Metabolic inflammation: Connecting obesity and insulin resistance

被引:203
作者
Dali-Youcef, Nassim [1 ,2 ]
Mecili, Mustapha [3 ]
Ricci, Romeo [1 ,2 ]
Andres, Emmanuel [3 ]
机构
[1] Hop Univ Strasbourg, Lab Biochim & Biol Mol, F-67091 Strasbourg, France
[2] Univ Strasbourg, CNRS, INSERM, Inst Genet & Biol Mol & Cellulaire, F-67404 Illkirch Graffenstaden, France
[3] Hop Univ Strasbourg, Clin Med B, Serv Med Interne & Malad Metab, F-67091 Strasbourg, France
关键词
Macrophages; metaflammation; NF kappa B; type; 2; diabetes; visceral obesity; C-REACTIVE PROTEIN; NECROSIS-FACTOR-ALPHA; ENDOPLASMIC-RETICULUM STRESS; ADIPOSE-TISSUE INFLAMMATION; MONOCYTE CHEMOATTRACTANT PROTEIN-1; RECEPTOR SUBSTRATE-1; GUT MICROBIOTA; HEPATIC STEATOSIS; MACROPHAGE RECRUITMENT; LIVER INFLAMMATION;
D O I
10.3109/07853890.2012.705015
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Insulin resistance is a pathological condition that arises when insulin signaling is impaired, forcing beta-cells to produce more insulin in order to cope with body demands and to maintain glucose homeostasis. When the pancreas is no more able to support an appropriate insulin secretion, insulin resistance becomes decompensated and hyperglycemia is detected. One of the mechanisms leading to insulin resistance is low-grade inflammation that involves a number of protagonists such as inflammatory cytokines, lipids and their metabolites, reactive oxygen species (ROS), hypoxia and endoplasmic reticulum stress, and changes in gut microbiota profiles. We review here the molecular aspects of metabolic inflammation converging to insulin resistance and secondarily to type 2 diabetes. We also discuss the place of high-sensitivity C-reactive protein (hsCRP) in the assessment of metabolic inflammation and potential therapeutic interventions aimed to impede inflammation and therefore prevent insulin resistance.
引用
收藏
页码:242 / 253
页数:12
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