Abstract
miR-146a, an anti-inflammatory microRNA, is shown to be a negative regulator of adipocyte inflammation. However, the functional contribution of miR-146a in the development of obesity is not defined. In order to determine whether miR-146a influences diet-induced obesity, mice that were either wild type (WT) or miR-146a deficient (KO) were fed with high (60% kcal) fat diet (HFD) for 16 weeks. Deficiency of miR-146a did not influence obesity measured as HFD-induced body weight and fat mass gain, or metabolism of glucose and insulin tolerance. In addition, adipocyte apoptosis, adipose tissue collagen and macrophage accumulation as detected by TUNEL, Picro Sirius and F4/80 immunostaining, respectively, were comparable between the two groups of mice. Although, miR-146a deficiency had no influence on HFD-induced hepatic lipid accumulation, interestingly, it significantly increased obesity-induced inflammatory responses in liver tissue. The present study demonstrates that miR-146a deficiency had no influence on the development of HFD-induced obesity and adipose tissue remodeling, whereas it significantly increased hepatic inflammation in obese mice. This result suggests that miR-146a regulates hepatic inflammation during development of obesity.
Highlights
Using miR-146a deficient mice, in the present study, we examined the contribution of miR-146a to the development of diet-induced obesity, adipose tissue inflammation, remodeling, glucose and insulin tolerance, hepatic steatosis and inflammation in mice
In order to understand whether miR-146a expression is influenced by obesity in adipose tissue, adipose tissue mRNA from male mice (C57BL/6) fed either a 10% Kcal low fat diet (LFD) or a 60% Kcal high fat diet (HFD) for 16 weeks. miR qPCR analyses using Taqman primers against miR-146a and snoRNA202 showed that miR-146a abundance was significantly increased in epididymal adipose tissue from HFD-induced obese mice compared to LFD fed mice (Fig. 1A)
Obesity development is strongly associated with extensive remodeling of adipose tissue including hypertrophy and apoptosis of adipocytes, infiltration and accumulation of macrophages, and adipose tissue fibrosis
Summary
Using miR-146a deficient mice, in the present study, we examined the contribution of miR-146a to the development of diet-induced obesity (body weight gain), adipose tissue inflammation, remodeling (e.g. fibrosis, apoptosis, macrophage accumulation), glucose and insulin tolerance, hepatic steatosis and inflammation in mice. Our study demonstrates that miR-146a deficiency in mice had no influence on the development of high fat diet (HFD)-induced (i) obesity (body weight gain), (ii) adipose tissue inflammation, (iii) adipose tissue remodeling www.nature.com/scientificreports/. MiR-146a deficiency strongly increased inflammation in the liver tissue without influencing lipid deposition in the liver
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