Buechler Christa, Krautbauer Sabrina, Eisinger Kristina
Christa Buechler, Sabrina Krautbauer, Kristina Eisinger, Department of Internal Medicine I, University Hospital of Regensburg, 93042 Regensburg, Germany.
World J Diabetes. 2015 May 15;6(4):548-53. doi: 10.4239/wjd.v6.i4.548.
The increasing prevalence of obesity causes a major interest in white adipose tissue biology. Adipose tissue cells are surrounded by extracellular matrix proteins whose composition and remodeling is of crucial importance for cell function. The expansion of adipose tissue in obesity is linked to an inappropriate supply with oxygen and hypoxia development. Subsequent activation of hypoxia inducible factor 1 (HIF-1) inhibits preadipocyte differentiation and initiates adipose tissue fibrosis. Thereby adipose tissue growth is limited and excess triglycerides are stored in ectopic tissues. Stressed adipocytes and hypoxia contribute to immune cell immigration and activation which further aggravates adipose tissue fibrosis. There is substantial evidence that adipose tissue fibrosis is linked to metabolic dysfunction, both in rodent models and in the clinical setting. Peroxisome proliferator activated receptor gamma agonists and adiponectin both reduce adipose tissue fibrosis, inflammation and insulin resistance. Current knowledge suggests that antifibrotic drugs, increasing adipose tissue oxygen supply or HIF-1 antagonists will improve adipose tissue function and thereby ameliorate metabolic diseases.
肥胖患病率的不断上升引发了人们对白色脂肪组织生物学的极大兴趣。脂肪组织细胞被细胞外基质蛋白所包围，其组成和重塑对细胞功能至关重要。肥胖状态下脂肪组织的扩张与氧气供应不足和缺氧的发展有关。随后缺氧诱导因子1（HIF-1）的激活会抑制前脂肪细胞分化并引发脂肪组织纤维化。由此脂肪组织的生长受到限制，多余的甘油三酯则储存在异位组织中。应激的脂肪细胞和缺氧会促使免疫细胞迁移和激活，这进一步加剧了脂肪组织纤维化。有大量证据表明，在啮齿动物模型和临床环境中，脂肪组织纤维化都与代谢功能障碍有关。过氧化物酶体增殖物激活受体γ激动剂和脂联素都能减少脂肪组织纤维化、炎症和胰岛素抵抗。目前的知识表明，抗纤维化药物、增加脂肪组织氧气供应或HIF-1拮抗剂将改善脂肪组织功能，从而改善代谢性疾病。
