Leptin affects adenylate cyclase activity in H9c2 cardiac cell line: effects of short- and long-term exposure |
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| Institution: | 1. Department ofFrom the Departments of Biochemistry and Biophysics “F. Cedrangolo” (GI, SN, MP, AS, EC), Naples, Italy;2. Department of Geriatric Medicine and Metabolic Diseases (MB, GP), Second University of Naples, Naples, Italy;1. Department of Internal Medicine, Section on Hypertensive Diseases, Ochsner Clinic Foundation, New Orleans, Louisiana, USA;1. Department of Cardiology, University of Athens, Hippokration Hospital, Athens, Greece;1. Joslin Diabetes Center and Department of Medicine, Harvard Medical School, Boston, MA 02215 USA;2. Diabetes Unit, Endocrine Division, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215 USA;1. From the Department of Medicine, Duke University Medical Center, Durham, North Carolina. *Present address: University Federico II, Division of Cardiology, Naples, Italy.;1. Division of Health Promotion and Exercise (KI-T), National Institute of Health and Nutrition, Shinjyuku, TokyoJapan;2. Chubu National Hospital (TO), Obu, Aichi, Japan;3. Department of Kinesiology and Health Education (HT), University of Texas at Austin, Austin, Texas, USA;1. Department of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA;2. Roudebush VA Medical Center, Indianapolis, IN 46202, USA |
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| Abstract: | Leptin has been hypothesized to be a pathophysiologic link between obesity and cardiovascular diseases. Because the adenylate cyclase (AC) system is a main effector of β-adrenergic receptors and leptin has been shown to modulate AC activity in other cell lines, a leptin impact on cardiac AC activity was hypothesized. Therefore, acute and chronic effects of leptin on a rat cardiac cell line (H9c2) were investigated. Leptin affected both basal (+13% at 30 min and −16.4% after 18 h v untreated cells) and catecholamine-stimulated AC activity (isoproterenol + leptin at 30 min or 18 h was +21% v untreated cells; norepinephrine + leptin at 30 min was +38.8% v untreated cells; and norepinephrine + leptin at 18 h was +6% v untreated cells). Thus, long-term leptin treatment was associated with a reduced AC activity and a different responsiveness to catecholamines. The AC activity on leptin treatment was accompanied by changes in levels of proteins structurally or functionally related to AC complex (AC, Gαs, Gαi, p21-ras). These data indicate that the AC complex is profoundly affected at more than one level by leptin treatment in the H9c2 cardiac cell line. Differences in AC activity after short- and long-term exposure to leptin and the interaction between leptin and catecholamine might provide further insight to the understanding of the development of hypertension and congestive heart failure in obese patients. |
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