Proline oxidase-adipose triglyceride lipase pathway restrains adipose cell death and tissue inflammation
| Autor: | G Rotilio, Katia Aquilano, Maria Rosa Ciriolo, Sara Baldelli, D Lettieri Barbato, Stefano Cannata, Sergio Bernardini |
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| Jazyk: | angličtina |
| Rok vydání: | 2014 |
| Předmět: |
medicine.medical_specialty
Adipose tissue macrophages Adipose tissue Peroxisome proliferator-activated receptor Apoptosis Inflammation White adipose tissue Biology Mitochondrion Mice 3T3-L1 Cells Internal medicine Proline Oxidase medicine Animals PPAR alpha RNA Messenger RNA Small Interfering Settore BIO/10 Settore MED/49 - Scienze Tecniche Dietetiche Applicate Molecular Biology chemistry.chemical_classification Original Paper Proline oxidase Forkhead Box Protein O1 Forkhead Transcription Factors Lipase Cell Biology Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha Diet Mitochondria Up-Regulation Endocrinology Adipose Tissue chemistry Adipose triglyceride lipase RNA Interference medicine.symptom Reactive Oxygen Species Transcription Factors |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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