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Effect of caloric restriction on learning impairment in the hippocampus of ob/ob mice; through enhanced O‐GlcNAcylation and Ca 2+ homeostasis
Author(s) -
Lee Jong Youl,
Jeon Byeong Tak,
Heo Rok Won,
Jeong Eun Ae,
Yi Chinok,
Roh Gu Seob
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.lb206
Subject(s) - endocrinology , medicine , hippocampus , hippocampal formation , insulin resistance , homeostasis , diabetes mellitus , intracellular , chemistry , biology , biochemistry
Diabetes may adversely affect cognitive function, although the specific underlying mechanisms are unknown. On the other hand, caloric restriction (CR) increases longevity and improves memory. We examined the effects of CR on serum metabolic parameters and hippocampal protein expression in ob/ob mice, a model of obesity‐induced diabetes. We found that CR reduced hepatic steatosis and insulin resistance in ob/ob mice. In the hippocampus of these mice, CR increased the expression of O‐linked‐N‐acetylglucosamine (O‐GlcNAc) and GlcNAc transferase and decreased the expression of calcium/calmodulin‐dependent protein kinase P. It also decreased hippocampal lipocalin‐2 and phosphorylated tau. Furthermore, CR lessened the learning deficits that are typically seen in ob/ob mice. These findings indicate that CR may reverse obesity‐related brain glucose impairment and intracellular Ca 2+ dysfunction and relieve learning impairment in diabetes.

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