DELETION OF MICRORNA-22 ENHANCES THERMOGENIC GENE EXPRESSION IN WHITE ADIPOSE TISSUE OF OBESE MICE

Background Obesity is a major risk factor for several cardiovascular and metabolic disorders. In the last years, diverse studies have suggested that browning of white adipose tissue (WAT) may be used as a novel strategy for treatment of diseases associated to obesity. We recently reported that loss of microRNA‐22 attenuated the fat mass gain induced by high fat (HF) diet. In addition, loss of microRNA‐22 enhanced energy expenditure in mice fed a HF diet, suggesting that microRNA‐22 may play a critical role in the control of metabolic disorders observed in obesity. However, the possible mechanisms by which microRNA‐22 mediates the gain of WAT in response to HF feeding are unclear. In the present study, we investigated the contribution of microRNA‐22 in browning of WAT. Methods Male microRNA‐22 knockout (miR22KO) and wild type (WT) mice were fed a chow diet or HF diet for 12 weeks. Body weight gain was monitored weekly. Epididymal fat was collected and expression of genes involved in browning of WAT was evaluated by qPCR. Results miR22KO and WT mice fed HF diet displayed increased body weight gain when compared to their respective controls fed a chow diet. Loss of microRNA‐22 did not attenuate the body weight gain mediated by HF diet. Both miR22KO and WT mice fed HF diet exhibited increased epididymal fat mass compared to their respective controls. However, deletion of microRNA‐22 attenuated the gain of fat mass induced by HF diet. Analysis of gene expression demonstrated that miR22KO mice fed either a chow or HF diet displayed higher expression levels of UCP1 in WAT. In addition, miR22KO mice fed HF diet exhibited increased expression levels of Cidea and Prdm16 in WAT when compared to WT mice fed HF diet. Conclusions These findings suggest that loss of microRNA‐22 induces thermogenic gene expression in WAT of obese mice. Support or Funding Information Funding: Sao Paulo Research Foundation (FAPESP #2015/21859‐5; #2017/01558‐6). This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .