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| 1 | Incretin based therapies:A novel treatment approach for non-alcoholic fatty liver disease显示文摘Non-alcoholic fatty liver disease is considered a hepatic manifestation of metabolic syndrome(MS).The current treatment of non-alcoholic fatty liver disease(NAFLD)principally includes amelioration of MS components by lifestyle modifications but the lack of success in their implementation and sustainment arises the need for effective pharmacological agent in fatty liver treatment.Incretins are gut derived hormones secreted into the circulation in response to nutrient ingestion that enhances glucose-stimulated insulin secretion.Glucagon-like peptide-1(GLP-1)is the most important incretin.Its receptor agonist and inhibitors of dipeptidyl peptidase-4(DPP-4)are used in treatment of type2 diabetes mellitus.DPP-4 serum activity and hepatic expression are shown to be elevated in several hepatic diseases.There are several experimental and clinical trials exploring the efficacy of incretin based therapies in NAFLD treatment.They suggest that GLP-1 analogues might have beneficial effect on hepatic steatosis acting as insulin sensitizers and directly by stimulating GLP-1 receptors expressed on hepatocytes.The use of DPP-4 inhibitors also results in hepatic fat reduction but the mechanism of action remains unclear.There is growing evidence that incretin based therapies have beneficial effects on hepatocytes,however further study analysis are needed to assess the long term effect of incretin based therapies on NAFLD. | Kristina Blaslov Tomislav Bulum Karin Zibar Lea Duvnjak | 2014 | World Journal of Gastroenterology2014，20，23： | 10 |
| 2 | MK-0626,a selective DPP-4 inhibitor,attenuates hepatic steatosis in ob/ob mice显示文摘AIM:To investigate the mechanism and in vivo effects of MK-0626,a dipeptidyl peptidase-4 inhibitor,on hepatic steatosis using ob/ob mice.METHODS:We analyzed obese(ob/ob)8-wk-old male mice that had been randomly divided into two groups of ob/ob mice(n=16 each)and were treated with1.5 or 3 mg/kg MK-0626 and two control groups of untreated ob/ob mice and lean littermates(n=16 each).All mice were fed a normal chow diet with or without MK-0626 for either four or eight weeks.Blood samples were collected,and total hepatectomy was performed.RESULTS:The administration of dietary MK-0626 ameliorated the hepatic lipid accumulation in ob/ob micetreated with 3 mg/kg MK-0626(3 MK),P<0.05,vs untreated ob/ob mice(ob/ob).The MK-0626 treatment reduced the serum alanine aminotransferase levels(both treatment groups,P<0.05 vs ob/ob)and glucoses/insulin levels/calculated HOMA scores(1.5 MK,P<0.05vs ob/ob;3 MK,P<0.01 vs ob/ob)and increased the serum adiponectin levels(3 MK,P<0.05 vs ob/ob)in a dose-dependent manner.The MK-0626 treatment increased the m RNA expression of peroxisome proliferator-activated receptorα/microsomal triglyceride transfer protein(1.5 MK,P<0.05 vs ob/ob;3 MK,P<0.01vs ob/ob)but reduced the sterol regulatory element binding transcription factor-1c/fatty acid synthase/stearoyl-Co A desaturase-1(both treatment groups,P<0.01 vs ob/ob).The MK-0626 treatment increased the activity of AMP-activated protein kinase(AMPK)(both treatment groups,P<0.01 vs ob/ob).CONCLUSION:MK-0626 could attenuate hepatic steatosis through enhancing AMPK activity,inhibiting hepatic lipogenic gene expression,enhancing triglyceride secretion from liver and increasing serum adiponectin levels. | Tatsuya Ohyama Ken Sato Yuichi Yamazaki Hiroaki Hashizume Norio Horiguchi Satoru Kakizaki Masatomo Mori Motoyasu Kusano Masanobu Yamada | 2014 | World Journal of Gastroenterology2014，20，43： | 4 |
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