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Caloric restriction improves diabetes-induced cognitive deficits by attenuating neurogranin-associated calcium signaling in high-fat diet-fed mice

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dc.contributor.authorKim, H-
dc.contributor.authorKang, H-
dc.contributor.authorHeo, RW-
dc.contributor.authorJeon, BT-
dc.contributor.authorYi, CO-
dc.contributor.authorShin, HJ-
dc.contributor.authorKim, J-
dc.contributor.authorJeong, SY-
dc.contributor.authorKwak, W-
dc.contributor.authorKim, WH-
dc.contributor.authorKang, SS-
dc.contributor.authorRoh, GS-
dc.date.accessioned2018-05-04T00:24:00Z-
dc.date.available2018-05-04T00:24:00Z-
dc.date.issued2016-
dc.identifier.issn0271-678X-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/14791-
dc.description.abstractDiabetes-induced cognitive decline has been recognized in human patients of type 2 diabetes mellitus and mouse model of obesity, but the underlying mechanisms or therapeutic targets are not clearly identified. We investigated the effect of caloric restriction on diabetes-induced memory deficits and searched a molecular mechanism of caloric restriction-mediated neuroprotection. C57BL/6 mice were fed a high-fat diet for 40 weeks and RNA-seq analysis was performed in the hippocampus of high-fat diet-fed mice. To investigate caloric restriction effect on differential expression of genes, mice were fed high-fat diet for 20 weeks and continued on high-fat diet or subjected to caloric restriction (2 g/day) for 12 weeks. High-fat diet-fed mice exhibited insulin resistance, glial activation, blood-brain barrier leakage, and memory deficits, in that we identified neurogranin, a down-regulated gene in high-fat diet-fed mice using RNA-seq analysis: neurogranin regulates Ca(2+)/calmodulin-dependent synaptic function. Caloric restriction increased insulin sensitivity, reduced high-fat diet-induced blood-brain barrier leakage and glial activation, and improved memory deficit. Furthermore, caloric restriction reversed high-fat diet-induced expression of neurogranin and the activation of Ca(2+)/calmodulin-dependent protein kinase II and calpain as well as the downstream effectors. Our results suggest that neurogranin is an important factor of high-fat diet-induced memory deficits on which caloric restriction has a therapeutic effect by regulating neurogranin-associated calcium signaling.-
dc.language.isoen-
dc.subject.MESHAnimals-
dc.subject.MESHCalcium Signaling-
dc.subject.MESHCaloric Restriction-
dc.subject.MESHCognition Disorders/diet therapy-
dc.subject.MESHCognition Disorders/etiology-
dc.subject.MESHDiabetes Mellitus, Type 2/complications-
dc.subject.MESHDiet, High-Fat-
dc.subject.MESHGene Expression Profiling-
dc.subject.MESHHippocampus/metabolism-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred C57BL-
dc.subject.MESHNeurogranin/genetics-
dc.subject.MESHSequence Analysis, RNA-
dc.titleCaloric restriction improves diabetes-induced cognitive deficits by attenuating neurogranin-associated calcium signaling in high-fat diet-fed mice-
dc.typeArticle-
dc.identifier.pmid26661177-
dc.identifier.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4908619/-
dc.contributor.affiliatedAuthor김, 정현-
dc.contributor.affiliatedAuthor정, 선용-
dc.type.localJournal Papers-
dc.identifier.doi10.1177/0271678X15606724-
dc.citation.titleJournal of cerebral blood flow and metabolism-
dc.citation.volume36-
dc.citation.number6-
dc.citation.date2016-
dc.citation.startPage1098-
dc.citation.endPage1110-
dc.identifier.bibliographicCitationJournal of cerebral blood flow and metabolism, 36(6). : 1098-1110, 2016-
dc.identifier.eissn1559-7016-
dc.relation.journalidJ00271678X-
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Journal Papers > School of Medicine / Graduate School of Medicine > Medical Genetics
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