RESUMO
BACKGROUND AND AIMS: Epicardial adipose tissue (EAT) is a visceral AT, surrounding myocardium and coronary arteries. Its volume is higher in Type 2 diabetic (DM2) patients, associated with cardiovascular disease risk. Lipoprotein lipase (LPL) hydrolyses triglycerides (TG) from circulating lipoproteins, supplying fatty acids to AT, contributing to its expansion. We aimed to evaluate LPL expression and activity in EAT from DM2 and no DM2 patients, and its regulators ANGPTL4, GPIHBP1 and PPARγ levels, together with VLDLR expression and EAT LPL association with VLDL characteristics. METHODS: We studied patients undergoing coronary by-pass graft (CABG) divided into CABG-DM2 (nâ¯=â¯21) and CABG-noDM2 (nâ¯=â¯29), and patients without CABG (No CABG, nâ¯=â¯30). During surgery, EAT and subcutaneous AT (SAT) were obtained, in which LPL activity, gene and protein expression, its regulators and VLDLR protein levels were determined. Isolated circulating VLDLs were characterized. RESULTS: EAT LPL activity was higher in CABG-DM2 compared to CABG-noDM2 and No CABG (p=0.002 and p<0.001) and in CABG-noDM2 compared to No CABG (p=0.02), without differences in its expression. ANGPTL4 levels were higher in EAT from No CABG compared to CABG-DM2 and CABG-noDM2 (p<0.001). GPIHBP1 levels were higher in EAT from CABG-DM2 and CABG-noDM2 compared to No CABG (p= 0.04). EAT from CABG-DM2 presented higher PPARγ levels than CABG-noDM2 and No CABG (p=0.02 and p=0.03). No differences were observed in VLDL composition between groups, although EAT LPL activity was inversely associated with VLDL-TG and TG/protein index (p<0.05). CONCLUSIONS: EAT LPL regulation would be mainly post-translational. The higher LPL activity in DM2 could be partly responsible for the increase in EAT volume.
Assuntos
Proteína 4 Semelhante a Angiopoietina/análise , Diabetes Mellitus Tipo 2/enzimologia , Gordura Intra-Abdominal/enzimologia , Lipase Lipoproteica/análise , Receptores de Lipoproteínas/análise , Adiposidade , Idoso , Estudos de Casos e Controles , Diabetes Mellitus Tipo 2/diagnóstico , Diabetes Mellitus Tipo 2/fisiopatologia , Ativação Enzimática , Ácidos Graxos/sangue , Feminino , Humanos , Gordura Intra-Abdominal/fisiopatologia , Lipoproteínas VLDL/sangue , Masculino , Pessoa de Meia-Idade , PPAR gama/metabolismo , Pericárdio , Receptores de LDL/análise , Triglicerídeos/sangueRESUMO
Avaliou-se o efeito do GH in vitro sobre a expressão gênica do receptor LDL (RLDL) e da HMG-CoA redutase, bem como sobre a proliferação celular e acúmulo de lípides intracelulares em células mesangiais cultivadas em meio com soro deficiente de lipoproteínas (LPDS) durante 1, 2, 4 e 6 dias. A expressão coordenada entre o RLDL e a HMG-CoA redutase foi observada nas células mesangiais cultivadas em meio com LPDS. O GH aaumentou a proliferação das células mesangiais, dependente da sua concentração. A exposição prolongada ao GH induziu o aumento da expressão de RNAm do RLDL e da HMG-CoA redutase na células mesangiais, bem como o acúmulo de lípides neutros no citoplasma. Nos estudos in vivo...