https://scholars.lib.ntu.edu.tw/handle/123456789/384359
標題: | Adiponectin receptor 1 overexpression reduces lipid accumulation and hypertrophy in the heart of diet-induced obese mice-possible involvement of oxidative stress and autophagy | 作者: | Chou, I.-P. Chiu, Y.-P. SHIH-TORNG DING Liu, B.-H. Lin, Y.Y. CHING-YI CHEN |
關鍵字: | Adiponectin receptor 1; Autophagy; Diet-induced obesity; Hypertrophic heart; Lipid accumulation; Oxidative stress | 公開日期: | 2014 | 卷: | 39 | 期: | 4 | 起(迄)頁: | 173-179 | 來源出版物: | Endocrine Research | 摘要: | Background: Studies show that adiponectin and its receptors (AdipoR1 and 2) play important roles in regulating glucose and lipid metabolism in mice. Obesity, type II diabetes and cardiovascular disease are highly correlated with downregulated adiponectin signaling; however, research has not clarified the functions of AdipoR1 in vivo. Methods: In this study, mice were induced to overexpress the AdipoR1 transgene so that its functions could be studied in relation to hypertrophic cardiomyopathy. Wild-type and AdipoR1-transgenic male mice were fed ad libitum with a standard chow diet or else a high-fat/sucrose diet (HFSD) for 24 weeks, beginning at 6-7 weeks of age. Results: After receiving the 24-week HFSD, AdipoR1-transgenic mice did not become obese, nor did they develop heart hypertrophy. The AdipoR1 transgene decreased the elevating cardiac troponin I expression caused by the HFSD. While the HFSD induced mRNA expression of CD36 and CPTI, AdipoR1 reversed it. Suppression of cardiac SOD mRNA expression by the HFSD was improved by the AdipoR1 transgene. The HFSD caused a higher autophagic gene expression of Beclin 1 and Lamp 2A in the heart, whereas the AdipoR1 transgene ameliorated them. Conclusions: The AdipoR1 transgene enabled mice to resist diet-induced obesity while decreasing lipid accumulation, oxidative stress and autophagic damage. These effects might contribute to the improvement of heart functions in diet-induced obese mice. ? 2014 Informa Healthcare USA, Inc. |
URI: | http://www.scopus.com/inward/record.url?eid=2-s2.0-84911472579&partnerID=MN8TOARS http://scholars.lib.ntu.edu.tw/handle/123456789/384359 |
DOI: | 10.3109/07435800.2013.879165 | SDG/關鍵字: | adiponectin; adiponectin receptor 1; beclin 1; lysosome associated membrane protein 2; sucrose; troponin I; adiponectin receptor; adiponectin receptor 1, mouse; apoptosis regulatory protein; Becn1 protein, mouse; biological marker; CD36 antigen; manganese superoxide dismutase; sugar intake; superoxide dismutase; troponin I; animal experiment; animal model; animal tissue; Article; autophagy; Beclin 1 gene; controlled study; gene; gene overexpression; heart function; hypertrophic cardiomyopathy; Lamp 2 A gene; lean body weight; lipid diet; lipid storage; male; mouse; nonhuman; nucleotide sequence; obesity; oxidative stress; sugar intake; transgene; transgenic mouse; wild type; adverse effects; animal; cardiomegaly; cross breeding; enzymology; gene expression regulation; genetics; heart ventricle; lipid metabolism; metabolism; obesity; pathophysiology; randomization; Animals; Antigens, CD36; Apoptosis Regulatory Proteins; Autophagy; Biological Markers; Cardiomegaly; Crosses, Genetic; Diet, High-Fat; Dietary Sucrose; Gene Expression Regulation; Heart Ventricles; Lipid Metabolism; Male; Mice, Transgenic; Obesity; Oxidative Stress; Random Allocation; Receptors, Adiponectin; Superoxide Dismutase; Troponin I |
顯示於: | 動物科學技術學系 |
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