Department of Food and Nutrition, Brain Korea 21 Project, Yonsei University, Seoul, Korea.
Biotechnol J. 2010 Jan;5(1):99-112. doi: 10.1002/biot.200900228.
One of the major goals of this review was to identify obesity-specific gene profiles in animal models to help comprehend the pathogenic mechanisms and the prediction of the phenotypic outcomes of obesity and its associated metabolic diseases. The genomic examination of insulin-sensitive tissues, such as the adipose and hepatic tissues, has provided a wealth of information about the changes in gene expression in obesity and its associated metabolic diseases. The overexpression of genes related to inflammation, immune response, adhesion molecules, and lipid metabolism is a major characteristic of white adipose tissue, while the overexpression of the genes related to lipid metabolism, adipocyte differentiation, defense, and stress responses is noticeable in the non-alcoholic fatty liver of obese rodents. The hepatic-gene expression profiles led us to hypothesize that in obese rodents, the livers are supplied with large amounts of free fatty acids under conditions associated with obesity either through increased fatty acid biosynthesis or through decreased fatty acid oxidation, which may lead to increased mitochondrial respiratory activity. The wide list of genes that were identified in previous studies could be a source of potential therapeutic targets because most of these genes are involved in the key mechanisms of obesity development, from adipocyte differentiation to the disturbance of metabolism.
本次综述的主要目标之一是在动物模型中确定肥胖特异性基因谱，以帮助理解肥胖及其相关代谢疾病的发病机制和表型结果的预测。对胰岛素敏感组织（如脂肪组织和肝脏组织）的基因组研究提供了大量关于肥胖及其相关代谢疾病中基因表达变化的信息。与炎症、免疫反应、黏附分子和脂质代谢相关的基因的过度表达是白色脂肪组织的一个主要特征，而与脂质代谢、脂肪细胞分化、防御和应激反应相关的基因的过度表达在肥胖啮齿动物的非酒精性脂肪肝中是显而易见的。肝脏基因表达谱使我们假设，在肥胖啮齿动物中，肝脏在与肥胖相关的条件下通过增加脂肪酸合成或减少脂肪酸氧化而供应大量的游离脂肪酸，这可能导致线粒体呼吸活性增加。在之前的研究中确定的广泛的基因列表可能是潜在治疗靶点的来源，因为这些基因中的大多数都参与了肥胖发展的关键机制，从脂肪细胞分化到代谢紊乱。
