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Titolo:
Impaired beta-adrenergic signaling pathway in white adipocytes of sucklingfa/fa Zucker rats: a defect in receptor coupling
Autore:
Mory, G; Wiel, M; Adli, H; Diot-Dupuy, F; Ferre, P; Bazin, R;
Indirizzi:
INSERM U465, Ctr Biomed Cordeliers, F-75270 Paris 06, France INSERM U465 Paris France 06 Biomed Cordeliers, F-75270 Paris 06, France
Titolo Testata:
INTERNATIONAL JOURNAL OF OBESITY
fascicolo: 11, volume: 25, anno: 2001,
pagine: 1592 - 1598
SICI:
0307-0565(200111)25:11<1592:IBSPIW>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
BROWN-ADIPOSE-TISSUE; G-PROTEINS; FA-FA; BETA-3-ADRENERGIC RECEPTOR; 3T3-F442A ADIPOCYTES; ADENYLATE-CYCLASE; GENETIC OBESITY; EXPRESSION; MECHANISM; BINDING;
Keywords:
beta(1)-adrenoceptors; beta(3)-adrenoceptors; Gs protein; Gi protein; adenylyl cyclase; lipolysis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Bazin, R INSERM U465, Ctr Biomed Cordeliers, 15 Rue Ecole Med, F-75270 Paris 06, France INSERM U465 15 Rue Ecole Med Paris France 06 70 Paris 06, France
Citazione:
G. Mory et al., "Impaired beta-adrenergic signaling pathway in white adipocytes of sucklingfa/fa Zucker rats: a defect in receptor coupling", INT J OBES, 25(11), 2001, pp. 1592-1598

Abstract

BACKGROUND: In fa/fa Zucker rats, leptin receptor deficiency is responsible for both a deficit of energy expenditure and hyperphagia which lead to massive obesity and insulin resistance in adulthood. This obesity is also characterised by alterations of the beta -adrenergic signaling pathway. OBJECTIVE: To determine whether alterations in beta -adrenergic pathway could occur at the onset of obesity when fa/fa rats are not yet hyperinsulinemic. ANIMALS: Fourteen-day-old suckling fa/fa and Fa/fa littermates (from heterozygous lean (Fa/fa) female and homozygous obese (fa/fa) male mating). MEASUREMENTS: Membranes were prepared from isolated adipocytes after collagenase treatment of inguinal adipose tissue. The response of adenylyl-cyclase activity to stimulation by isoprenaline, GTP gamma -S or forskolin was studied. B-max and K-d of (beta (1) + beta (2)) and of beta (3) adrenoceptors were measured using H-3-CGP saturation binding experiments. mRNA concentration of beta (1) and beta (3)-AR was determined by semi-quantitative RT-PCR. G(s)alpha protein was quantified by Western blotting and Gi protein by ADP-ribosylation. RESULTS: Despite an almost normal body weight, inguinal fat pad weight wasincreased two-fold by the expression of fa mutation. This increase was entirely accounted for by fat cell hypertrophy (x2.5 in volume). In fa/fa compared to Falfa pups, response of adenylyl cyclase to isoprenaline was decreased two-fold but responses to GTP(gamma)S or forskolin were unchanged. Density Of (beta (1) + beta (2)) and beta (3)-AR was not affected by the fa/fa genotype, as well as G(s)alpha and Gi concentration. CONCLUSION: Response of inguinal fat cells to catecholamines was decreasedwithout any quantitative modifications of the different elements of the adenylyl cyclase cascade. This suggests an alteration in the coupling betweenbeta -AR and G proteins. Due to the important increase in fat cell volume we hypothesize that changes in the physical properties of plasma membranes and/or changes in cytoskeleton - extracellular-matrix interactions could disturb the beta -adrenergic pathway responsiveness. In addition to the excess of lipid storage, which occurs very early at the onset of obesity, the impairment of the responsiveness to catecholamines reported in this study might worsen the obesity syndrome.

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Documento generato il 29/09/20 alle ore 00:44:00