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Hiroshi Sakura

Researcher at University of Tokyo

Publications -  44
Citations -  2897

Hiroshi Sakura is an academic researcher from University of Tokyo. The author has contributed to research in topics: Diabetes mellitus & Insulin. The author has an hindex of 20, co-authored 41 publications receiving 2803 citations.

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Journal ArticleDOI

Insulin resistance and growth retardation in mice lacking insulin receptor substrate-1.

TL;DR: The data suggest that mice homozygous for targeted disruption of the IRS-1 gene were born alive but were retarded in embryonal and postnatal growth and the exis-tence of both IRS- 1-dependent and IRS-2-independent pathways for signal transduction of insulin and IGFs is suggested.
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A subtype of diabetes mellitus associated with a mutation of mitochondrial DNA

TL;DR: Diabetes mellitus associated with the A-->G mutation at position 3243 of mitochondrial leucine transfer RNA represents a subtype of diabetes found in both patients with IDDM and patients with NIDDM in Japan.
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Pancreatic β-Cell-specific Targeted Disruption of Glucokinase Gene DIABETES MELLITUS DUE TO DEFECTIVE INSULIN SECRETION TO GLUCOSE

TL;DR: GK-deficient mice serve as an animal model of the insulin-secretory defect in human non-insulin-dependent diabetes mellitus and provide the first direct proof that GK serves as a glucose sensor molecule for insulin secretion and plays a pivotal role in glucose homeostasis.
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Ethidium Bromide-induced Inhibition of Mitochondrial Gene Transcription Suppresses Glucose-stimulated Insulin Release in the Mouse Pancreatic β-Cell Line βHC9

TL;DR: Investigation of the involvement of mitochondrial function in insulin secretion in pancreatic β-cell line with low dose ethidium bromide revealed that treatment by EB caused morphological changes only in mitochondria and not in other organelles such as nuclei, endoplasmic reticula, Golgi bodies, or secretory granules.
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Decreased response inhibition in middle-aged male patients with type 2 diabetes

TL;DR: The results showed that middle-aged, newly diagnosed and medication-free patients with type 2 diabetes have a particular neuropsychological deficit in inhibitory control of impulsive response, which is an independent effect of diabetes apart from being overweight.