[Objectives]To explore the mechanism of Gegen Qinlian Decoction in treating type 2 diabetes mellitus(T2DM)complicated with non-alcoholic fatty liver disease(NAFLD)by analyzing the effective components of Gegen Qinlian...[Objectives]To explore the mechanism of Gegen Qinlian Decoction in treating type 2 diabetes mellitus(T2DM)complicated with non-alcoholic fatty liver disease(NAFLD)by analyzing the effective components of Gegen Qinlian Decoction.[Methods]TCMSP database was used to analyze the active components of Gegen Qinlian Decoction,and pubchem and Swiss ADME databases were also used to predict drug targets,extract T2DM complicated with NAFLD targets from OMIM and Genecards databases.Venny plot was drawn to obtain intersection targets,and finally Cytoscape was used to make core target maps and drug-target-disease network maps.Using DAVID and Metascape database to analyze the intersection targets,the gene ontology information of Go and KEGG was obtained.Microbial informatics technology was used to visualize GO,and Cytoscape was used to make drug-target-disease network map-enrichment pathway map.[Results]The network pharmacological analysis showed that Gegen Qinlian Decoction acted on the key targets of type 2 diabetes mellitus complicated with non-alcoholic fatty liver disease,such as ALB and ALT1,through many components,and achieved the purpose of treating this disease.The chemical constituents of the drug include formononetin,5-hydroxyisomucronulatol-2,5-2-O-glucoside,cholesteryl laurate,isoliquiritigenin,etc.[Conclusions]This study provides a new idea and theoretical support for future drug research and clinical practice.展开更多
Objective To explore the relationship between serum osteocalcin levels and glucolipid metabolism in elderly type 2 diabetic patients with non-alcoholic fatty liver disease(NAFLD).Methods Data collected from 97 pa-tien...Objective To explore the relationship between serum osteocalcin levels and glucolipid metabolism in elderly type 2 diabetic patients with non-alcoholic fatty liver disease(NAFLD).Methods Data collected from 97 pa-tients with type 2 diabetes mellitus(T2DM)admitted to the Department of Geriatric Endocrinology of the First Affiliated hospital of Zhengzhou University from June展开更多
OBJECTIVE:To observe the effect of Jiangtang Xiaoke(JTXK) granule on endoplasmic reticulum(ER)stress in high fat diet(HFD)-induced type 2 diabetes mellitus(T2 DM) KK-Ay mice.METHODS:KK-Ay mice were fed with HFD to ind...OBJECTIVE:To observe the effect of Jiangtang Xiaoke(JTXK) granule on endoplasmic reticulum(ER)stress in high fat diet(HFD)-induced type 2 diabetes mellitus(T2 DM) KK-Ay mice.METHODS:KK-Ay mice were fed with HFD to induce the T2 DM model,while normal control C57 BL/6 J mice were given standard feed.Fasting blood glucose(FBG) in all mice was measured weekly and oral glucose tolerance tests(OGTTs) were performed at 4 and 10 weeks after start of treatment to determine glucose metabolism.Serum fasting insulin(FINS) and insulin sensitivity index(ISI) were measured to determine insulin sensitivity.m RNA expressions of eukaryotic initiation factor-2 alpha(e IF2α),glucose regulated protein 78(GRP78),activating transcription factor 4(ATF4),and C/EBP homology protein(CHOP) were assessed by reverse transcription polymerase chain reaction and the protein expressions of p-e IF2α,GRP78,and CHOP were assessed by Western blotting.RESULTS:JTXK granule significantly reduced FBG and free fatty acid levels and improved OGTT at the120 min of the 10-week treatment in T2 DM KK-Ay mice.FINS and Hb Alc levels were reduced and insulin sensitivities were increased in KK-Ay diabetic mice,which were improved with the treatment of JTXK granule,especially at the 7 and 3.5 g/kg doses.JTXK granule at the 3.5 g/kg dose was most effective in reducing both gene and protein expressions of e IF2α,GRP78,and CHOP.CONCLUSION:ER stress response is increased in T2 DM KK-Ay mice.Treatment with JTXK granule attenuates glucose disorders,improves insulin sensitivity,and reduces serum FFA in T2 DM KK-Ay mice.The mechanisms may be attributed to regulation of the signaling ER stress pathway via decreasing e IF2α phosphorylation and suppressing e IF2α-ATF4-CHOP activation.展开更多
基金Guangxi Key R&D Program Project(GuiKe AB18221095)National and Autonomous Region-Level College Student Innovation and Entrepreneurship Training Funding Project(202210599009)High-level Talent Research Project of Youjiang Medical University for Nationalities(01002018079).
