Role Of LncRNA In The Pathophysiology Of NAFLD And T2DM

Nonalcoholic fatty liver disease?NAFLD?is a kind of hepatic excess fat deposition in cells leads to acquired and hepatic metabolic stress system disease,more closely associated with insulin resistance and genetic predisposition,and high blood sugar,high blood pressure,obesity,and dyslipidemia associated with multiple metabolic pathway disorders.Insulin resistance is the central component of metabolic syndrome.The incidence of non-alcoholic fatty liver?NAFLD?in the general population is 20-30%,but in the population with impaired glucose metabolism,the proportion is as high as 70-90%.Type 2 diabetes mellitus?T2DM?is a common endocrine metabolic disease,and insulin resistance is a pathophysiological bridge between NAFLD and T2DM.These two diseases occur together can synergy,can cause more serious disease and higher mortality rates,increases the likelihood of diabetes complications,including macro and microvascular complications,has increased the more serious NAFLD?including cirrhosis of the liver,hepatocellular carcinoma,and death?.Therefore,it is very important to control NAFLD in T2DM patients,and vice versa.At present,the pathogenesis of these two diseases is not clear.Diabetes and NAFLD are mutual risk factors.When they occur together,diabetes is more difficult to manage,and NAFLD is more likely to make progress.Long non-coding RNA?lncRNAs?is involved in the regulation of multiple cellular biological processes and plays a vital role in the development and progression of many diseases.In order to better understand the lncRNA whether to participate in the occurrence of NAFLD and T2DM,we selected 15 in peroxidase,the proliferation of activated receptor signal of steroid biosynthesis and sheath lipid metabolic signaling pathways of lncRNA associated with cardiovascular disease.The expression levels of lncRNA in serum of NAFLD,T2DM patients and healthy controls were detected by fluorescence quantitative PCR.The results showed that four of the 15 lncrnas in NAFLD and T2DM patients had significant changes,including saf,fendrr,MHRT and dio3os.the expression of SAF was significantly downregulated in the patients with NAFLD?P<0.01?and T2DM?P<0.05?as compared with the normal control F_?2,120?=3.896,P=0.23.For FENDRR?Fig.1B?,the results of one-way ANOVA revealed that significant difference between the groups F_?2,120?=4.094,P<0.05.The post tests indicated that the expression of FENDRR was significantly increased in the NAFLD group as compared with the T2DM group?P<0.01?,whereas no statistical significance was detected in other groups.Likewise,as Fig.1C showed,MHRT was also observed to be upregulated in the NAFLD group as compared with the T2DM individuals?P<0.05?without any changes in other groups.At last,the expression ofDIO3OS was found to be upregulated in the NAFLD group as compared with the T2DM groupand control group?Fig.1D,P<0.05?.In conclusion,we found 4 new lncrnas that may be involved in the development of type2 diabetes and non-alcoholic fatty liver,including saf,fendrr,MHRT and dio3os.Further in-depth studies may provide new insights into the pathogenesis of NAFLD and T2DM.