<総説>糖尿病と脂質代謝異常

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In the past decade, significant observations with important insights have been made in our understanding of the causation of hyperlipidemia and atherogenesis. Atherosclerosis is now the major cause of death in diabetics, and there is increasing concern about the possible role of hyperlipidemia in the acceleration of atherosclerosis in the patients. This review will deal with the theories of hyperlipidemia or hyperlipoproteinemia, and the various pathogenic factors as well as the treatment will be discussed with particular reference to the investigations in diabetes mellitus. There are multiple factors at work in the hyperlipidemia observed in diabetes mellitus. First, the activity of lipoprotein lipase (LPL) which is secreted from adipocytes and muscle cells to migrate to capillary walls all over the body is generally and considerably decreased in uncontrolled diabetes mellitus. Since the enzyme plays the most important role in the removal of triglyceride-rich lipoproteins such as chylomicron and very-low density lipoprotein (VLDL) from circulation, its deficiency results in the lowered clearance of these lipoproteins as is often the case with diabetic patients. When insulin deficiency, whether absolute or relative, is evident, it causes most frequently hypertriglyceridemia associated with the increase of VLDL (type IV hyperlipidemia) and also, if less frequently, hypertriglyceridemia associated with both chylomicronemia and the increase of VLDL (type V hyperlipidemia). This sort of LPL deficiency caused by insulin lack is observed in both types of diabetes, insulin dependent diabetes mellitus (IDDM) and non-insulin dependent diabetes mellitus (NIDDM). Besides insulin, C apolipoproteins affect LPL activity, C_<II> being stimulatory and C_<III> inhibitory, although clear roles of them in diabetic hyperlipidemia remain to be settled. Second, hyperinsulinemia or insulin resistance which is well established for patients with NIDDM contributes to hypertriglyceridemia as a result of the enhancement of synthesis of endogenous triglyceride in the liver. Obesity and the excess of calory intake which are so often associated with NIDDM demonstrate hyperinsulinemia as well, and thus cause hypertriglyceridemia in the same line as NIDDM. Third, there are some evidences for the delayed clearance of cholesterol-rich lipoproteins in uncontrolled diabetes mellitus. The delay would seem to be caused by the alteration of lipid contents in lipoprotein particles or the conformational change of apolipoprotein B. This apoprotein resides in VLDL, IDL and LDL, and is essentially important in the recognition of LDL by LDL receptor. Hyperglycemia-induced glycosylation of apolipoprotein B has been reported to impair the receptor-induced uptake of LDL in the cells. Similar mechanism might work at E apolipoprotein, which is important in hepatic uptake of remnant proteins including chylomicron-remnant and IDL. Thus, abnormalities of lipid metabolism in diabetes mellitus are complicated and caused by multiple factors, involving derangement in lipids, lipoproteins, apolipoproteins and enzyme systems.
近畿大学の論文
1987-12-25

<総説>糖尿病と脂質代謝異常

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