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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Mccann, S. M. Mastronardi, C. A. Dees, W. L. Srivastava, V. K. Yu, W. H. |
| Description | Author Affiliation: Mastronardi CA ( Pennington Biomedical Research Center, Louisiana State University, 6400 Perkins Road, Baton Rouge, LA 70808-4124, USA.); |
| Abstract | Our hypothesis is that leptin release is controlled neurohormonally. Conscious, male rats bearing indwelling, external, jugular catheters were injected with the test drug or 0.9% NaCl (saline), and blood samples were drawn thereafter to measure plasma leptin. Anesthesia decreased plasma leptin concentrations within 10 min to a minimum at 120 min, followed by a rebound at 360 min. Administration (i.v.) of lipopolysaccharide (LPS) increased plasma leptin to almost twice baseline by 120 min, and it remained on a plateau for 360 min, accompanied by increased adipocyte leptin mRNA. Anesthesia largely blunted the LPS-induced leptin release at 120 min. Isoproterenol (beta-adrenergic agonist) failed to alter plasma leptin but reduced LPS-induced leptin release significantly. Propranolol (beta-receptor antagonist) produced a significant increase in plasma leptin but had no effect on the response to LPS. Phentolamine (alpha-adrenergic receptor blocker) not only increased plasma leptin (P < 0.001), but also augmented the LPS-induced increase (P < 0.001). alpha-Bromoergocryptine (dopaminergic-2 receptor agonist) decreased plasma leptin (P < 0.01) and blunted the LPS-induced rise in plasma leptin release (P < 0.001). We conclude that leptin is at least in part controlled neurally because anesthesia decreased plasma leptin and blocked its response to LPS. The findings that phentolamine and propranolol increased plasma leptin concentrations suggest that leptin release is inhibited by the sympathetic nervous system mediated principally by alpha-adrenergic receptors because phentolamine, but not propranolol, augmented the response to LPS. Because alpha-bromoergocryptine decreased basal and LPS-induced leptin release, dopaminergic neurons may inhibit basal and LPS-induced leptin release by suppression of release of prolactin from the adenohypophysis. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 25 |
| Volume Number | 98 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2001-12-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Leptin Secretion Lipopolysaccharides Toxicity Neurosecretory Systems Drug Effects Physiology Adipocytes Metabolism Adrenergic Alpha-Antagonists Pharmacology Adrenergic Beta-Agonists Adrenergic Beta-Antagonists Anesthesia Animals Bromocriptine Dopamine Agonists Isoproterenol Blood Genetics Models, Neurological Phentolamine Propranolol RNA, Messenger Sympathetic Nervous System Research Support, U.S. Gov't, P.H.S. Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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