{"title":"DIET-INDUCED ACCUMULATION OF AGES CONTRIBUTE TO METABOLIC DISEASES ONSET BY INTERFERING WITH SREBP-1C ACTIVITY","authors":"F. Rigoldi","doi":"10.18143/JISANH_V3I2_1437","DOIUrl":null,"url":null,"abstract":"Literature data have evidenced the diet-induced accumulation of Advanced Glycation End-Products (AGEs) associated to several dysmetabolic conditions, as obesity, insulin resistance, and type 2 diabetes. We have recently reported in different animal models of diet-induced metabolic disorders the causal link between AGEs and the dysregulated activation of the lipogenic transcription factor SREBP1c. We have thus analyzed in different target tissues of dysmetabolism the effect of the AGEs/SREBP1c axis overactivation on selective pathways involved in the antioxidant and inflammatory response, as well as in structural and metabolic adaptation. Our most recent findings have demonstrated that the inhibition of AGEs production by the administration of the anti- glycative compound pyridoxamine to mice fed a high-fat or high-fructose diet is able to prevent the AGEs/SREBP1c-depending impairments.","PeriodicalId":17323,"journal":{"name":"Journal of the International Society of Antioxidants in Nutrition & Health","volume":"27 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2016-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of the International Society of Antioxidants in Nutrition & Health","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.18143/JISANH_V3I2_1437","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Literature data have evidenced the diet-induced accumulation of Advanced Glycation End-Products (AGEs) associated to several dysmetabolic conditions, as obesity, insulin resistance, and type 2 diabetes. We have recently reported in different animal models of diet-induced metabolic disorders the causal link between AGEs and the dysregulated activation of the lipogenic transcription factor SREBP1c. We have thus analyzed in different target tissues of dysmetabolism the effect of the AGEs/SREBP1c axis overactivation on selective pathways involved in the antioxidant and inflammatory response, as well as in structural and metabolic adaptation. Our most recent findings have demonstrated that the inhibition of AGEs production by the administration of the anti- glycative compound pyridoxamine to mice fed a high-fat or high-fructose diet is able to prevent the AGEs/SREBP1c-depending impairments.