The role of lipids in the pathogenesis and treatment of type 2 diabetes and associated co-morbidities

被引:52
作者
Erion, Derek M. [1 ]
Park, Hyun-Jun [2 ]
Lee, Hui-Young [2 ,3 ]
机构
[1] Takeda Pharmaceut, 350 Massachusetts Ave, Cambridge, MA 02139 USA
[2] Gachon Univ, Dept Mol Med, Incheon 21999, South Korea
[3] Gachon Univ, Sch Med, Lee Gil Ya Canc & Diabet Inst, Korea Mouse Metab Phenotyping Ctr, Incheon 21999, South Korea
基金
新加坡国家研究基金会;
关键词
Cardiovascular disease; Diabetic dyslipidemia; Lipid metabolites; Insulin resistance; Type; 2; diabetes; HEPATIC INSULIN-RESISTANCE; FATTY LIVER-DISEASE; TRANSFER PROTEIN INHIBITOR; OF-FUNCTION MUTATIONS; ADIPOSE-TISSUE; BODY-FAT; CARDIOVASCULAR-DISEASE; GLYCOGEN-SYNTHESIS; GLUCOSE-PRODUCTION; GLYCEMIC CONTROL;
D O I
10.5483/BMBRep.2016.49.3.268
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In the past decade, the incidence of type 2 diabetes (T2D) has rapidly increased, along with the associated cardiovascular complications. Therefore, understanding the pathophysiology underlying T2D, the associated complications and the impact of therapeutics on the T2D development has critical importance for current and future therapeutics. The prevailing feature of T2D is hyperglycemia due to excessive hepatic glucose production, insulin resistance, and insufficient secretion of insulin by the pancreas. These contribute to increased fatty acid influx into the liver and muscle causing accumulation of lipid metabolites. These lipid metabolites cause dyslipidemia and non-alcoholic fatty liver disease, which ultimately contributes to the increased cardiovascular risk in T2D. Therefore, understanding the mechanisms of hepatic insulin resistance and the specific role of liver lipids is critical in selecting and designing the most effective therapeutics for T2D and the associated co-morbidities, including dyslipidemia and cardiovascular disease. Herein, we review the effects and molecular mechanisms of conventional anti-hyperglycemic and lipid-lowering drugs on glucose and lipid metabolism.
引用
收藏
页码:139 / 148
页数:10
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