Sciences to Good Health, Adelaide Medical School, The University of Adelaide, Adelaide 5000, Australia;2. Department of Clinical Biochemistry, Bispebjerg and Frederiksberg Hospital, Copenhagen, Denmark;3. Department of Endocrinology, Zhongda Hospital, Institute of Diabetes, School of Medicine, Southeast University, Nanjing 210009, China;4. Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide 5000, Australia;5. Department of Gastroenterology and Hepatology, Royal Adelaide Hospital, Adelaide, Australia;1. Department of Internal Medicine and Clinical Nutrition, Institute of Medicine at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden;2. Department of Endocrinology, Sahlgrenska University Hospital, Gothenburg, Sweden;3. Department of Clinical Chemistry Sahlgrenska University Hospital, Gothenburg, Sweden;4. Wallenberg Center for Molecular and Translational Medicine, University of Gothenburg, Gothenburg, Sweden |
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| Abstract: | Evidence for pre-receptor, receptor and post-receptor glucagon defects was investigated in adipocytes from cortisol-treated rats. A decrease in glucagon binding due to a decreased number of receptors was observed. No changes in receptor affinity were detected. Both, the lipolytic response of glucagon and the ability of glucagon to increase basal and theophylline-stimulated cAMP accumulation remained unaltered. Moreover, a hyperglucagonemia accompanied by an increase in glucagon degradation in the serum of cortisol-treated rats was observed. Such alterations could represent a new mechanism by which glucocorticoids exert their biological actions. |
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