AJP - Regulatory, Integrative and Comparative Physiology, Vol 266, Issue 4 1141-R1147, Copyright © 1994 by American Physiological Society

ARTICLES

Antilipolytic effects of alpha 2-adrenergic agonists, neuropeptide Y, adenosine, and PGE1 in mammal adipocytes

I. Castan, P. Valet, N. Quideau, T. Voisin, L. Ambid, M. Laburthe, M. Lafontan and C. Carpene
Institut National de la Sante et de la Recherche Medicale U317, Institut L. Bugnard, Toulouse, France.

Lipolysis is stimulated by different hormones, depending on the species, but is also regulated by antilipolytic modulators, such as catecholamines (alpha 2-agonists), neuropeptide Y (NPY), adenosine, and prostaglandin E1 (PGE1), for which species-specific variations are poorly described. Comparison of the efficiency of these antilipolytic systems showed that PGE1 or phenylisopropyladenosine was able to totally inhibit lipolysis activation in nine mammalian species. However, the antilipolytic responses to clonidine or UK-14304 were fully developed in hamster and rabbit but blunted in the adipocytes of jerboa, rat, guinea pig, garden dormouse, and dormouse. A powerful antilipolytic effect of NPY was found only in the garden dormouse. Only human and dog adipocytes exhibited antilipolytic responses to alpha 2-adrenergic and NPY stimulation. These observations were explained by differences in alpha 2-adrenergic and NPY/peptide YY receptor number. Thus, inhibitory regulation of lipolysis in white adipocytes seems to be composed of two systems: a constitutive one that is related to paracrine mediators (adenosine, prostaglandins) and a regulatory one including neuroendocrine messengers such as catecholamines and NPY.

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