microRNAs (miRNAs), a class of endogenous non-coding RNA about 22 nucleotide long, regulate gene expression at the post-transcription level by inhibiting the translation or inducing the degradation of their target mRNAs in organisms. A lot of studies reveal that miRNAs in adipose tissues are involved in adipocyte differentiation and lipid metabolism and modulated by multiple transcription factors, adipocytokines and environmental factors, which form a complex regulatory network maintaining the homeostasis of adipose tissues. The discovery of circulating miRNAs adds new elements to the regulatory network. To study the metabolic diseases such as obesity, we should keep a new insight into the complex dynamic network. In this review, we summarize the latest studies of miRNAs in adipose tissues, which might provide new strategies for the treatment of obesity and other related diseases.
Adipokines ; metabolism ; Adipose Tissue ; metabolism ; Cell Differentiation ; Gene Expression Regulation ; Humans ; Lipid Metabolism ; MicroRNAs ; metabolism ; Obesity ; metabolism ; RNA, Messenger ; Transcription Factors ; metabolism

Objective To investigate the effects of intestinal ischemia-reperfusion (I/R) on the brain in rats. Methods Sixty-four healthy male SD rats weighing 250-300 g were randomly allocated to one of 2 groups (n = 32 each): sham operation group (S) and intestinal I/R group (I/R). Intestinal I/R was produced by occlusion of superior mesenteric artery (SMA) for 90 min followed by reperfusion. Eight animals were sacrificed at each of the following time points: 2, 6, 12 and 24 h of reperfusion (T1-4) in each group. After a median sternotomyblood samples were taken from left ventricle for measurement of plasma TNF-α and IL-6 (by ELISA). Intestine and brain tissue was harvested for microscopic examination and detection of apoptosis ( by TUNEL). The cognitive function was tested using Morris water maze at 24 h. Results No abnormality was found in intestine and brain tissue in group S. Intestinal damage and neurodegeneration were detected in group I/R. Intestinal I/R significantly increased cerebral apoptosis in group I/R compared with group S. Plasma TNF-a and IL-6 concentrations were significantly higher at T1-4 in group I/R than in group S. The escape latency and swimming distance were significantly increased, while the number of crossing the platform was decreased in group I/R compared with group S. There was no significant difference in the swimming speed between the 2 groups. Conclusion Intestinal I/R can induce brain injury and lead to cognitive dysfunction. I/R-induced release of inflammatory mediators and neuronal apoptosis are involved in the underlying mechanism.