title: Hamster adipocyte alpha 2-adrenoceptor changes during fat mass modifications are not directly dependent on adipose tissue norepinephrine content.
abstract: It is questioned whether alterations of the sympathetic nervous system can explain the specific increment of the adipocyte alpha 2-adrenoceptor observed during white adipose tissue (WAT) enlargement and fat cell size increment. The impact of a 6-hydroxydopamine-induced sympathectomy, validated by determination of the WAT norepinephrine content, was tested on isolated white fat cell alpha 2-adrenoceptor function and binding [( 3H]RX 821002 and [3H]UK 14304 binding). Chemical sympathectomy of standard adult hamsters, neither alters the alpha 2-adrenergic-dependent antilipolysis nor the adipocyte alpha 2-adrenergic binding. A slight hypersensitivity of the beta 1-adrenergic lipolytic response was observed, without modification in beta-adrenergic binding [( 125I]cyanopindolol binding). Compared with controls, caloric restriction (10 days) of adult hamsters induced a large decrease in adipocyte alpha 2-adrenoceptor (P less than 0.001) with a parallel decrement in the mean fat cell size (P less than 0.001) and alpha 2-adrenergic responsiveness while there was no significant variation of the WAT norepinephrine content (on a per pad basis). 6-Hydroxydopamine treatment of the restricted animals (from day 6 to day 9) induced a higher preservation of adipocyte alpha 2-adrenoceptor density (P less than 0.001), no change in alpha 2-adrenergic responsiveness, and higher preservation of mean fat cell size (P less than 0.05) than in the restricted only animals. No significant modification in the beta-adrenergic binding was observed whatever the conditions. It was concluded that the specific increment in the adipocyte alpha 2-adrenoceptor during fat mass enlargement was not directly dependent on sympathetic nervous system alterations. Nevertheless, the sympathetic-dependent mobilization of the fat stores, after induction of caloric restriction, can indirectly modulate the alpha 2-adrenoceptor density in the adipocyte by promoting changes in white fat cell size.
authors.affiliation: Institut National de la Santé et de la Recherche Médicale (I.N.S.E.R.M. U. 317), Université Paul Sabatier, Toulouse, France.
authors.forename: J S
authors.initials: JS
authors.lastname: Saulnier-Blache
authors.forename: C
authors.initials: C
authors.lastname: Atgie
authors.forename: C
authors.initials: C
authors.lastname: Carpene
authors.forename: N
authors.initials: N
authors.lastname: Quideau
authors.forename: M
authors.initials: M
authors.lastname: Lafontan
mesh_terms: D000273:Adipose Tissue / Q000294:innervation / Q000378:metabolism*; D000316:Adrenergic alpha-Agonists / Q000378:metabolism; D000317:Adrenergic alpha-Antagonists; D000818:Animals; D000068438:Brimonidine Tartrate; D006224:Cricetinae; D004146:Dioxanes / Q000378:metabolism; D002149:Energy Intake; D005508:Food Deprivation; D006892:Hydroxydopamines; D019329:Idazoxan / Q000031:analogs & derivatives; D008066:Lipolysis; D008297:Male; D008647:Mesocricetus; D009638:Norepinephrine / Q000378:metabolism*; D016627:Oxidopamine; D010869:Pindolol / Q000031:analogs & derivatives / Q000378:metabolism; D011810:Quinoxalines / Q000378:metabolism; D011942:Receptors, Adrenergic, alpha / Q000378:metabolism*; D013563:Sympathectomy, Chemical
chemical_list: D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D004146:Dioxanes; D006892:Hydroxydopamines; D011810:Quinoxalines; D011942:Receptors, Adrenergic, alpha; C047975:cyanopindolol; D000068438:Brimonidine Tartrate; D016627:Oxidopamine; D010869:Pindolol; C058525:2-methoxyidazoxan; D009638:Norepinephrine; D019329:Idazoxan