<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Fu Y</submitter><funding>Natural Science Foundation of Beijing Municipality</funding><funding>Beijing Outstanding Young Scientist Program</funding><funding>National Natural Science Foundation of China</funding><funding>Fund for Beijing Science &amp;amp; Technology Development of TCM</funding><funding>CAMS Initiative for Innovative Medicine</funding><pagination>15938</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9786790</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>23(24)</volume><pubmed_abstract>Voglibose is an α-glycosidase inhibitor that improves postprandial hyperglycemia and increases glucagon-like peptide-1 (GLP-1) secretion in patients with type 2 diabetes. Recently, there has been increasing interest in the anti-inflammatory effects of voglibose on the intestine, but the underlying mechanism is not clear. This study evaluated the effects and mechanisms of voglibose on glycemic control and intestinal inflammation. Type 2 diabetic KKAy mice were treated with voglibose (1 mg/kg) by oral gavage once daily. After 8 weeks, glucose metabolism, levels of short-chain fatty acids (SCFAs), systematic inflammatory factors, intestinal integrity and inflammation were evaluated using hematoxylin and eosin staining, immunohistochemistry, immunofluorescence and Western blot analysis. Voglib</pubmed_abstract><journal>International journal of molecular sciences</journal><pubmed_title>Voglibose Regulates the Secretion of GLP-1 Accompanied by Amelioration of Ileal Inflammatory Damage and Endoplasmic Reticulum Stress in Diabetic KKAy Mice.</pubmed_title><pmcid>PMC9786790</pmcid><funding_grant_id>JJ-2020-25</funding_grant_id><funding_grant_id>2022-I2M-2-002</funding_grant_id><funding_grant_id>BJJWZYJH01201910023028</funding_grant_id><funding_grant_id>7202137</funding_grant_id><funding_grant_id>2021-I2M-1-026</funding_grant_id><funding_grant_id>81900480</funding_grant_id><funding_grant_id>2022-I2M-JB0011</funding_grant_id><funding_grant_id>81973379</funding_grant_id><pubmed_authors>Lei L</pubmed_authors><pubmed_authors>Li C</pubmed_authors><pubmed_authors>Cao H</pubmed_authors><pubmed_authors>Chen L</pubmed_authors><pubmed_authors>Huan Y</pubmed_authors><pubmed_authors>Fu Y</pubmed_authors><pubmed_authors>Liu Q</pubmed_authors><pubmed_authors>Li P</pubmed_authors><pubmed_authors>Zhang L</pubmed_authors><pubmed_authors>Liu S</pubmed_authors><pubmed_authors>Feng C</pubmed_authors><pubmed_authors>Shen Z</pubmed_authors><pubmed_authors>Ji W</pubmed_authors><pubmed_authors>Gao X</pubmed_authors><pubmed_authors>Zhai J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Voglibose Regulates the Secretion of GLP-1 Accompanied by Amelioration of Ileal Inflammatory Damage and Endoplasmic Reticulum Stress in Diabetic KKAy Mice.</name><description>Voglibose is an α-glycosidase inhibitor that improves postprandial hyperglycemia and increases glucagon-like peptide-1 (GLP-1) secretion in patients with type 2 diabetes. Recently, there has been increasing interest in the anti-inflammatory effects of voglibose on the intestine, but the underlying mechanism is not clear. This study evaluated the effects and mechanisms of voglibose on glycemic control and intestinal inflammation. Type 2 diabetic KKAy mice were treated with voglibose (1 mg/kg) by oral gavage once daily. After 8 weeks, glucose metabolism, levels of short-chain fatty acids (SCFAs), systematic inflammatory factors, intestinal integrity and inflammation were evaluated using hematoxylin and eosin staining, immunohistochemistry, immunofluorescence and Western blot analysis. Voglib</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2026-04-29T03:22:28.721Z</modification><creation>2025-04-07T02:58:21.79Z</creation></dates><accession>S-EPMC9786790</accession><cross_references><pubmed>36555580</pubmed><doi>10.3390/ijms232415938</doi></cross_references></HashMap>