Potential regulatory mechanisms of lncRNA in diabetes and its complications.

Long non-coding RNAs (lncRNAs) are transcripts longer than 200 nucleotides without protein-coding potential. Although these molecules were initially considered as "junk products" of transcription without biological relevance, recent advances in research have shown that lncRNA plays an important role, not only in cellular processes such as proliferation, differentiation, and metabolism, but also in the pathological processes of cancers, diabetes, and neurodegenerative diseases. In this review, we focus on the potential regulatory roles of lncRNA in diabetes and the complications associated with diabetes.

[The effects of arecoline on the lipid metabolism of 3T3-L1 adipocytes].

OBJECTIVE: To observe the effects of arecoline on lipid metabolism in 3T3-L1 adipocytes and explore its possible mechanisms. METHODS: 3T3-L1 pre-adipocytes were induced into adipocytes with the classic "cocktail" method, subsequently, adipocytes were treated with arecoline at the concentrations of 0, 25, 50 and 100 µmol/L for 72 hours. After 72 hours, cell vability was measured with MTT method, lipid droplet accumulation in the cytoplasm was observed with oil red O staining, the protein expression of fatty acid synthase (FAS), adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) were detected by Western blot assay. RESULTS: There were a large number of lipid droplets in the cytoplasm in the differentiated 3T3-L1 adipocytes. MTT results showed that 0~100 µmol/L arecoline had no significant effect on cell vability; oil red O staining found arecoline reduced lipid amount in 3T3-L1 adipocytes; Western blot results showed that compared with 0 µmol/L arecoline group (the control group), arecoline significantly reduced the protein level of FAS and increased the protein levels of ATGL and HSL, and 50 µmol/L arecoline group was the most significant. CONCLUSIONS: Arecoline significantly increased lipolysis of 3T3-L1 adipocyte, which might be associated with decreased the FAS expression of key enzyme of lipid synthesis and increased the ATGL and HSL expression of key enzyme of adipolysis.

[The effects of dihydromyricetin on cognitive dysfunction in type 2 diabetes mice].

OBJECTIVE: To observe the effects of dihydromyricetin(DHM) on cognitive dysfunction and expression of brain derived neurotrophic factor(BDNF) protein in hippocampus of type 2 diabetic mice(T2DM). METHODS: Forty C57BL/6J mice were randomly divided into two groups, normal control group (n=8):normal diet feeding; T2DM model group (n=32):high-glucose and high-fat combined with 100 mg/kg streptozocin(STZ) treatment (five mice died during modeling and three failed). Twenty-four diabetic mice were modeled successfully and divided into three groups (T2DM group, T2DM+L-DHM group and T2DM+H-DHM group). Three groups mice were fed with high-glucose and high-fat diet, and treated with equal volume of normal saline, 125 mg/(kg·d) DHM or 250 mg/(kg·d) DHM for 16 weeks respectively. The control mice were fed with normal diet and treated with equal volume of saline (once a day, gavage) for 16 weeks. After 16 weeks, the body weight and fasting blood glucose were measured, intraperitoneal glucose tolerance test and related behavioral experiment were performed. Finally, the expression of BDNF protein in hippocampus of mice was detected by Western blot. RESULTS: The model of type 2 diabetes mellitus was established successfully with high-glucose and high-fat combined with 100 mg/kg STZ. After 16 weeks, the body weight of T2DM group was significantly decreased, the fasting blood glucose was significantly increased and the glucose tolerance was significantly abnormal compared with the normal control group. Compared with T2DM group, the body weight of T2DM+DHM groups mice was increased, while the levels of fasting blood glucose were decreased. And H-DHM could significantly improve the abnormal glucose tolerance of T2DM mice. Behavior test results showed that the ability of learning and memory of T2DM mice was significant decreased compared with control group, but these phenomena were improved in T2DM+DHM groups mice, and T2DM+H-DHM group was more obvious. Western blot analysis showed that the expression of BDNF protein in hippocampus of T2DM group was significantly lower than that of control group, while T2DM+DHM group was significant increased compared with T2DM mice. CONCLUSIONS: Dihydromyricetin can improve the cognitive dysfunction in type 2 diabetic mice. The mechanism may be through hypoglycemic effect and activation of BDNF protein expression in hippocampus.

[Ameliorative effects and the mechanism of lyceum barbarum polysaccharide on insulin resistance of HepG2 cell].

OBJECTIVE: To observe the effects of lyceum barbarum polysaccharide (LBP) on insulin resistance of HepG2 cells and investigate its possible mechanism. METHODS: IR-HepG2 cell model was induced with high glucose and high insulin in combination for 24 hours,with 104/vaccination in the 96-well plates, hole density after adherent cells (30 µg/ml、100 µg/ml、300 µg/ml) LBP cultivate 48 h, 200 µl/hole, each all had four holes. The effects of LBP at different concentrations on HepG2 cell activity and insulin resistance were tested. Intracellular malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were detected. The expressions of related proteins in insulin signal transduction pathways such as insulin receptor substrate-2(IRS-2), phosphatidylinositol-3-kinase(PI3-K), protein kinase B(Akt) and glucose transport-2(GLUT2) were determined. RESULTS: Compared with normal control group, the content of MDA was increased significantly and the activity of SOD and the expression levels of IRS-2,PI-3K,Akt and GLUT2 were decreased significantly in the IR model group. Compared with IR model group, medium and high concentrations of LBP decreased the content of MDA and increased the activity of SOD and the expression levels of IRS-2, PI-3K, Akt and GLUT2 in insulin-resistant HepG2 cells. MTT showed that at the same time, the OD value gradually decreased with the increase of LBP's concentration; under the same concentration of LBP, the OD value also gradually decreased with the extension of time, which indicated that LBP inhibited the proliferation of HepG2 cells with time and concentration-dependent manner. Glucose consumption experiment indicated that medium and high concentration of LBP could increase the glucose consumption of insulin-resistant HepG2 cells significantly, but low concentration of LBP had no significant impacted on glucose consumption of insulin-resistant HepG2 cells. CONCLUSIONS: Medium and high concentration of LBP can improve insulin resistance of HepG2 cell, its mechanisns may be associated with decreasing the level of oxidative stress and increasing the protein expressions of insulin signaling pathway.