Lozano-Bartolome, JavierLlaurado, GemmaPortero-Otin, ManelAltuna-Coy, AntonioRojo-Martinez, GemmaVendrell, JoanJorba, RosaRodriguez-Gallego, EstherChacon, Matilde R2023-01-252023-01-252018-02-01Lozano-Bartolomé J, Llauradó G, Portero-Otin M, Altuna-Coy A, Rojo-Martínez G, Vendrell J, et al. Altered Expression of miR-181a-5p and miR-23a-3p Is Associated With Obesity and TNFα-Induced Insulin Resistance. J Clin Endocrinol Metab. 2018 Apr 1;103(4):1447-1458http://hdl.handle.net/10668/12089The proinflammatory cytokine TNFα is a key player in insulin resistance (IR). The role of miRNAs in inflammation associated with IR is poorly understood. To investigate miR-181a-5p and miR-23a-3p expression profiles in obesity and to study their role in TNFα-induced IR in adipocytes. Two separate cohorts were used. Cohort 1 was used in adipose tissue (AT) expression studies and included 28 subjects with body mass index (BMI) Expression of miR-181a-5p and miR-23a-3p was reduced in adipose tissue from obese and diabetic subjects and was inversely correlated to adiposity and homeostasis model assessment of IR index. Overexpression of miR-181a-5p and miR-23a-3p in adipocytes upregulated insulin-stimulated AKT activation and reduced TNFα-induced IR, regulating PTEN and S6K expression. Serum levels of miR-181a-5p were reduced in case vs control subjects at baseline, suggesting a prognostic value. Variable importance in projection scores revealed miR-181a-5p had more effect on the model than insulin or glucose at 120 minutes. miR-181a-5p and miR-23a-3p may prevent TNFα-induced IR in adipocytes through modulation of PTEN and S6K expression.enProto-Oncogene Proteins c-aktSignal TransductionTumor Necrosis Factor-alphaUp-RegulationAdipocytesAdultAgedFemaleHumansInsulinInsulin ResistanceIntra-Abdominal FatMaleMicroRNAsMiddle AgedObesityPTEN PhosphohydrolaseAltered Expression of miR-181a-5p and miR-23a-3p Is Associated With Obesity and TNFα-Induced Insulin Resistance.research article29409019Restricted accessTejido AdiposoInsulinaHomeostasisInflamaciónGlucosaResistencia a la insulinaMicroARNs10.1210/jc.2017-019091945-7197https://academic.oup.com/jcem/article-pdf/103/4/1447/24565597/jc.2017-01909.pdf