Queiroz Jean César Farias de, Alonso-Vale Maria Isabel Cardoso, Curi Rui, Lima Fabio Bessa
Laboratório de Fisiologia Celular, Departamento de Fisiologia e Biofísica, ICB, USP, São Paulo, SP, Brasil.
Arq Bras Endocrinol Metabol. 2009 Jul;53(5):582-94. doi: 10.1590/s0004-27302009000500011.
Obesity is one of the major Public Health problems. Obese individuals are more susceptible to develop cardiovascular diseases and type 2 diabetes mellitus. The obesity results from the increase in size and number of the adipocytes. The balance between adipogenesis and adiposity determines the degree of obesity. Mature adipocytes secrete adipokines, such as TNFalpha, IL-6, leptine and adiponectin, and lipokine, the palmitoleic acid omega-7. The production of adipokines is increased in obesity, contributing to the onset of peripheral insulin resistance. The knowledge about the molecular events that regulate the differentiation of pre-adipocytes and mesenchymal stem cells into adipocytes (adipogenesis) is important for the comprehension of the genesis of obesity. Activation of transcription factor PPARgamma plays an essential role in the adipogenesis. Certain fatty acids are PPARgamma ligands and can control adipogenesis. Moreover, some fatty acids act as signaling molecules regulating their differentiation into adipocytes or death. Accordingly, the lipid composition of the diet and PPARgamma agonists can regulate the balance between adipogenesis and death of adipocytes and, therefore, the obesity.
肥胖是主要的公共卫生问题之一。肥胖个体更容易患心血管疾病和2型糖尿病。肥胖是由脂肪细胞大小和数量增加导致的。脂肪生成与肥胖之间的平衡决定了肥胖程度。成熟脂肪细胞分泌脂肪因子，如肿瘤坏死因子α、白细胞介素-6、瘦素和脂联素，以及脂质因子ω-7棕榈油酸。肥胖时脂肪因子的产生增加，导致外周胰岛素抵抗的发生。了解调节前脂肪细胞和间充质干细胞分化为脂肪细胞（脂肪生成）的分子事件，对于理解肥胖的发生机制很重要。转录因子PPARγ的激活在脂肪生成中起关键作用。某些脂肪酸是PPARγ配体，可控制脂肪生成。此外，一些脂肪酸作为信号分子调节其向脂肪细胞的分化或死亡。因此，饮食中的脂质组成和PPARγ激动剂可以调节脂肪生成与脂肪细胞死亡之间的平衡，进而调节肥胖。
