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Yasuo Ido

Researcher at Boston University

Publications -  76
Citations -  10032

Yasuo Ido is an academic researcher from Boston University. The author has contributed to research in topics: AMPK & AMP-activated protein kinase. The author has an hindex of 43, co-authored 69 publications receiving 9356 citations. Previous affiliations of Yasuo Ido include University of Texas Health Science Center at Houston & Boston Medical Center.

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Hyperglycemic Pseudohypoxia and Diabetic Complications

TL;DR: Several lines of evidence support the likelihood that the increased cytosolic ratio of free NADH/NAD+ caused by hyperglycemia, referred to as pseudohypoxia, is a characteristic feature of poorly controlled diabetes that mimics the effects of true hypoxia on vascular and neural function and plays an important role in the pathogenesis of diabetic complications.
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AMPK and SIRT1: a long-standing partnership?

TL;DR: The evidence that AMPK and SIRT1 both regulate each other and share many common target molecules is examined and the possibility that their dysregulation predisposes to disorders such as type 2 diabetes and atherosclerotic cardiovascular disease is discussed.
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SIRT1 Regulates Hepatocyte Lipid Metabolism through Activating AMP-activated Protein Kinase *

TL;DR: It is shown that polyphenols, including resveratrol and the synthetic polyphenol S17834, increase SIRT1 deacetylase activity, LKB1 phosphorylation at Ser428, and AMPK activity, which suggests that Sirt1 functions as a novel upstream regulator for L KB1/AMPK signaling and plays an essential role in the regulation of hepatocyte lipid metabolism.
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SIRT1 Modulation of the Acetylation Status, Cytosolic Localization, and Activity of LKB1 POSSIBLE ROLE IN AMP-ACTIVATED PROTEIN KINASE ACTIVATION

TL;DR: The results suggest that LKB1 deacetylation is regulated by SIRT1 and that this in turn influences its intracellular localization, association with STRAD, kinase activity, and ability to activate AMPK.
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Energy metabolism in uncoupling protein 3 gene knockout mice.

TL;DR: It is demonstrated that UCP3 has uncoupling activity and that its absence may lead to increased production of ROS, and the consequence of increased mitochondrial coupling in U CP3 KO mice on metabolism and the possible role of yet unidentified compensatory mechanisms, remains to be determined.