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Yasushi Fukushima

Researcher at University of Tokyo

Publications -  99
Citations -  6001

Yasushi Fukushima is an academic researcher from University of Tokyo. The author has contributed to research in topics: Insulin receptor & Receptor. The author has an hindex of 42, co-authored 96 publications receiving 5594 citations. Previous affiliations of Yasushi Fukushima include Saitama Medical University.

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Angiotensin II–Induced Insulin Resistance Is Associated With Enhanced Insulin Signaling

TL;DR: Investigation of the effects of chronic AII infusion on blood pressure and insulin sensitivity in rats fed a normal or high-salt diet suggests increased oxidative stress, possibly through impaired insulin signaling located downstream from PI 3-kinase activation, is involved in AII-induced insulin resistance.
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Dexamethasone-induced insulin resistance in 3T3-L1 adipocytes is due to inhibition of glucose transport rather than insulin signal transduction.

TL;DR: The GLUT1 decrease may be involved in the dexamethasone-induced decrease in basal glucose transport activity, and the mechanism of dexamethylamethas one-induced insulin resistance in glucose transportactivity (rather than the inhibition of phosphatidylinositol 3-kinase activation resulting from a decreased IRS-1 content) is likely to underlie impaired glucose transporter regulation.
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Blockade of the Stromal Cell–Derived Factor-1/CXCR4 Axis Attenuates In vivo Tumor Growth by Inhibiting Angiogenesis in a Vascular Endothelial Growth Factor–Independent Manner

TL;DR: The data indicate that the SDF-1/CXCR4 pathway might be a general target for anticancer strategies and that blocking this system could be cooperatively effective in combination with other antiangiogenic therapies, such as blockade of VEGF.
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Humoral regulation of resistin expression in 3T3-L1 and mouse adipose cells

TL;DR: It is found that resistin expression in 3T3-L1 adipocytes was significantly upregulated by high glucose concentrations and was suppressed by insulin, suggesting that these factors affect insulin sensitivity and fat tissue mass in part by altering the expression and eventual secretion of resistin from adipose cells.