Hui Ping Yaw, S. Ton, K. A. Kadir, Tee Yee Tan, Y. W. Teo, Michael Yohanes
{"title":"Effects of Glycyrrhetic Acid (GE) on Some Gluconeogenic Enzymes, Lipoprotein Lipase and Peroxisome Proliferator-Activated Receptors Alpha and Gamma","authors":"Hui Ping Yaw, S. Ton, K. A. Kadir, Tee Yee Tan, Y. W. Teo, Michael Yohanes","doi":"10.2174/1874847301004010014","DOIUrl":null,"url":null,"abstract":"The aim of this study was to examine the role of glycyrrhetic acid (GE) as a potential compound in the amelio- ration of metabolic syndrome. Rats given intraperitoneal injection of GE were sacrificed after 24 hours. Blood was col- lected for the determination of glucose, insulin and lipid profiles; while tissues were used for 11� -HSD1, gluconeogenic enzymes activities, PPAR-� /-� and LPL expression by RT-PCR. Intraperitoneal injection of 50mg/kg GE to normal rats significantly lowered blood glucose while insulin level and HOMA-IR showed no significant changes. H6PDH activities increased in the liver, kidney, subcutaneous and visceral adipose tissues and quadriceps femoris but decreased in the ab- dominal muscle. PEPCK activities were significantly reduced in the kidney and decreased in the liver but showed an in- crease in the subcutaneous and visceral adipose tissues. G6Pase activities were found to be reduced in both the liver and kidney. 11� -HSD1 activities increased in the liver but decreased in all other tissues. There were improvements in lipid profiles in GE-treated rats. Up-regulation of LPL activity was seen in all tissues except quadriceps femoris. PPAR-� ex- pression was up-regulated in the liver, heart and abdominal muscle while down-regulated in the kidney and quadriceps femoris but were undetectable in the subcutaneous and visceral adipose tissues. PPAR-� expression was up-regulated in all tissues except the kidney. GE prevented hyperglycaemia and improved lipid profiles possibly through 11� -HSD1 inhi- bition instead of via PPAR agonism.","PeriodicalId":403551,"journal":{"name":"The Open Bioactive Compounds Journal","volume":"22 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2013-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"11","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Open Bioactive Compounds Journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/1874847301004010014","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 11
Abstract
The aim of this study was to examine the role of glycyrrhetic acid (GE) as a potential compound in the amelio- ration of metabolic syndrome. Rats given intraperitoneal injection of GE were sacrificed after 24 hours. Blood was col- lected for the determination of glucose, insulin and lipid profiles; while tissues were used for 11� -HSD1, gluconeogenic enzymes activities, PPAR-� /-� and LPL expression by RT-PCR. Intraperitoneal injection of 50mg/kg GE to normal rats significantly lowered blood glucose while insulin level and HOMA-IR showed no significant changes. H6PDH activities increased in the liver, kidney, subcutaneous and visceral adipose tissues and quadriceps femoris but decreased in the ab- dominal muscle. PEPCK activities were significantly reduced in the kidney and decreased in the liver but showed an in- crease in the subcutaneous and visceral adipose tissues. G6Pase activities were found to be reduced in both the liver and kidney. 11� -HSD1 activities increased in the liver but decreased in all other tissues. There were improvements in lipid profiles in GE-treated rats. Up-regulation of LPL activity was seen in all tissues except quadriceps femoris. PPAR-� ex- pression was up-regulated in the liver, heart and abdominal muscle while down-regulated in the kidney and quadriceps femoris but were undetectable in the subcutaneous and visceral adipose tissues. PPAR-� expression was up-regulated in all tissues except the kidney. GE prevented hyperglycaemia and improved lipid profiles possibly through 11� -HSD1 inhi- bition instead of via PPAR agonism.