Obesity is associated with development of diverse diseases, including cardiovascular diseases and dyslipidemia. MiRNA-22 (miR-22) is a critical regulator of cardiac function and targets genes involved in metabolic processes. Previously, we generated miR-22 null mice and we showed that loss of miR-22 blunted cardiac hypertrophy induced by mechanohormornal stress. In the present study, we examined the role of miR-22 in the cardiac and metabolic alterations promoted by high-fat (HF) diet. We found that loss of miR-22 attenuated the gain of fat mass and prevented dyslipidemia induced by HF diet, although the body weight gain, or glucose intolerance and insulin resistance did not seem to be affected. Mechanistically, loss of miR-22 attenuated the increased expression of genes involved in lipogenesis and inflammation mediated by HF diet. Similarly, we found that miR-22 mediates metabolic alterations and inflammation induced by obesity in the liver. However, loss of miR-22 did not appear to alter HF diet induced cardiac hypertrophy or fibrosis in the heart. Our study therefore establishes miR-22 as an important regulator of dyslipidemia and suggests it may serve as a potential candidate in the treatment of dyslipidemia associated with obesity.
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December 2017
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Wheat germ agglutinin staining of the adult mouse heart transverse section. In their study, Diniz et al., shows microRNA-22 regulates dyslipidemia and energy expenditure. For more information please see pages 2885-2900. Image kindly provided by Da-Zhi Wang
Research Article|
December 04 2017
Loss of microRNA-22 prevents high-fat diet induced dyslipidemia and increases energy expenditure without affecting cardiac hypertrophy
Gabriela Placoná Diniz;
1Department of Cardiology, Boston Children’s Hospital, Harvard Medical School, Boston, Massachusetts, U.S.A.
2Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, SP, Brazil
Correspondence: Gabriela P. Diniz ([email protected]) or Da-Zhi Wang ([email protected])
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Zhan-Peng Huang;
Zhan-Peng Huang
1Department of Cardiology, Boston Children’s Hospital, Harvard Medical School, Boston, Massachusetts, U.S.A.
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Jianming Liu;
Jianming Liu
1Department of Cardiology, Boston Children’s Hospital, Harvard Medical School, Boston, Massachusetts, U.S.A.
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Jinghai Chen;
Jinghai Chen
1Department of Cardiology, Boston Children’s Hospital, Harvard Medical School, Boston, Massachusetts, U.S.A.
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Jian Ding;
Jian Ding
1Department of Cardiology, Boston Children’s Hospital, Harvard Medical School, Boston, Massachusetts, U.S.A.
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Renata Inzinna Fonseca;
Renata Inzinna Fonseca
2Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, SP, Brazil
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Maria Luiza Barreto-Chaves;
Maria Luiza Barreto-Chaves
2Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, SP, Brazil
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Jose Donato, Jr;
Jose Donato, Jr
3Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, SP, Brazil
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Xiaoyun Hu;
Xiaoyun Hu
1Department of Cardiology, Boston Children’s Hospital, Harvard Medical School, Boston, Massachusetts, U.S.A.
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Da-Zhi Wang
1Department of Cardiology, Boston Children’s Hospital, Harvard Medical School, Boston, Massachusetts, U.S.A.
Correspondence: Gabriela P. Diniz ([email protected]) or Da-Zhi Wang ([email protected])
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Publisher: Portland Press Ltd
Received:
September 18 2017
Revision Received:
November 01 2017
Accepted:
November 03 2017
Accepted Manuscript online:
November 03 2017
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© 2017 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society
2017
Clin Sci (Lond) (2017) 131 (24): 2885–2900.
Article history
Received:
September 18 2017
Revision Received:
November 01 2017
Accepted:
November 03 2017
Accepted Manuscript online:
November 03 2017
Citation
Gabriela Placoná Diniz, Zhan-Peng Huang, Jianming Liu, Jinghai Chen, Jian Ding, Renata Inzinna Fonseca, Maria Luiza Barreto-Chaves, Jose Donato, Xiaoyun Hu, Da-Zhi Wang; Loss of microRNA-22 prevents high-fat diet induced dyslipidemia and increases energy expenditure without affecting cardiac hypertrophy. Clin Sci (Lond) 15 December 2017; 131 (24): 2885–2900. doi: https://doi.org/10.1042/CS20171368
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