Sodium Butyrate Protects Against High Fat Diet-Induced Cardiac Dysfunction and Metabolic Disorders in Type II Diabetic Mice
文献类型：期刊论文
| 作者 | Zhang, Ling1,2; Du, Jianfeng2; Wang, Hao2; Zhao, Yu Tina2; Zhao, Ting C.2; Yano, Naohiro3; Dubielecka, Patrycja M.4; Zhuang, Shougang4; Chin, Y. Eugene5; Qin, Gangjian6 |
| 刊名 | JOURNAL OF CELLULAR BIOCHEMISTRY
 |
| 出版日期 | 2017 |
| 卷号 | 118期号:8页码:2395-2408 |
| 关键词 | HISTONE DEACETYLASE DIABETES CARDIOVASCULAR DISEASE OBESITY CARDIAC FUNCTION METABOLIC SYNDROME |
| ISSN号 | 0730-2312 |
| DOI | 10.1002/jcb.25902 |
| 文献子类 | Article |
| 英文摘要 | Histone deacetylases are recently identified to act as key regulators for cardiac pathophysiology and metabolic disorders. However, the function of histone deacetylase (HDAC) in controlling cardiac performance in Type II diabetes and obesity remains unknown. Here, we determine whether HDAC inhibition attenuates high fat diet (HFD)-induced cardiac dysfunction and improves metabolic features. Adult mice were fed with either HFD or standard chow food for 24 weeks. Starting at 12 weeks, mice were divided into four groups randomly, in which sodium butyrate (1%), a potent HDAC inhibitor, was provided to chow and HFD-fed mice in drinking water, respectively. Glucose intolerance, metabolic parameters, cardiac function, and remodeling were assessed. Histological analysis and cellular signaling were examined at 24 weeks following euthanization of mice. HFD-fed mice demonstrated myocardial dysfunction and profound interstitial fibrosis, which were attenuated by HDAC inhibition. HFD-induced metabolic syndrome features insulin resistance, obesity, hyperinsulinemia, hyperglycemia, lipid accumulations, and cardiac hypertrophy, these effects were prevented by HDAC inhibition. Furthermore, HDAC inhibition attenuated myocyte apoptosis, reduced production of reactive oxygen species, and increased angiogenesis in the HFD-fed myocardium. Notably, HFD induced decreases in MKK3, p38, p38 regulated/activated protein kinase (PRAK), and Akt-1, but not p44/42 phosphorylation, which were prevented by HDAC inhibition. These results suggest that HDAC inhibition plays a critical role to preserve cardiac performance and mitigate metabolic disorders in obesity and diabetes, which is associated with MKK3/p38/PRAK pathway. The study holds promise in developing a new therapeutic strategy in the treatment of Type II diabetic-induced heart failure and metabolic disorders. J. Cell. Biochem. 118: 2395-2408, 2017. (c) 2017 Wiley Periodicals, Inc. |
| 学科主题 | Biochemistry & Molecular Biology ; Cell Biology |
| WOS关键词 | HISTONE DEACETYLASE ; INSULIN-RESISTANCE ; HDAC INHIBITION ; MYOCARDIAL-ISCHEMIA ; REPERFUSION INJURY ; INFARCTED HEARTS ; DISEASE ; OBESITY ; HYPERTROPHY ; SENSITIVITY |
| 语种 | 英语 |
| CSCD记录号 | CSCD:31641108 |
| WOS记录号 | WOS:000403053000046 |
| 出版者 | WILEY |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.144/handle/331004/1263]  |
| 专题 | 中国科学院上海生命科学研究院营养科学研究所 |
| 作者单位 | 1.Rhode Isl Hosp, Dept Emergency Med, Providence, RI USA; 2.Boston Univ, Sch Med, Roger Williams Med Ctr, Dept Surg, 50 Maude St, Providence, RI 02908 USA; 3.Brown Univ, Women & Infants Hosp, Providence, RI 02912 USA; 4.Rhode Isl Hosp, Dept Med, Providence, RI 02903 USA; 5.Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Key Lab Stem Cell Biol, Shanghai, Peoples R China; 6.Northwestern Univ, Feinberg Sch Med, Feinberg Cardiovasc Res Inst, Chicago, IL 60611 USA, |
| 推荐引用方式 GB/T 7714 | Zhang, Ling,Du, Jianfeng,Wang, Hao,et al. Sodium Butyrate Protects Against High Fat Diet-Induced Cardiac Dysfunction and Metabolic Disorders in Type II Diabetic Mice[J]. JOURNAL OF CELLULAR BIOCHEMISTRY,2017,118(8):2395-2408. |
| APA | Zhang, Ling.,Du, Jianfeng.,Wang, Hao.,Zhao, Yu Tina.,Zhao, Ting C..,...&,.(2017).Sodium Butyrate Protects Against High Fat Diet-Induced Cardiac Dysfunction and Metabolic Disorders in Type II Diabetic Mice.JOURNAL OF CELLULAR BIOCHEMISTRY,118(8),2395-2408. |
| MLA | Zhang, Ling,et al."Sodium Butyrate Protects Against High Fat Diet-Induced Cardiac Dysfunction and Metabolic Disorders in Type II Diabetic Mice".JOURNAL OF CELLULAR BIOCHEMISTRY 118.8(2017):2395-2408. |
入库方式： OAI收割
来源：上海营养与健康研究所
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