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RESEARCH PRODUCT

Systemic Oxidative Stress and Visceral Adipose Tissue Mediators of NLRP3 Inflammasome and Autophagy Are Reduced in Obese Type 2 Diabetic Patients Treated with Metformin.

Dolores Periañez-gómezMilagros RochaCarlos MorillasSandra López-domènechVictor M. VictorRubén Díaz-rúaFrancesca IannantuoniSegundo ÁNgel Gómez-abrilZaida Abad-jiménez

subject

0301 basic medicinemedicine.medical_specialtyvisceral adipose tissue (VAT)obesityautophagyendocrine system diseasesPhysiologyinflammatory cytokinesClinical BiochemistryATG5Adipose tissue030209 endocrinology & metabolismLeukocyte homeostasisType 2 diabetesBiochemistryArticleProinflammatory cytokine03 medical and health sciences0302 clinical medicineInternal medicinemedicineoxidative stressMolecular Biologytype 2 diabetes (T2D)business.industrylcsh:RM1-950nutritional and metabolic diseasesInflammasomeCell Biologymedicine.diseaseMetforminlcsh:Therapeutics. Pharmacology030104 developmental biologyEndocrinologybusinessmetforminInflammasome complexmedicine.drug

description

Obesity is a low-grade inflammatory condition affecting a range of individuals, from metabolically healthy obese (MHO) subjects to type 2 diabetes (T2D) patients. Metformin has been shown to display anti-inflammatory properties, though the underlying molecular mechanisms are unclear. To study whether the effects of metformin are mediated by changes in the inflammasome complex and autophagy in visceral adipose tissue (VAT) of obese patients, a biopsy of VAT was obtained from a total of 68 obese patients undergoing gastric bypass surgery. The patients were clustered into two groups: MHO patients and T2D patients treated with metformin. Patients treated with metformin showed decreased levels of all analyzed serum pro-inflammatory markers (TNF&alpha

10.3390/antiox9090892https://pubmed.ncbi.nlm.nih.gov/32967076