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ORIGINAL ARTICLE: The approach to the mechanism of calcitonin gene‐related peptide‐inducing inhibition of food intake
Author(s) -
Sun J.Y.,
Jing M.Y.,
Wang J.F.,
Weng X.Y.
Publication year - 2010
Publication title -
journal of animal physiology and animal nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.651
H-Index - 56
eISSN - 1439-0396
pISSN - 0931-2439
DOI - 10.1111/j.1439-0396.2009.00937.x
Subject(s) - medicine , endocrinology , anorectic , neuropeptide , cholecystokinin , calcitonin gene related peptide , leptin , calcitonin , neuropeptide y receptor , chemistry , ghrelin , glucagon , peptide hormone , somatostatin , insulin , hormone , biology , food intake , obesity , receptor
Summary The aim of this study was to investigate the anorectic mechanism of calcitonin gene‐related peptide (CGRP) in rats. Intraperitoneal injection of CGRP (50 μ g/kg) resulted in decline (p < 0.05) in the food intake of rats at 0.5, 1, 2 and 4 h in comparison with saline control. Compared with saline‐treated group, the levels of hypothalamic 3′,5′‐cyclic adenosine monophosphate (cAMP) and plasma glucagon were increased (p < 0.05) in CGRP‐treated group, but insulin level was decreased (p < 0.05). No significant changes (p > 0.05) in the plasma leptin were observed between two treatment groups. Calcitonin gene‐related peptide injection down regulated (p < 0.05) both neuropeptide Y (NPY) and melanin‐concentrating hormone (MCH) genes at mRNA levels, but up regulated (p < 0.05) the expression of cholecystokinin (CCK) gene. The correlations analysis showed that food intake was negatively correlated (p < 0.05) with CCK mRNA, cAMP and glucagon levels. Moreover, there existed negative correlations (p < 0.05) between MCH mRNA and glucagon levels, and positive correlations (p < 0.05) between insulin and leptin levels. The results showed that cAMP acting as the second messenger may play a vital role in the anorectic effects of CGRP. Calcitonin gene‐related peptide could stimulate anorexigenic neuropeptides (i.e. CCK) and/or inhibit orexigenic neuropeptides (i.e. NPY and MCH) expression, and ultimately suppressed food intake that was functionally coupled to cAMP/PKA pathway activation.