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Hypoxia and adipose tissue function and dysfunction in obesity

机译：肥胖者的缺氧和脂肪组织功能障碍

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The rise in the incidence of obesity has led to a major interest in the biology of white adipose tissue. The tissue is a major endocrine and signaling organ, with adipocytes, the characteristic cell type, secreting a multiplicity of protein factors, the adipokines. Increases in the secretion of a number of adipokines occur in obesity, underpinning inflammation in white adipose tissue and the development of obesity-associated diseases. There is substantial evidence, particularly from animal studies, that hypoxia develops in adipose tissue as the tissue mass expands, and the reduction in PO2 is considered to underlie the inflammatory response. Exposure of white adipocytes to hypoxic conditions in culture induces changes in the expression of 1,000 genes. The secretion of a number of inflammation-related adipokines is upregulated by hypoxia, and there is a switch from oxidative metabolism to anaerobic glycolysis. Glucose utilization is increased in hypoxic adipocytes with corresponding increases in lactate production. Importantly, hypoxia induces insulin resistance in fat cells and leads to the development of adipose tissue fibrosis. Many of the responses of adipocytes to hypoxia are initiated at PO2 levels above the normal physiological range for adipose tissue. The other cell types within the tissue also respond to hypoxia, with the differentiation of preadipocytes to adipocytes being inhibited and preadipocytes being transformed into leptin-secreting cells. Overall, hypoxia has pervasive effects on the function of adipocytes and appears to be a key factor in adipose tissue dysfunction in obesity.
机译：肥胖症的发病率上升已引起人们对白色脂肪组织生物学的极大兴趣。该组织是主要的内分泌和信号传导器官，其脂肪细胞是特征性的细胞类型，分泌多种蛋白质因子，脂肪因子。肥胖中许多脂肪因子的分泌增加，这是白色脂肪组织炎症和肥胖相关疾病发展的基础。有大量证据，尤其是从动物研究中得出的证据表明，随着组织质量的增长，脂肪组织中会发生缺氧，而PO2的减少被认为是炎症反应的基础。将白色脂肪细胞暴露于培养物中的低氧条件下会诱导> 1,000个基因的表达发生变化。缺氧会上调许多与炎症相关的脂肪因子的分泌，并且存在从氧化代谢到厌氧糖酵解的转变。缺氧脂肪细胞中的葡萄糖利用增加，而乳酸的产生相应增加。重要的是，缺氧会诱导脂肪细胞中的胰岛素抵抗，并导致脂肪组织纤维化的发展。脂肪细胞对缺氧的许多反应是在脂肪组织的正常生理范围以上的PO2水平开始的。组织内的其他细胞类型也对缺氧有反应，前脂肪细胞向脂肪细胞的分化被抑制，前脂肪细胞转化为瘦素分泌细胞。总的来说，缺氧对脂肪细胞的功能具有普遍的影响，并且似乎是肥胖中脂肪组织功能障碍的关键因素。

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