title: Selective reduction of alpha 2-adrenergic responsiveness in hamster adipose tissue during prolonged starvation.
abstract: The influence of fasting on the dual adrenergic control of adipose tissue lipolysis was investigated in hamsters because in this species the adipocytes exhibit both beta-stimulatory and alpha 2-inhibitory adrenergic responses. In adipocytes from fed animals, the number of alpha 2-receptors (identified with [3H]clonidine and [3H]RX 821002) was greater than that of beta-receptors. As in humans, the alpha 2-adrenoceptor number was greater in adipocyte membranes from subcutaneous (inguinal and popliteal) than from internal (perirenal and epididymal) adipose tissues. Despite this difference in alpha 2-adrenoceptor number, the antilipolytic responses to the alpha 2-agonists clonidine and UK 14304 were similar in the two tissues. Food deprivation for a period of 1-6 days induced a net depletion of both adipose tissues. In 6-day starved animals the number of adipocyte alpha 2-adrenoceptors and the maximal antilipolytic effect of UK 14304 were less than 50% of those in fed controls. In contrast, the antilipolytic responses to phenylisopropyladenosine or prostaglandin E1 remained unchanged. Starvation induced a decrease in alpha 2-adrenoceptor number and an increase in beta-adrenergic sensitivity that were greater in adipocytes from subcutaneous than from internal fad pads. The data suggest that the adipocyte beta- and alpha 2-adrenoceptors are independently regulated during starvation. In the adipocyte, the alpha 2-antilipolytic responses and the alpha 2-adrenoceptor levels are dependent on the extent of the adipose mass; they are particularly reduced in emaciated hamsters.
authors.affiliation: Institut National de la Santé et de la Recherche Médicale, U 317, Toulouse, France.
authors.forename: C
authors.initials: C
authors.lastname: Carpéné
authors.forename: J
authors.initials: J
authors.lastname: Galitzky
authors.forename: J S
authors.initials: JS
authors.lastname: Saulnier-Blache
authors.forename: M
authors.initials: M
authors.lastname: Lafontan
mesh_terms: D000243:Adenosine Deaminase / Q000494:pharmacology; D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism*; D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000527:Alprostadil / Q000494:pharmacology; D000818:Animals; D001798:Blood Proteins / Q000378:metabolism; D000068438:Brimonidine Tartrate; D002478:Cells, Cultured; D003000:Clonidine / Q000494:pharmacology*; D006224:Cricetinae; D005230:Fatty Acids, Nonesterified / Q000097:blood; D008066:Lipolysis / Q000187:drug effects; D008297:Male; D008647:Mesocricetus; D010660:Phenylisopropyladenosine / Q000494:pharmacology; D011810:Quinoxalines / Q000494:pharmacology*; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D012016:Reference Values; D013217:Starvation
chemical_list: D000318:Adrenergic beta-Agonists; D001798:Blood Proteins; D005230:Fatty Acids, Nonesterified; D011810:Quinoxalines; D011943:Receptors, Adrenergic, beta; D010660:Phenylisopropyladenosine; D000068438:Brimonidine Tartrate; D000243:Adenosine Deaminase; D000527:Alprostadil; D003000:Clonidine