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Short-term effects of EGCG (10–500 μM) were examined using isolated perfused rat livers and mitochondrial, microsomal, and cytosolic assays. EGCG strongly suppressed gluconeogenesis from lactate, glycerol, and alanine, while enhancing glycolysis, glycogenolysis, and fatty acid oxidation, with redox shifts and altered permeability. Mechanistically, it induced mild mitochondrial uncoupling, inhibited pyruvate carboxylase and glucose-6-phosphatase, and modulated key enzymes. UDP ATP remained unchanged, and membrane-disruptive properties raised hepatotoxicity concerns in compromised livers.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":40,"@type":76,"position":81},"https://docshare.wps.com/document/research-report/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/short-term-actions-of-epigalocatechin-3-gallate-in-the-liver-a-mechanistic-insight-into-hypoglycemic-and-potential-toxic-effects/439805/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/short-term-actions-of-epigalocatechin-3-gallate-in-the-liver-a-mechanistic-insight-into-hypoglycemic-and-potential-toxic-effects/439805.png","ImageObject",300,407,{"name":92,"@type":93},"Stanley","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-02","2026-09-29",true,{"@type":102,"interactionType":103,"userInteractionCount":14},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"How does EGCG affect gluconeogenesis in isolated rat livers?","Question",{"text":112,"@type":113},"EGCG markedly inhibits gluconeogenesis from lactate, glycerol, and alanine, reducing glucose production up to the reported levels.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"What metabolic shifts accompany EGCG treatment besides gluconeogenesis inhibition?",{"text":117,"@type":113},"EGCG stimulates glycolysis and glycogenolysis and increases oleic acid oxidation, accompanied by changes in oxygen uptake depending on the metabolic condition.",{"name":119,"@type":110,"acceptedAnswer":120},"Which mechanistic actions are linked to EGCG’s hepatic effects?",{"text":121,"@type":113},"EGCG causes mild mitochondrial uncoupling, inhibits pyruvate carboxylase and glucose-6-phosphatase, shifts NADH/NAD+ ratios toward oxidation, and alters redox-sensitive fluxes, while hepatic ATP content remains unchanged.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},439805,1790927989,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":39,"category_name":40,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":14,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":139,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":145},2336477405376,"https://ap-avatar.wpscdn.com/davatar_29158cc5080c5b710cf443261637dec0","RESEARCH ARTICLE  \nShort-term actions of epigalocatechin-3-gallate in the liver: a mechanistic insight into hypoglycemic and potential toxic effects  \nCarla Indianara Bonetti 1, Bruna Lopes Correia 1, Francielle Cristina Nakamura Manicardi2, Nairana Mithieli de Queiroz Eskuarek Melo2, Vanesa de Oliveira Pateis2,  \nJurandir Fernando Comar3, Anacharis Babeto de S´a-Nakanishi3, Adelar Bracht2 and L ´ıvia Bracht3   \n1 Post-Graduate Program in Pharmaceutical Sciences, State University of Maring´a, Maring´a, Brazil  \n2 Post-Graduate Program in Biochemistry, State University of Maring´a, Maring´a, Brazil  \n3 Department of Biochemistry, State University of Maring´a, Maring´a, Brazil  \nKeywords  \ngluconeogenesis; glycogenolysis; glycolysis; hepatotoxiciy; redox state; β-oxidation  \nCorrespondence  \nL. Bracht, Department of Biochemistry, State University of Maring´a, Avenida Colombo 5790, Jardim Universit´ario, Maring´a, Brazil  \nTel: +55 44 30114711  \nE-mail: lbracht@uem. br  \n(Received 23 May 2025, revised 19 August 2025, accepted 28 August 2025)  \ndoi:10.1002/2211-5463.70118  \nEdited by Sandro Sonnino  \nEpigallocatechin-3-gallate (EGCG), the main catechin in green tea, is associated with antidiabetic and anti-obesity effects, although its acute hepatic actions remain unclear. We investigated short-term effects of EGCG (10–500 