Metabolic balancing acts of vitamin A in type-2 diabetes and obesity  

作　　者：Rajendra Raghow 

机构地区：[1]Department of Veterans Affairs Medical Center,Memphis,TN 38104,United States [2]Department of Pharmacology,University of Tennessee Health Science Center,Memphis,TN 38163,United States

出　　处：《World Journal of Diabetes》2012年第10期174-177,共4页世界糖尿病杂志（英文版）（电子版）

摘　　要：Using mice that lack retinaldehyde dehydrogenase 1 gene(Raldh1-/-mice),Kierfer et al demonstrated that retinoids(metabolites of Vitamin A) play an important role in the regulation of cellular metabolisms and energetics.The Aldh1a1-/-mice were leaner and less prone to accumulate subcutaneous and visceral fat,and to acquire insulin resistance on high fat diet.Their lower fasting glucose levels concomitant with reduced hepatic expression of glucose 6-phosphatase and phosphoenol pyruvate carboxy kinase genes indicated that Aldh1a1-/-mice were defective in gluconeogenesis.These mice also had lower plasma levels of triglycerides,very low-density lipoprotein and lowdensity lipoprotein-triacylglycerol,while their skeletal muscles elicited higher expression of carnitine palmatoyl transferase,medium chain acyl-A dehydrogenase,peroxisome proliferation activated receptor(PPARα and PPARδ.Thus,the improved lipid and lipoprotein profiles of Raldh1a1-/-mice resulted from a combination of reduced lipogenesis and enhanced fatty acid oxidation by retinoids.The mechanistic details of how retinoids integrate fasting glucose,hepatic gluconeogenesis and adaptive thermogenesis independent of body mass deserve further study.Using mice that lack retinaldehyde dehydrogenase 1 gene (Raldh1-/- mice), Kierfer et al demonstrated that retinoids (metabolites of Vitamin A) play an important role in the regulation of cellular metabolisms and energetics. The Aldh1a1-/- mice were leaner and less prone to accumulate subcutaneous and visceral fat, and to acquire insulin resistance on high fat diet. Their lower fasting glucose levels concomitant with reduced hepatic expression of glucose 6-phosphatase and phosphoenol pyruvate carboxy kinase genes indicated that Aldh1a1-/- mice were defective in gluconeogenesis. These mice also had lower plasma levels of triglycerides, very low-density lipoprotein and low-density lipoprotein-triacylglycerol, while their skeletal muscles elicited higher expression of carnitine palmatoyl transferase, medium chain acyl-A dehydrogenase, peroxisome proliferation activated receptor (PPARα and PPARδ. Thus, the improved lipid and lipoprotein profiles of Raldh1a1-/- mice resulted from a combination of reduced lipogenesis and enhanced fatty acid oxidation by retinoids. The mechanistic details of how retinoids integrate fasting glucose, hepatic gluconeogenesis and adaptive thermogenesis independent of body mass deserve further study.

关 键 词：RETINALDEHYDE DEHYDROGENASE 1 VITAMIN A RETINOIDS GLUCONEOGENESIS type 2 DIABETES 

分 类 号：R587.1[医药卫生—内分泌] R589.2[医药卫生—内科学]