Objective To reveal the effects and related mechanisms of chlorogenic acid(CGA)on intestinal glucose homeostasis.Methods Forty male Sprague-Dawley rats were randomly and equally divided into four groups:normal chow(NC...Objective To reveal the effects and related mechanisms of chlorogenic acid(CGA)on intestinal glucose homeostasis.Methods Forty male Sprague-Dawley rats were randomly and equally divided into four groups:normal chow(NC),high-fat diet(HFD),HFD with low-dose CGA(20 mg/kg,HFD-LC),and HFD with high-dose CGA(90 mg/kg,HFD-HC).The oral glucose tolerance test was performed,and fast serum insulin(FSI)was detected using an enzyme-linked immunosorbent assay.The m RNA expression levels of glucose transporters(Sglt-1 and Glut-2)and proglucagon(Plg)in different intestinal segments(the duodenum,jejunum,ileum,and colon)were analyzed using quantitative real-time polymerase chain reaction.SGLT-1 protein and the morphology of epithelial cells in the duodenum and jejunum was localized by using immunofluorescence.Results At both doses,CGA ameliorated the HFD-induced body weight gain,maintained FSI,and increased postprandial 30-min glucagon-like peptide 1 secretion.High-dose CGA inhibited the HFD-induced elevation in Sglt-1 expression.Both CGA doses normalized the HFD-induced downregulation of Glut-2 and elevated the expression of Plg in all four intestinal segments.Conclusion An HFD can cause a glucose metabolism disorder in the rat intestine and affect body glucose homeostasis.CGA can modify intestinal glucose metabolism by regulating the expression of intestinal glucose transporters and Plg,thereby controlling the levels of blood glucose and insulin to maintain glucose homeostasis.展开更多
Nonalcoholic fatty liver disease (NAFLD) is the most prevalent cause of chronic liver disease worldwide. NAFLD is considerably more frequent in patients with type 2 diabetes mellitus (T2DM) than in the general populat...Nonalcoholic fatty liver disease (NAFLD) is the most prevalent cause of chronic liver disease worldwide. NAFLD is considerably more frequent in patients with type 2 diabetes mellitus (T2DM) than in the general population and is also more severe histologically in this group. Sodium-glucose co-transporter-2 (SGLT2) inhibitors, the newest class of antidiabetic agents, appear to represent a promising option for the management of NAFLD in patients with T2DM. In a number of studies, treatment with SGLT2 inhibitors resulted in a reduction in hepatic steatosis and in transaminase levels. However, existing studies are small, their follow-up period was short and none evaluated the effects of SGLT2 inhibitors on liver histology. Accordingly, larger studies are needed to verify these preliminary results and define the role of SGLT2 inhibitors in the treatment of NAFLD in patients with T2DM.展开更多
AIM:To investigate the effects of the somatostatin analogue,octreotide,on maltose and sucrase activities and expression of glucose transporter type 2(GLUT2) in obese rat intestinal mucosa.METHODS:We divided 49 Sprague...AIM:To investigate the effects of the somatostatin analogue,octreotide,on maltose and sucrase activities and expression of glucose transporter type 2(GLUT2) in obese rat intestinal mucosa.METHODS:We divided 49 Sprague-Dawley rats into a group of 31 high fat diet-induced obese rats and a group of 18 normal controls.The obese rats were separated into an octreotide treated group of 16 rats and an obese group of 15.The intervention group was injected with octreotide at 40μg/kg body weight every 12 h for 8 d.Rat body weight was measured weekly to calculate Lee's index.After euthanization,maltase and sucrase activities in the small intestine were measuredby activity assays,and the fasting plasma glucose level was measured.The expression of GLUT2 in small intestinal mucosa was analyzed by immunohistochem-istry,reverse transcriptase polymerase chain reaction and Western blotting assays.RESULTS:Body weight,Lee's index,fasting plasma glucose level,maltase activity in small intestinal mucosa,mucosa and apical GLUT2,GLUT2 mRNA and protein expression levels were all significantly higher in the obese group than in the normal control group(605.61±141.00 vs 378.54±111.75,337.61 ±10.82 vs 318.73±20.10,8.60±1.38 vs 7.33± 0.70,156.01±58.81 vs 50.43±30.49,390 744.2 ±62 469.21 vs 170 546.50±50 646.14,26 740.18 ±3809.60 vs 354.98±57.19,0.26±0.11 vs 0.07 ±0.02,and 2.08±0.59 vs 1.27±0.38,respectively,all P<0.01).Sucrase activity did not differ between the two groups.Octreotide intervention significantly decreased the body weight and fasting plasma glucose level of obese rats(508.27±94.39 vs 605.61±141.00,7.58±1.51 vs 8.60±1.38,respectively,all P<0.05).The intestinal mucosa and apical GLUT2,expression of GLUT2 mRNA and protein were also significantly lower in the octreotide intervention group than in the obese group(269 975.2 ±53 730.94 vs 390 744.2±62 469.21,3758.06± 364.51 vs 26 740.18±3809.60,0.08±0.02 vs 0.26± 0.11,and 1.31±0.27 vs 2.08±0.59,respectively,all P<0.01).CONCLUSION:High fat dietinduced obesity is associated with elevated intestinal maltase activity,GLUT2 expression,and permanent apical GLUT2 in the small intestinal mucosa of rats.Octreotide can inhibit these effects.展开更多
