Diabetic dyslipidaemia: from basic research to clinical practice*

摘要: The recognition that the increase of plasma triglyceride rich lipoproteins (TRLs) is associated with multiple alterations other species are potentially atherogenic has expanded picture diabetic dyslipidaemia. discovery heterogeneity within major lipoprotein classes VLDL, LDL and HDL opened new avenues to reveal specific pertubations large VLDL 1 particles in Type 2 diabetes initiates a sequence events generates remnants, small dense particles. Together these components comprise lipid triad. Notably malignant nature dyslipidaemia not completely shown by measures used clinical practice. key question what mechanisms behind dyslipidaemia? Despite advances recent years, our understanding assembly secretion still surprisingly incomplete. To date it unclear how liver able regulate amount triglycerides incorporated into produce either or current evidence suggests machinery driving includes (i) low insulin signalling via PI-3 kinase pathway enhances accumulation "nascent " (ii) up-regulation SREBP-1C stimulates de novo lipogenesis (iii) excess availability "polar molecules" hepatocytes stabilizes apo B 100. Recent data suggest all steps could be fundamentally altered explaining overproduction as well ability suppress production diabetes. discoveries have established transcription factors including PPARs, SREBP-1 LXRs regulators liver. These observations target tailor more efficient drugs treat