期刊
OBESITY
卷 24, 期 2, 页码 417-423出版社
WILEY
DOI: 10.1002/oby.21388
关键词
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资金
- NIH [R00AT004197, R15DK10396]
- University of Toledo
- USDA/NIFA [2010-38903-20740]
- Wolfe Innovation Fund (University of Toledo)
- NIFA [688362, 2010-38903-20740] Funding Source: Federal RePORTER
ObjectiveObesity-induced diabetes has increased over the years and has become one of the risk factors for stroke. We investigated the influence of diet-induced obesity and hyperglycemia on permanent distal middle cerebral artery occlusion (pMCAO)-induced ischemic stroke in mice. MethodsMale C57/Bl6 mice were treated with a high-fat/high-carbohydrate diet [HFCD/obese and hyperglycemia (O/H)] or a normal diet (control) for 3.5 months, subjected to pMCAO, and sacrificed after 7 days. ResultsInfarct volume analysis showed no differences between the O/H and control group, whereas neurological deficits were significantly higher in the O/H group compared to the control group. Sirtuin (Sirt1) was overexpressed and NADPH oxidase was reduced in the O/H group. O/H mice had significantly lower expression of Wnt and glycogen synthase kinase 3 and , a key component in the Wnt signaling pathway. Translocation of apoptosis inducing factor (AIF) to the nucleus was observed in both the O/H and control groups, but O/H mice showed a higher expression of AIF in the nucleus. ConclusionsThese data suggest that impaired Wnt signaling and active apoptosis result in reduced post-stroke recovery in obese and hyperglycemic mice.
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