Glycation and Hypoxia: Two Key Factors for Adipose Tissue Dysfunction

被引:14
作者
Matafome, Paulo [1 ,2 ]
Rodrigues, Tiago [1 ]
Seica, Raquel [1 ]
机构
[1] Univ Coimbra, Fac Med, Inst Biomed Res Light & Image IBILI, Physiol Lab, P-3000354 Coimbra, Portugal
[2] Coimbra Hlth Sch ESTeSC, Inst Politecn Coimbra, Coimbra, Portugal
关键词
Adipose tissue; microvascular function; hypoxia; glycation; inflammation; insulin resistance; RENIN-ANGIOTENSIN SYSTEM; METHYLGLYOXAL INDUCES APOPTOSIS; INSULIN SIGNALING PATHWAYS; ENDOTHELIAL GROWTH-FACTOR; ACTIVATED PROTEIN-KINASE; OXIDATIVE STRESS MARKERS; TYPE-1 RECEPTOR BLOCKER; FATTY-ACID OXIDATION; END-PRODUCTS AGES; RED-BLOOD-CELLS;
D O I
10.2174/0929867322666150209155633
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
Many aspects of adipose tissue pathophysiology in metabolic diseases have been described in the last years. One of such aspects is certainly hypoxia, which was shown to develop in adipose tissue of obese individuals and animal models. Recent data suggest two main factors for adipose tissue hypoxia: adipocyte hypertrophy and vascular dysfunction. In addition, glycation was also shown to induce morphological and functional alterations in adipose tissue. In particular, methylglyoxal directly formed from glucose was shown to potently induce AGE formation in vivo and to contribute to metabolic and vascular alterations in adipose tissue. Glycation and hypoxia are both thought to be on the basis of low grade inflammatory activation, further increasing metabolic dysregulation in adipose tissue. This review summarizes the current knowledge about the factors that contribute for tissue hypoxia and the role of glycation, not only at the vascular level, but also at the metabolic, oxidative and inflammatory levels.
引用
收藏
页码:2417 / 2437
页数:21
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