Peter Spégel , Andreas Lindqvist , Monica Sandberg , Nils Wierup
{"title":"葡萄糖依赖型胰岛素多肽降低高血糖大鼠支链氨基酸","authors":"Peter Spégel , Andreas Lindqvist , Monica Sandberg , Nils Wierup","doi":"10.1016/j.regpep.2013.12.009","DOIUrl":null,"url":null,"abstract":"<div><p><span><span>Hypersecretion of the incretin hormone<span> glucose-dependent insulinotropic polypeptide (GIP) has been associated with obesity and glucose intolerance. This condition has been suggested to be linked to GIP resistance. Besides its insulinotropic effect, GIP also directly affects </span></span>glucose uptake<span> and lipid metabolism. This notwithstanding, effects of GIP on other circulating metabolites than glucose have not been thoroughly investigated. Here, we examined effects of infusion of various concentrations of GIP in normo- and hyperglycemic rats on serum metabolite profiles. We found that, despite a decrease in serum glucose levels (−</span></span> <!-->26%, p<!--> <!--><<!--> <span>0.01), the serum metabolite profile was largely unaffected by GIP infusion in normoglycemic rats. Interestingly, levels of branched chain amino acids<span> and the ketone body β-hydroxybutyrate were decreased by 21% (p</span></span> <!--><<!--> <!-->0.05) and 27% (p<!--> <!--><<!--> <!-->0.001), respectively, in hyperglycemic rats infused with 60<!--> <!-->ng/ml GIP. Hence, our data suggest that GIP provokes a decrease in BCAA levels and ketone body production. Increased concentrations of these metabolites have been associated with obesity and T2D.</p></div>","PeriodicalId":20853,"journal":{"name":"Regulatory Peptides","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2014-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.regpep.2013.12.009","citationCount":"1","resultStr":"{\"title\":\"Glucose-dependent insulinotropic polypeptide lowers branched chain amino acids in hyperglycemic rats\",\"authors\":\"Peter Spégel , Andreas Lindqvist , Monica Sandberg , Nils Wierup\",\"doi\":\"10.1016/j.regpep.2013.12.009\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p><span><span>Hypersecretion of the incretin hormone<span> glucose-dependent insulinotropic polypeptide (GIP) has been associated with obesity and glucose intolerance. This condition has been suggested to be linked to GIP resistance. Besides its insulinotropic effect, GIP also directly affects </span></span>glucose uptake<span> and lipid metabolism. This notwithstanding, effects of GIP on other circulating metabolites than glucose have not been thoroughly investigated. Here, we examined effects of infusion of various concentrations of GIP in normo- and hyperglycemic rats on serum metabolite profiles. We found that, despite a decrease in serum glucose levels (−</span></span> <!-->26%, p<!--> <!--><<!--> <span>0.01), the serum metabolite profile was largely unaffected by GIP infusion in normoglycemic rats. Interestingly, levels of branched chain amino acids<span> and the ketone body β-hydroxybutyrate were decreased by 21% (p</span></span> <!--><<!--> <!-->0.05) and 27% (p<!--> <!--><<!--> <!-->0.001), respectively, in hyperglycemic rats infused with 60<!--> <!-->ng/ml GIP. Hence, our data suggest that GIP provokes a decrease in BCAA levels and ketone body production. Increased concentrations of these metabolites have been associated with obesity and T2D.</p></div>\",\"PeriodicalId\":20853,\"journal\":{\"name\":\"Regulatory Peptides\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2014-02-10\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/j.regpep.2013.12.009\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Regulatory Peptides\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0167011514000032\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Regulatory Peptides","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0167011514000032","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Hypersecretion of the incretin hormone glucose-dependent insulinotropic polypeptide (GIP) has been associated with obesity and glucose intolerance. This condition has been suggested to be linked to GIP resistance. Besides its insulinotropic effect, GIP also directly affects glucose uptake and lipid metabolism. This notwithstanding, effects of GIP on other circulating metabolites than glucose have not been thoroughly investigated. Here, we examined effects of infusion of various concentrations of GIP in normo- and hyperglycemic rats on serum metabolite profiles. We found that, despite a decrease in serum glucose levels (− 26%, p < 0.01), the serum metabolite profile was largely unaffected by GIP infusion in normoglycemic rats. Interestingly, levels of branched chain amino acids and the ketone body β-hydroxybutyrate were decreased by 21% (p < 0.05) and 27% (p < 0.001), respectively, in hyperglycemic rats infused with 60 ng/ml GIP. Hence, our data suggest that GIP provokes a decrease in BCAA levels and ketone body production. Increased concentrations of these metabolites have been associated with obesity and T2D.
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Regulatory Peptides provides a medium for the rapid publication of interdisciplinary studies on the physiology and pathology of peptides of the gut, endocrine and nervous systems which regulate cell or tissue function. Articles emphasizing these objectives may be based on either fundamental or clinical observations obtained through the disciplines of morphology, cytochemistry, biochemistry, physiology, pathology, pharmacology or psychology.
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