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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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- Author(s): Kim H;Kim H; Kang H; Kang H; Heo RW; Heo RW; Jeon BT; Jeon BT; Yi CO; Yi CO; Shin HJ; Shin HJ; Kim J; Kim J; Jeong SY; Jeong SY; Kwak W; Kwak W; Kim WH; Kim WH; Kang SS; Kang SS; Roh GS; Roh GS
- Source:
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism [J Cereb Blood Flow Metab] 2016 Jun; Vol. 36 (6), pp. 1098-110. Date of Electronic Publication: 2015 Oct 05.- Publication Type:
Journal Article; Research Support, Non-U.S. Gov't- Language:
English - Source:
- Additional Information
- Source: Publisher: SAGE Publications Country of Publication: United States NLM ID: 8112566 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1559-7016 (Electronic) Linking ISSN: 0271678X NLM ISO Abbreviation: J Cereb Blood Flow Metab Subsets: MEDLINE
- Publication Information: Publication: 2016- : Thousand Oaks, CA : SAGE Publications
Original Publication: New York : Raven Press, c1981- - Subject Terms: Calcium Signaling* ; Caloric Restriction*; Cognition Disorders/*diet therapy ; Diabetes Mellitus, Type 2/*complications ; Neurogranin/*genetics; Animals ; Cognition Disorders/etiology ; Diet, High-Fat ; Gene Expression Profiling ; Hippocampus/metabolism ; Mice ; Mice, Inbred C57BL ; Sequence Analysis, RNA
- Abstract: Diabetes-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.
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Sci Rep. 2013;3:1392. (PMID: 23462742) - Contributed Indexing: Keywords: Calcium; caloric restriction; cognitive impairment; diabetes; hippocampus
- Accession Number: 132654-77-4 (Neurogranin)
- Publication Date: Date Created: 20151215 Date Completed: 20170809 Latest Revision: 20181113
- Publication Date: 20221213
- Accession Number: PMC4908619
- Accession Number: 10.1177/0271678X15606724
- Accession Number: 26661177
- Source:
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