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Objective:To investigate the effect of metformin on autophagy in muscle cells exposed to palmitic acid, and to explore its mechanism.Methods:L6 rat myoblasts were incubated with palmitic acid at various concentrations(0.1, 0.2, 0.4, 0.6 mmol/L) and metformin(0.5, 1, 2, 5, 10 mmol/L) for 24 h. CCK8 method was used to detect the survival rate of muscle cells. After muscle cells were treated with palmitic acid and metformin for 24 h, mRNA and protein expressions of microtubule-associated protein11ight chain3(LC3Ⅱ), Beclin 1, p62, and silent mating type information regulation2 homolog-3(SIRT3) were detected by RT-PCR and Western blot, respectively. AMP-activated protein kinase(AMPK) phosphorylation level was detected by Western blot.Results:Palmitic acid dose-dependently decreased the survival rate of muscle cells, which was attenuated by metformin at the concentration of 2 mmol/L. After muscle cells were incubated with 0.4 mmol/L palmitic acid and 2 mmol/L metformin for 24 h, palmitic acid significantly reduced the mRNA and protein expressions of LC3Ⅱ, Beclin1, and SIRT3 as well as phosphorylation level of AMPK(all P<0.05), and increased p62 mRNA and protein expressions( P<0.05). Those effects were all antagonized by metformin(all P<0.05). Conclusions:Metformin treatment may promote the autophagy of muscle cells exposed to palmitic acid through AMPK/STRT3 pathway.
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Objective@#To investigate the effect of metformin on autophagy in muscle cells exposed to palmitic acid, and to explore its mechanism.@*Methods@#L6 rat myoblasts were incubated with palmitic acid at various concentrations(0.1, 0.2, 0.4, 0.6 mmol/L) and metformin(0.5, 1, 2, 5, 10 mmol/L) for 24 h. CCK8 method was used to detect the survival rate of muscle cells. After muscle cells were treated with palmitic acid and metformin for 24 h, mRNA and protein expressions of microtubule-associated protein11ight chain3(LC3Ⅱ), Beclin 1, p62, and silent mating type information regulation2 homolog-3(SIRT3) were detected by RT-PCR and Western blot, respectively. AMP-activated protein kinase(AMPK) phosphorylation level was detected by Western blot.@*Results@#Palmitic acid dose-dependently decreased the survival rate of muscle cells, which was attenuated by metformin at the concentration of 2 mmol/L. After muscle cells were incubated with 0.4 mmol/L palmitic acid and 2 mmol/L metformin for 24 h, palmitic acid significantly reduced the mRNA and protein expressions of LC3Ⅱ, Beclin1, and SIRT3 as well as phosphorylation level of AMPK(all P<0.05), and increased p62 mRNA and protein expressions(P<0.05). Those effects were all antagonized by metformin(all P<0.05).@*Conclusions@#Metformin treatment may promote the autophagy of muscle cells exposed to palmitic acid through AMPK/STRT3 pathway.
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Objective:To observe the hypoglycemic and weight loss effects of liraglutide in type 2 diabetes mellitus (T2DM) com-plicated with obesity, and explore new treatment strategies for T2DM complicated with obesity. Methods: Totally 38 T2DM patients complicated with obesity with dissatisfactory blood sugar control treated with oral hypoglycemic drugs or insulin were enrolled and divid-ed into group A ( overweight group, 28 kg·m-2 >BMI≥24 kg·m-2 , 18 cases) and group B ( obesity group, BMI≥28 kg·m-2 , 20 cases) according to the body mass index ( BMI) . Liraglutide was used in all the participants for 12 weeks. The height, weight, BMI,HbA1c, fasting blood glucose(FBG),2-hour postprandial blood glucose(2hPG), fasting insulin(FINS),2-hour postprandial in-sulin (2hPINS),fast-c peptide(FCP), 2-hour postprandial c-peptide(2hCP) and insulin resistance index (HOMA-IR), pancreaticβcell function index( HOMA-β) of the two groups were detected before and after the liraglutide treatment. Results:After the treatment with liraglutide, HbA1c, FPG, 2hPG, FCP,2hCP,HOMA-β,HOMA-IR were significantly decreased (P<0. 01) than before in the two groups, while there were no significant differences between the groups(P>0. 05). However, the body weight in group B was sig-nificantly lower than before (P<0. 01), while there were no significant change in group A(P>0. 05). Conclusion: Liraglutide can effectively control blood glucose level, ameliorate insulin resistance and obviously decrease the body weight in the T2DM patients com-plicated with obesity.
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Aim To investigate the effect of oxymatrine on lipid metabolism regulated genes in liver in fat-in-duced insulin resistance in ApoE -/- mice.Methods Seventeen C57BL/6J male mice were selected in normal control group.Sixty-eight ApoE -/- mice with high fat diet for 1 6 weeks,were randomly divided into model group,oxymatrine low,middle and high dose groups.Then they were gavaged for 8 weeks.Body weight and general biochemical indicators were deter-mined in mice.The mRNA and protein expression lev-els of LPL,FAT/CD36,CPT1 ,UCP2,SREBP-1 c,FAS and ACC were examined by real-time PCR and West-ern blot in the liver.Results Compared with model group,oxymatrine reduced body weight(BW),fasting blood glucose (FBG),cholesterol (TC ),triglyceride (TG),free fatty acids(FFA),fasting plasma insulin (FINS)and insulin resistance index(HOMA-IR)(P <0.05),while improved glucose infusion rate (GIR). Oxymatrine down-regulated the mRNA and protein ex-pression of LPL,FAT/CD36,UCP2,SREBP-1 c,FAS and ACC(P <0.05),and up-regulated the mRNA and protein expression of CPT1 in varying degrees (P <0.05).Conclusion Oxymatrine can regulate the ex-pression of lipid metabolism regulated genes in liver and improve insulin resistance in ApoE -/- mice in-duced by high fat diet.