文摘[Objectives]To explore the mechanism of Gegen Qinlian Decoction in treating type 2 diabetes mellitus(T2DM)complicated with non-alcoholic fatty liver disease(NAFLD)by analyzing the effective components of Gegen Qinlian Decoction.[Methods]TCMSP database was used to analyze the active components of Gegen Qinlian Decoction,and pubchem and Swiss ADME databases were also used to predict drug targets,extract T2DM complicated with NAFLD targets from OMIM and Genecards databases.Venny plot was drawn to obtain intersection targets,and finally Cytoscape was used to make core target maps and drug-target-disease network maps.Using DAVID and Metascape database to analyze the intersection targets,the gene ontology information of Go and KEGG was obtained.Microbial informatics technology was used to visualize GO,and Cytoscape was used to make drug-target-disease network map-enrichment pathway map.[Results]The network pharmacological analysis showed that Gegen Qinlian Decoction acted on the key targets of type 2 diabetes mellitus complicated with non-alcoholic fatty liver disease,such as ALB and ALT1,through many components,and achieved the purpose of treating this disease.The chemical constituents of the drug include formononetin,5-hydroxyisomucronulatol-2,5-2-O-glucoside,cholesteryl laurate,isoliquiritigenin,etc.[Conclusions]This study provides a new idea and theoretical support for future drug research and clinical practice.
文摘Objective To explore the relationship between serum osteocalcin levels and glucolipid metabolism in elderly type 2 diabetic patients with non-alcoholic fatty liver disease(NAFLD).Methods Data collected from 97 pa-tients with type 2 diabetes mellitus(T2DM)admitted to the Department of Geriatric Endocrinology of the First Affiliated hospital of Zhengzhou University from June
基金the National Natural Science Foundation of China(No.NSFC81703971,NSFC81274041)Co-construction Project of Beijing Education Commission(No.0101216-2013,0101216-2014)+1 种基金the Key Drug Development Program(No.2012ZX09103201-005)the 111 project of MOE(No.B07007)
文摘OBJECTIVE:To observe the effect of Jiangtang Xiaoke(JTXK) granule on endoplasmic reticulum(ER)stress in high fat diet(HFD)-induced type 2 diabetes mellitus(T2 DM) KK-Ay mice.METHODS:KK-Ay mice were fed with HFD to induce the T2 DM model,while normal control C57 BL/6 J mice were given standard feed.Fasting blood glucose(FBG) in all mice was measured weekly and oral glucose tolerance tests(OGTTs) were performed at 4 and 10 weeks after start of treatment to determine glucose metabolism.Serum fasting insulin(FINS) and insulin sensitivity index(ISI) were measured to determine insulin sensitivity.m RNA expressions of eukaryotic initiation factor-2 alpha(e IF2α),glucose regulated protein 78(GRP78),activating transcription factor 4(ATF4),and C/EBP homology protein(CHOP) were assessed by reverse transcription polymerase chain reaction and the protein expressions of p-e IF2α,GRP78,and CHOP were assessed by Western blotting.RESULTS:JTXK granule significantly reduced FBG and free fatty acid levels and improved OGTT at the120 min of the 10-week treatment in T2 DM KK-Ay mice.FINS and Hb Alc levels were reduced and insulin sensitivities were increased in KK-Ay diabetic mice,which were improved with the treatment of JTXK granule,especially at the 7 and 3.5 g/kg doses.JTXK granule at the 3.5 g/kg dose was most effective in reducing both gene and protein expressions of e IF2α,GRP78,and CHOP.CONCLUSION:ER stress response is increased in T2 DM KK-Ay mice.Treatment with JTXK granule attenuates glucose disorders,improves insulin sensitivity,and reduces serum FFA in T2 DM KK-Ay mice.The mechanisms may be attributed to regulation of the signaling ER stress pathway via decreasing e IF2α phosphorylation and suppressing e IF2α-ATF4-CHOP activation.