التفاصيل البيبلوغرافية
| العنوان: |
Loss of microRNA-22 prevents high-fat diet induced dyslipidemia and increases energy expenditure without affecting cardiac hypertrophy. |
| المؤلفون: |
Diniz, Gabriela Placoná, Zhan-Peng Huang, Jianming Liu, Jinghai Chen, Jian Ding, Fonseca, Renata Inzinna, Barreto-Chaves, Maria Luiza, Donato Jr, Jose, Xiaoyun Hu, Da-Zhi Wang |
| المصدر: |
Clinical Science; 12/15/2017, Vol. 131 Issue 24, p2885-2900, 16p |
| مصطلحات موضوعية: |
MICRORNA, HIGH-fat diet, DYSLIPIDEMIA, CALORIC expenditure, CARDIAC hypertrophy |
| مستخلص: |
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. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
