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Toshiyuki Maki

Researcher at University of Tokyo

Publications -  12
Citations -  2608

Toshiyuki Maki is an academic researcher from University of Tokyo. The author has contributed to research in topics: Adipokine & Adiponectin. The author has an hindex of 10, co-authored 12 publications receiving 2461 citations.

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Targeted disruption of AdipoR1 and AdipoR2 causes abrogation of adiponectin binding and metabolic actions.

TL;DR: Adenovirus-mediated expression of AdipoR1 and R2 in the liver of Lepr−/− mice increased AMP-activated protein kinase (AMPK) activation and peroxisome proliferator-activated receptor (PPAR)-α signaling pathways, respectively, and abolished adiponectin binding and actions, leading to insulin resistance and marked glucose intolerance in vivo.
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Insulin/Foxo1 Pathway Regulates Expression Levels of Adiponectin Receptors and Adiponectin Sensitivity

TL;DR: The expression of AdipoR1/R2 appears to be inversely regulated by insulin in physiological and pathophysiological states such as fasting/refeeding, insulin deficiency, and hyper-insulinemia models via the insulin/phosphoinositide 3-kinase/Foxo1 pathway and is correlated with adiponectin sensitivity.
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Peroxisome proliferator-activated receptor (PPAR)alpha activation increases adiponectin receptors and reduces obesity-related inflammation in adipose tissue: comparison of activation of PPARalpha, PPARgamma, and their combination.

TL;DR: ptive activation of peroxisome proliferator-activated receptor (PPAR)alpha, PPARgamma, and both of them in combination in obese diabetic KKAy mice markedly improved insulin sensitivity and dual activation of PPARalpha and -gamma enhances the action of adip onectin by increasing both adiponectin and AdipoRs, which can result in the amelioration of obesity-induced insulin resistance.
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Adiponectin inhibits the growth and peritoneal metastasis of gastric cancer through its specific membrane receptors AdipoR1 and AdipoR2.

TL;DR: The results suggest that the antitumor effect of adiponectin was, at least partially, dependent on the direct effects on tumor cells.