基金supported by the National Natural Science foundation of China(No.31071531)the Scientific Research Fund of the Hunan Provincial Education Department(No.14A071)the China National Tobacco Corp Hunan Branch(15-17Aa04)
文摘Objective To reveal the effects and related mechanisms of chlorogenic acid(CGA)on intestinal glucose homeostasis.Methods Forty male Sprague-Dawley rats were randomly and equally divided into four groups:normal chow(NC),high-fat diet(HFD),HFD with low-dose CGA(20 mg/kg,HFD-LC),and HFD with high-dose CGA(90 mg/kg,HFD-HC).The oral glucose tolerance test was performed,and fast serum insulin(FSI)was detected using an enzyme-linked immunosorbent assay.The m RNA expression levels of glucose transporters(Sglt-1 and Glut-2)and proglucagon(Plg)in different intestinal segments(the duodenum,jejunum,ileum,and colon)were analyzed using quantitative real-time polymerase chain reaction.SGLT-1 protein and the morphology of epithelial cells in the duodenum and jejunum was localized by using immunofluorescence.Results At both doses,CGA ameliorated the HFD-induced body weight gain,maintained FSI,and increased postprandial 30-min glucagon-like peptide 1 secretion.High-dose CGA inhibited the HFD-induced elevation in Sglt-1 expression.Both CGA doses normalized the HFD-induced downregulation of Glut-2 and elevated the expression of Plg in all four intestinal segments.Conclusion An HFD can cause a glucose metabolism disorder in the rat intestine and affect body glucose homeostasis.CGA can modify intestinal glucose metabolism by regulating the expression of intestinal glucose transporters and Plg,thereby controlling the levels of blood glucose and insulin to maintain glucose homeostasis.
文摘Nonalcoholic fatty liver disease (NAFLD) is the most prevalent cause of chronic liver disease worldwide. NAFLD is considerably more frequent in patients with type 2 diabetes mellitus (T2DM) than in the general population and is also more severe histologically in this group. Sodium-glucose co-transporter-2 (SGLT2) inhibitors, the newest class of antidiabetic agents, appear to represent a promising option for the management of NAFLD in patients with T2DM. In a number of studies, treatment with SGLT2 inhibitors resulted in a reduction in hepatic steatosis and in transaminase levels. However, existing studies are small, their follow-up period was short and none evaluated the effects of SGLT2 inhibitors on liver histology. Accordingly, larger studies are needed to verify these preliminary results and define the role of SGLT2 inhibitors in the treatment of NAFLD in patients with T2DM.
基金Supported by Grants from the National Natural Sciences Foundation of China,No.30870919Sichuan Provincial Department of Science and Technology,No.2010SZ0176
文摘AIM:To investigate the effects of the somatostatin analogue,octreotide,on maltose and sucrase activities and expression of glucose transporter type 2(GLUT2) in obese rat intestinal mucosa.METHODS:We divided 49 Sprague-Dawley rats into a group of 31 high fat diet-induced obese rats and a group of 18 normal controls.The obese rats were separated into an octreotide treated group of 16 rats and an obese group of 15.The intervention group was injected with octreotide at 40μg/kg body weight every 12 h for 8 d.Rat body weight was measured weekly to calculate Lee's index.After euthanization,maltase and sucrase activities in the small intestine were measuredby activity assays,and the fasting plasma glucose level was measured.The expression of GLUT2 in small intestinal mucosa was analyzed by immunohistochem-istry,reverse transcriptase polymerase chain reaction and Western blotting assays.RESULTS:Body weight,Lee's index,fasting plasma glucose level,maltase activity in small intestinal mucosa,mucosa and apical GLUT2,GLUT2 mRNA and protein expression levels were all significantly higher in the obese group than in the normal control group(605.61±141.00 vs 378.54±111.75,337.61 ±10.82 vs 318.73±20.10,8.60±1.38 vs 7.33± 0.70,156.01±58.81 vs 50.43±30.49,390 744.2 ±62 469.21 vs 170 546.50±50 646.14,26 740.18 ±3809.60 vs 354.98±57.19,0.26±0.11 vs 0.07 ±0.02,and 2.08±0.59 vs 1.27±0.38,respectively,all P<0.01).Sucrase activity did not differ between the two groups.Octreotide intervention significantly decreased the body weight and fasting plasma glucose level of obese rats(508.27±94.39 vs 605.61±141.00,7.58±1.51 vs 8.60±1.38,respectively,all P<0.05).The intestinal mucosa and apical GLUT2,expression of GLUT2 mRNA and protein were also significantly lower in the octreotide intervention group than in the obese group(269 975.2 ±53 730.94 vs 390 744.2±62 469.21,3758.06± 364.51 vs 26 740.18±3809.60,0.08±0.02 vs 0.26± 0.11,and 1.31±0.27 vs 2.08±0.59,respectively,all P<0.01).CONCLUSION:High fat dietinduced obesity is associated with elevated intestinal maltase activity,GLUT2 expression,and permanent apical GLUT2 in the small intestinal mucosa of rats.Octreotide can inhibit these effects.
