期刊
CURRENT OPINION IN LIPIDOLOGY
卷 17, 期 3, 页码 238-246出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/01.mol.0000226115.97436.c0
关键词
apolipoprotein B100; liver fat; stable isotopes; type 2 diabetes; very low density lipoproteint
Purpose of review Diabetic dyslipidaemia is a cluster of plasma lipid and lipoprotein abnormalities that are metabolically interrelated. The increase of large type 1 very low density lipoprotein particles in type 2 diabetes initiates a sequence of events that generates atherogenic remnants, small dense low-density lipoprotein and small dense high-density lipoprotein particles, Thus, it is of great importance to elucidate the mechanisms behind the overproduction of large very low density lipoprotein particles in diabetic dyslipidaemia. This' review discusses the pathophysiology of very low density lipoprotein metabolism in type 2 diabetes and recent concepts of lipid management of diabetic dyslipidaemia. Recent findings Results indicate that triglyceride and apolipoprotein production in types 1 and 2 very low density lipoprotein are significantly correlated, suggesting a coupling of the two processes governing the metabolism of these lipoprotein subpopulations. Insulin resistance, hyperglycaemia, and liver fat were associated with excess hepatic production, of type 1 but not type 2 very low density lipoprotein particles. These data provide support for the independent regulation of types 1 and 2 very low density lipoprotein apolipoprotein B production. Summary Recent data suggest that the assembly of very low density lipoprotein is fundamentally altered in type 2 diabetes, explaining, the overproduction of large type 1 very low density lipoprotein as well as the inability of insulin-to suppress production of type 1 very low density lipoprotein in type 2 diabetes. Future discoveries hopefully will delineate the regulatory steps to allow more targeted treatment of diabetic dyslipidaemia.
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