μM) using isolated perfused rat livers and complementary assays in mitochondrial, microsomal, and cytosolic fractions. EGCG markedly inhibited gluconeogenesis from lactate (up to 52%), glycerol (33%), and alanine (47%), while it stimulated glycolysis, glycogenolysis, and oleic acid oxidation (+42% total ketone bodies) . Oxygen uptake was stimulated under glycogenolytic and fatty acid oxidizing conditions but inhibited under gluconeogenic conditions. Mechanistic analyses revealed EGCGinduced mild mitochondrial uncoupling, inhibition of pyruvate carboxylaseand glucose-6-phosphatase (with no effect on fructose-1,6-bisphosphatase) and stimulation of phosphoenolpyruvate carboxykinase. EGCG shifted cytosolic and mitochondrial NADH/NAD+ ratios toward oxidation, increased mitochondrial and plasma membrane permeability (LDH leakage from 10 μM), and altered redox-sensitive fluxes, while the total hepatic ATP content remained unchanged. In summary, EGCG’s multifaceted actions suggest that suppression of gluconeogenesis may contribute to its antihyperglycemic effect and the stimulation of fatty acid oxidation to its anti-obesity action. Finally, EGCG’s membrane-disruptive properties raise concerns about potential hepatotoxicity in compromised livers.  \nAbbreviations  \nADP, adenosine diphosphate; AMP, adenosine monophosphate; AMPK, AMP-activated protein kinase; ATP, adenosine triphosphate; DCF, 20-70-dichlorofluorescein; DCFA-DA, 20-70-dichlorofluorescein diacetate; DCFH, reduced form of 20-70-dichlorofluorescein; DMSO, dimethylsulfoxide; EDTA, ethylenediamine tetraacetic acid; EGCG, epigallocatechin-3-gallate; EGTA, ethyleneglycol tetraacetic acid; FBPase- 1, fructose 1,6-bisphosphatase; G6Pase, glucose 6-phosphatase; GAPDH, glyceraldehyde 3-phosphate dehydrogenase reaction; GDP, guanosine diphosphate; GLUT4, glucose transporter 4; GP, glycogen phosphorylase; GTP, guanosine triphosphate; HEPES, 4-(2-hydroxyethyl)piperazine-1-ethanesulfonic acid; HPLC, high performance liquid chromatography; IRS-1, insulin receptor substrate 1; LDH, lactate dehydrogenase; NAD , oxidized nicotinamide adenine dinucleotide; NADH, reduced nicotinamide adenine dinucleotide; PC, pyruvate carboxylase; PEPCK, phosphoenolpyruvate carboxykinase; PGK, 3-phosphoglycerate kinase; PGM, phosphoglycero mutase; Pi, inorganic phosphate; RC, respiratory control ratio; ROS, reactive oxygen species; TIM, triose phosphate isomerase; TMPD, tetramethylphenylenediamine.  \nFEBS Open Bio 16 (2026) 199–221 ª 2025 The Author(s) . FEBS Open Bio published by John Wiley & Sons Ltd on behalf of 199  \nFederation of European Biochemical Societies.  \nThis is an open access article","cbCaiqy0ItdCnAMJ","https://ap.wps.com/l/cbCaiqy0ItdCnAMJ","pdf",5414908,23,"English","# Background\n## EGCG and reported bioactivities\n# Experimental Approach\n## Isolated perfused rat livers and fraction assays\n# Results\n## Effects on gluconeogenesis and glycolysis\n## Oxygen uptake and fatty acid oxidation\n## Mechanistic enzyme and redox changes\n# Conclusion and Implications\n## Antihyperglycemic, anti-obesity potential, and hepatotoxicity risk","[{\"question\":\"How does EGCG affect gluconeogenesis in isolated rat livers?\",\"answer\":\"EGCG markedly inhibits gluconeogenesis from lactate, glycerol, and alanine, reducing glucose production up to the reported levels.\"},{\"question\":\"What metabolic shifts accompany EGCG treatment besides gluconeogenesis inhibition?\",\"answer\":\"EGCG stimulates glycolysis and glycogenolysis and increases oleic acid oxidation, accompanied by changes in oxygen uptake depending on the metabolic condition.\"},{\"question\":\"Which mechanistic actions are linked to EGCG’s hepatic effects?\",\"answer\":\"EGCG causes mild mitochondrial uncoupling, inhibits pyruvate carboxylase and glucose-6-phosphatase, shifts NADH/NAD+ ratios toward oxidation, and alters redox-sensitive fluxes, while hepatic ATP content remains unchanged.\"}]","Short-term actions of epigalocatechin-3-gallate in the liver - a mechanistic insight into hypoglycemic and potential toxic effects | PDF",1790690258,58]