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Lipopolysaccharide-induced leptin release is neurally controlled.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Mastronardi, Claudio Alberto Yu, Wen Hsin Srivastava, Vinod K. Dees, William Mccann, S. M. |
| Copyright Year | 2001 |
| 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. |
| Starting Page | 55 |
| Ending Page | 71 |
| Page Count | 17 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://www.pnas.org/content/98/25/14720.full.pdf |
| PubMed reference number | 11724949v1 |
| Volume Number | 98 |
| Issue Number | 25 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Adipocytes Adrenergic Agonists Adrenergic Receptor Adrenergic alpha-Agonists Adrenergic alpha-Antagonists Adrenergic beta-Agonists Adrenergic beta-Antagonists Blood specimen Bromocriptine CNS disorder Dopamine Hydrochloride Dopaminergic Neurons Isoproterenol Lipopolysaccharides Phentolamine Pituitary Gland, Anterior Propranolol Sodium Chloride Substance Abuse Detection alpha-adrenergic receptor leptin |
| Content Type | Text |
| Resource Type | Article |
