Effect of Metformin on Adipose Tissue Degeneration During Obesity

Cesar Elpidio Rodríguez Cervantes, Clara Alba Betancourt
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Abstract

Obesity is associated with an increased inflammation involved in the development of atherosclerosis and insulin resistance. Macrophages are key in the genesis of these processes. Obesity induces macrophage accumulation in adipose tissue, they produce many of the inflammatory molecules secreted by adipose tissue like TNF-α, interleukins (IL-1β, IL-6, IL-8), as well as acute phase proteins such as haptoglobin (Hp), PAI-1 and C-reactive protein. The presence of these molecules in obesity relates this pathology to various inflammation degrees.The analysis of histological sections obtained from rabbit adipose tissue biopsy samples and processed by the hematoxylin-eosin and immunohistochemistry, showed the effect of metformin, a molecule which acts on the insulin metabolism, by the degeneration of this tissue during obesity. Metformin and its effects on metabolism are such that decreases the inflammation process suffered by adipose tissue, which is reflected by morphological changes in the distribution and migration of cells in the histological structure.
二甲双胍对肥胖期间脂肪组织变性的影响
肥胖与动脉粥样硬化和胰岛素抵抗相关的炎症增加有关。巨噬细胞是这些过程发生的关键。肥胖诱导巨噬细胞在脂肪组织中聚集,它们产生脂肪组织分泌的许多炎症分子,如TNF-α、白细胞介素(IL-1β、IL-6、IL-8),以及急性期蛋白,如触珠蛋白(Hp)、PAI-1和c反应蛋白。这些分子在肥胖中的存在与不同程度的炎症有关。利用苏木精-伊红和免疫组织化学对兔脂肪组织活检样本的组织学切片进行分析,发现二甲双胍(一种作用于胰岛素代谢的分子)通过肥胖期间该组织的变性而起作用。二甲双胍及其对代谢的影响可以减轻脂肪组织的炎症过程,这体现在组织结构中细胞分布和迁移的形态学改变上。
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