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Beneficial effects of PTP1B deficiency on brown adipocyte differentiation and protection against apoptosis induced by pro- and anti-inflammatory stimuli.

Abstract：

:Insulin is an inducer of brown fat adipogenesis through the activation of a signalling network that involves positive/negative modulators. Given the importance of brown adipose tissue (BAT) for basal thermogenic energy expenditure, we investigated the role of PTP1B in the acquisition of terminal differentiated phenotype and in the apoptotic responses of brown adipocytes. Immortalized brown preadipocytes lacking (PTP1B(-/-)) or expressing (PTP1B(+/+)) PTP1B have been generated. PTP1B deficiency accelerated a full program of brown adipogenesis including induction of transcription factors, coactivators, adipogenic markers and signalling molecules. Fully differentiated PTP1B(-/-) brown adipocytes were resistant to tumor necrosis factor (TNFalpha)-induced apoptosis as these cells were protected against caspase-8 activation, FLIP degradation, Bid cleavage and caspase-3 activation compared to wild-type controls. These events were recovered by PTP1B rescue. Survival signalling including phosphorylation of IRS-1 and Akt/PKB and BclxL expression were decreased in TNFalpha-treated PTP1B(-/-) cells but not in the wild-type. Similarly, PTP1B(-/-) brown adipocytes were protected against resveratrol-induced apoptosis. Phosphorylation of Akt/PKB and Foxo1 phosphorylation/acetylation decreased exclusively in resveratrol-treated wild-type cells, leading to nuclear localization of Foxo1 and up-regulation of Bim. Thus, PTP1B inhibition could be of benefit against obesity by counteracting TNFalpha-induced brown fat atrophy, and combined with resveratrol might improve low-grade inflammation.

journal_name

Cell Signal

journal_title

Cellular signalling

authors

Miranda S,González-Rodríguez A,Revuelta-Cervantes J,Rondinone CM,Valverde AM

doi

10.1016/j.cellsig.2009.11.019

subject

Has Abstract

pub_date

2010-04-01 00:00:00

pages

645-59

issue

4

eissn

0898-6568

issn

1873-3913

pii

S0898-6568(09)00366-0

journal_volume

22

pub_type

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