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Titolo:
Altered insulin secretion associated with reduced lipolytic efficiency in aP2(-/-) mice
Autore:
Scheja, L; Makowski, L; Uysal, KT; Wiesbrock, SM; Shimshek, DR; Meyers, DS; Morgan, M; Parker, RA; Hotamisligil, GS;
Indirizzi:
Harvard Univ, Sch Publ Hlth, Div Biol Sci, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 Hlth, Div Biol Sci, Boston, MA 02115 USA Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA Harvard UnivBoston MA USA 02115 bl Hlth, Dept Nutr, Boston, MA 02115 USA Bristol Myers Squibb Pharmaceut Res Inst, Dept Metab Dis, Princeton, NJ 08543 USA Bristol Myers Squibb Pharmaceut Res Inst Princeton NJ USA 08543 08543 USA
Titolo Testata:
DIABETES
fascicolo: 10, volume: 48, anno: 1999,
pagine: 1987 - 1994
SICI:
0012-1797(199910)48:10<1987:AISAWR>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
LIPID-BINDING PROTEIN; FATTY-ACID-BINDING; NECROSIS-FACTOR-ALPHA; BETA-ADRENERGIC-RECEPTOR; PANCREATIC-ISLETS; BROWN ADIPOCYTES; RAT ADIPOCYTES; MESSENGER-RNA; BETA-3-ADRENERGIC RECEPTOR; MOLECULAR-CLONING;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
68
Recensione:
Indirizzi per estratti:
Indirizzo: Hotamisligil, GS Harvard Univ, Sch Publ Hlth, Div Biol Sci, 665 HuntingtonAve, Boston, MA 02115 USA Harvard Univ 665 Huntington Ave Boston MA USA 02115 5 USA
Citazione:
L. Scheja et al., "Altered insulin secretion associated with reduced lipolytic efficiency in aP2(-/-) mice", DIABETES, 48(10), 1999, pp. 1987-1994

Abstract

Recent studies have shown that genetic deficiency of the adipocyte fatty acid-binding protein (aP2) results in minor alterations of plasma lipids andadipocyte development but provides significant protection from dietary obesity-induced hyperinsulinemia and insulin resistance. To identify potentialmechanisms responsible for this phenotype, we examined lipolysis and insulin secretion in aP2(-/-) mice. beta-Adrenergic stimulation resulted in a blunted rise of blood glycerol levels in aP2(-/-) compared with aP2(+/+) mice, suggesting diminished lipolysis in aP2(-/-) adipocytes. Confirming this, primary adipocytes isolated from aP2(-/-) mice showed attenuated glycerol and free fatty acid (FFA) release in response to dibutyryl cAMP. The decreased lipolytic response seen in the aP2(-/-) mice was not associated with altered expression levels of hormone-sensitive lipase or perilipin. The acute insulin secretory response to beta-adrenergic stimulation was also profoundly suppressed in aP2(-/-) mice despite comparable total concentrations and only minor changes in the composition of systemic FFAs. To address whether levels of specific fatty acids are different in aP2(-/-) mice, the plasma FFA profile after beta-adrenergic stimulation was determined. Significant reduction in both stearic and cis-11-eicoseneic acids and an increase in palmitoleic acid were observed. The response of aP2(-/-) mice to other insulin secretagogues such as arginine and glyburide was similar to that of aP2(+/+) mice, arguing against generally impaired function of pancreatic beta-cells. Finally no aP2 expression was detected in isolated pancreatic islet cells. These results provide support for the existence of an adipo-pancreatic axis, the proper action of which relies on the presence of aP2. Consequently, aP2's role in the pathogenesis of type 2 diabetes might involve regulation of both hyperinsulinemia and insulin resistance through its impact on both lipolysis and insulin secretion.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 10:24:47