脂肪组织
生物
胰岛素抵抗
胰岛素
肥胖
医学
碳水化合物代谢
新陈代谢
脂质代谢
2型糖尿病
代谢综合征
免疫系统
谷氨酰胺酶
葡萄糖稳态
作者
Wenkai Ren,Yaoyao Xia,Siyuan Chen,Guoyao Wu,Fuller W. Bazer,Beiyan Zhou,Bie Tan,Guoqiang Zhu,Jinping Deng,Yulong Yin
出处
期刊:Advances in Nutrition
[Oxford University Press]
日期:2019-03-01
卷期号:10 (2): 321-330
被引量:44
标识
DOI:10.1093/advances/nmy084
摘要
Obesity is a nutritional disorder resulting from a chronic imbalance between energy intake and expenditure. This disease is characterized by inflammation in multiple cell types, including macrophages. M1 macrophage responses are correlated with the progression of obesity or diabetes; therefore, strategies that induce repolarization of macrophages from an M1 to an M2 phenotype may be promising for the prevention of obesity- or diabetes-associated pathology. Glutamine (the most abundant amino acid in the plasma of humans and many other mammals including rats) is effective in inducing polarization of M2 macrophages through the glutamine-UDP-N-acetylglucosamine pathway and α-ketoglutarate produced via glutaminolysis, whereas succinate synthesized via glutamine-dependent anerplerosis or the γ-aminobutyric acid shunt promotes polarization of M1 macrophages. Interestingly, patients with obesity or diabetes show altered glutamine metabolism, including decreases in glutamine and α-ketoglutarate concentrations in serum but increases in succinate concentrations. Thus, manipulation of macrophage polarization through glutamine metabolism may provide a potential target for prevention of obesity- or diabetes-associated pathology.
科研通智能强力驱动
Strongly Powered by AbleSci AI