Interaction between Glucose and Lipid Metabolism: More than Diabetic Dyslipidemia

被引:188
作者
Parhofer, Klaus G. [1 ]
机构
[1] Univ Munich, Dept Med Grosshadern 2, Marchioninistr 15, D-81377 Munich, Germany
关键词
Diabetes mellitus; Diabetic dyslipidemia; Hyperlipoproteinemia type II; Hyperlipoproteinemias; Statin; HIGH-DENSITY-LIPOPROTEIN; CORONARY-HEART-DISEASE; HOMOZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA; EUROPEAN ATHEROSCLEROSIS SOCIETY; STATIN THERAPY; FATTY-ACIDS; CARDIOVASCULAR OUTCOMES; INSULIN-RESISTANCE; REDUCING LIPIDS; BETA-CELL;
D O I
10.4093/dmj.2015.39.5.353
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Glucose and lipid metabolism are linked to each other in many ways. The most important clinical manifestation of this interaction is diabetic dyslipidemia, characterized by elevated triglycerides, low high density lipoprotein cholesterol (HDL-C), and predominance of small-dense LDL particles. However, in the last decade we have learned that the interaction is much more complex. Hypertriglyceridemia and low HDL-C cannot only be the consequence but also the cause of a disturbed glucose metabolism. Furthermore, it is now well established that statins are associated with a small but significant increase in the risk for new onset diabetes. The underlying mechanisms are not completely understood but modulation of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG CoA)-reductase may play a central role as genetic data indicate that mutations resulting in lower HMG CoA-reductase activity are also associated with obesity, higher glucose concentrations and diabetes. Very interestingly, this statin induced increased risk for new onset type 2 diabetes is not detectable in subjects with familial hypercholesterolemia. Furthermore, patients with familial hypercholesterolemia seem to have a lower risk for type 2 diabetes, a phenomenon which seems to be dose-dependent (the higher the low density lipoprotein cholesterol, the lower the risk). Whether there is also an interaction between lipoprotein(a) and diabetes is still a matter of debate.
引用
收藏
页码:353 / 362
页数:10
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