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D-Psicose, a Sweet Monosaccharide, Ameliorate Hyperglycemia, and Dyslipidemia in C57BL/6J db/db Mice

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dc.contributor.authorBaek, S. H.-
dc.contributor.authorPark, S. J.-
dc.contributor.authorLee, H. G.-
dc.date.accessioned2022-12-20T18:45:51Z-
dc.date.available2022-12-20T18:45:51Z-
dc.date.created2022-08-27-
dc.date.issued2010-03-
dc.identifier.issn0022-1147-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/175347-
dc.description.abstractD-psicose has been implicated in glycemic control in recent animal and human studies. In this study, the effects of D-psicose on glycemic responses, insulin release, and lipid profiles were compared with those of D-glucose and D-fructose in a genetic diabetes model. C57BL/6J db/db mice were orally supplemented with 200 mg/kg BW of D-psicose, D-glucose, or D-fructose, respectively, while diabetes control or wild type mice were supplemented with water instead. D-psicose sustained weight gain by about 10% compared to other groups. The initial blood glucose level maintained from 276 to 305 mg/dL during 28 d in the D-psicose group, whereas a 2-fold increase was found in other groups (P < 0.05) among diabetic mice. D-psicose significantly improved glucose tolerance and the areas under the curve (AUC) for glucose among diabetes (P < 0.05), but had no effect on serum insulin concentration. The plasma lipid profile was not changed by supplemental monosacchrides, although the ratio of LDL-cholesterol/HDL-cholesterol was ameliorated by D-psicose. The administration of D-psicose reversed hepatic concentrations of triglyceride (TG) and total cholesterol (TC) by 37.88% and 62.89%, respectively, compared to the diabetes control (P < 0.05). The current findings suggest that D-psicose shows promise as an antidiabetic and may have antidyslipidemic effects in type 2 diabetes.-
dc.language영어-
dc.language.isoen-
dc.publisherWILEY-
dc.titleD-Psicose, a Sweet Monosaccharide, Ameliorate Hyperglycemia, and Dyslipidemia in C57BL/6J db/db Mice-
dc.typeArticle-
dc.contributor.affiliatedAuthorLee, H. G.-
dc.identifier.doi10.1111/j.1750-3841.2009.01434.x-
dc.identifier.scopusid2-s2.0-77953903384-
dc.identifier.wosid000275110200046-
dc.identifier.bibliographicCitationJOURNAL OF FOOD SCIENCE, v.75, no.2, pp.H49 - H53-
dc.relation.isPartOfJOURNAL OF FOOD SCIENCE-
dc.citation.titleJOURNAL OF FOOD SCIENCE-
dc.citation.volume75-
dc.citation.number2-
dc.citation.startPageH49-
dc.citation.endPageH53-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaFood Science & Technology-
dc.relation.journalWebOfScienceCategoryFood Science & Technology-
dc.subject.keywordPlusCHAIN FATTY-ACIDS-
dc.subject.keywordPlusDIETARY D-PSICOSE-
dc.subject.keywordPlusD-FRUCTOSE-
dc.subject.keywordPlusRATS-
dc.subject.keywordPlusBIOPRODUCTION-
dc.subject.keywordPlusCHOLESTEROL-
dc.subject.keywordPlusDERIVATIVES-
dc.subject.keywordPlusEXCRETION-
dc.subject.keywordPlusPRODUCTS-
dc.subject.keywordPlusGLUCOSE-
dc.subject.keywordAuthorC57BL/6J db/db mice-
dc.subject.keywordAuthorD-fructose-
dc.subject.keywordAuthorD-glucose-
dc.subject.keywordAuthorD-psicose-
dc.subject.keywordAuthortype 2 diabetes-
dc.identifier.urlhttps://ift.onlinelibrary.wiley.com/doi/10.1111/j.1750-3841.2009.01434.x-
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