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Proline oxidase–adipose triglyceride lipase pathway restrains adipose cell death and tissue inflammation

Identifieur interne : 000405 ( Main/Curation ); précédent : 000404; suivant : 000406

Proline oxidase–adipose triglyceride lipase pathway restrains adipose cell death and tissue inflammation

Auteurs : D. Lettieri Barbato [Italie] ; K. Aquilano [Italie] ; S. Baldelli [Italie] ; S M Cannata [Italie] ; S. Bernardini [Italie] ; G. Rotilio [Italie] ; M R Ciriolo [Italie]

Source :

Cell Death and Differentiation [ 1350-9047 ] ; 2013.

RBID : PMC:3857628

Abstract

The nutrient-sensing lipolytic enzyme adipose triglyceride lipase (ATGL) has a key role in adipose tissue function, and alterations in its activity have been implicated in many age-related metabolic disorders. In adipose tissue reduced blood vessel density is related to hypoxia state, cell death and inflammation. Here we demonstrate that adipocytes of poorly vascularized enlarged visceral adipose tissue (i.e. adipose tissue of old mice) suffer from limited nutrient delivery. In particular, nutrient starvation elicits increased activity of mitochondrial proline oxidase/dehydrogenase (POX/PRODH) that is causal in triggering a ROS-dependent induction of ATGL. We demonstrate that ATGL promotes the expression of genes related to mitochondrial oxidative metabolism (peroxisome proliferator-activated receptor-α, peroxisome proliferator-activated receptor-γ coactivator-1α), thus setting a metabolic switch towards fat utilization that supplies energy to starved adipocytes and prevents cell death, as well as adipose tissue inflammation. Taken together, these results identify ATGL as a stress resistance mediator in adipocytes, restraining visceral adipose tissue dysfunction typical of age-related metabolic disorders.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3857628

DOI: 10.1038/cdd.2013.137
PubMed: 24096872
PubMed Central: 3857628

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PMC:3857628

Le document en format XML

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<front><div type="abstract" xml:lang="en"><p>The nutrient-sensing lipolytic enzyme adipose triglyceride lipase (ATGL) has a key role in adipose tissue function, and alterations in its activity have been implicated in many age-related metabolic disorders. In adipose tissue reduced blood vessel density is related to hypoxia state, cell death and inflammation. Here we demonstrate that adipocytes of poorly vascularized enlarged visceral adipose tissue (i.e. adipose tissue of old mice) suffer from limited nutrient delivery. In particular, nutrient starvation elicits increased activity of mitochondrial proline oxidase/dehydrogenase (POX/PRODH) that is causal in triggering a ROS-dependent induction of ATGL. We demonstrate that ATGL promotes the expression of genes related to mitochondrial oxidative metabolism (peroxisome proliferator-activated receptor-<italic>α</italic>
, peroxisome proliferator-activated receptor-γ coactivator-1<italic>α</italic>
), thus setting a metabolic switch towards fat utilization that supplies energy to starved adipocytes and prevents cell death, as well as adipose tissue inflammation. Taken together, these results identify ATGL as a stress resistance mediator in adipocytes, restraining visceral adipose tissue dysfunction typical of age-related metabolic disorders.</p>
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Proline oxidase–adipose triglyceride lipase pathway restrains adipose cell death and tissue inflammation

Proline oxidase–adipose triglyceride lipase pathway restrains adipose cell death and tissue inflammation

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Abstract

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