NDLI: Cardiotrophin-1 (CT-1) Improves High Fat Diet-Induced Cognitive Deficits in Mice

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Cardiotrophin-1 (CT-1) Improves High Fat Diet-Induced Cognitive Deficits in Mice

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Cardiotrophin-1 (CT-1) Improves High Fat Diet-Induced Cognitive Deficits in Mice

Content Provider	Springer Nature Link
Author	Wang, Dongmei Liu, Ling Yan, Junqiang Wu, Wenlan Zhu, Xiaoying Wang, Yong
Copyright Year	2015
Abstract	Previous studies demonstrated that a high fat diet (HFD) results in a loss of working memory in mice correlated with neuroinflammatory changes as well as synaptodendritic abnormalities and brain insulin resistance. Cardiotrophin-1 (CT-1), a member of the gp130 cytokine family, has been shown to potentially play a critical role in obesity and the metabolic syndrome. Our recent studies have demonstrated that CT-1 attenuates cognitive impairment and glucose-uptake defects induced by amyloid-β in mouse brain through inhibiting GSK-3β activity. In this study, we evaluated the effect of CT-1 on cognitive impairment induced by brain insulin resistance in mice fed a HFD, and explored its potential mechanism. CT-1 (1 μg/day, intracerebroventricular injection) was given for 14 days to mice that were fed with either a HFD or normal diet for 18 weeks. After 20 weeks of treatment, our results showed that in the HFD group, CT-1 significantly improved learning and memory deficits and alleviated neuroinflammation demonstrated by decreasing brain levels of proinflammatory cytokine tumour necrosis factor-α and interleukin-1β, and increasing brain levels of anti-inflammatory cytokine IL-10. CT-1 significantly reduced body weight gain, restored normal levels of blood glucose, fatty acids and cholesterol. Furthermore, CT-1 significantly enhanced insulin/IGF signaling pathway as indicated by increasing the expression levels of insulin receptor substrate 1 (IRS-1) and the phosphorylation of Akt/GSK-3β, and reducing the phosphorylation of IRS-1 in the hippocampus compared to control. Moreover, CT-1 increased the level of the post-synaptic protein, PSD95, and drebrin, a dendritic spine-specific protein in the hippocampus. These results indicate a previously unrecognized potential of CT-1 in alleviating high-fat diet induced cognitive impairment.
Starting Page	843
Ending Page	853
Page Count	11
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	40
Issue Number	4
e-ISSN	15736903
Language	English
Publisher	Springer US
Publisher Date	2015-02-12
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	CT-1 High fat diet Cognitive deficits Insulin/IGF signaling Neuroinflammation Neurosciences Neurochemistry Biochemistry Cell Biology Neurology
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

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