Michael Bryer-Ash
University of British Columbia
8 Papers
72 Citations
Michael Bryer-Ash is an academic researcher from University of British Columbia. The author has contributed to research in topics: Insulin & Insulin receptor. The author has an hindex of 6, co-authored 8 publications.
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Papers
Tumor necrosis factor-alpha induces hepatic insulin resistance in obese Zucker (fa/fa) rats via interaction of leukocyte antigen-related tyrosine phosphatase with focal adhesion kinase.
TL;DR: Analysis of tyrosine phosphorylation patterns of liver homogenate proteins from TNF-alpha-neutralized fa/fa rats showed that focal adhesion kinase (FAK) was consistently hyperphosphorylated, which suggests that T NF-alpha may induce hepatic insulin resistance by preventing FAK phosphorylated in response to insulin treatment.
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Marked impairment of protein tyrosine phosphatase 1B activity in adipose tissue of obese subjects with and without type 2 diabetes mellitus
Anthony Cheung,Jyotirmoy Kusari,David Jansen,Debdutta Bandyopadhyay,Anasua B. Kusari,Michael Bryer-Ash +5 more
TL;DR: The data suggest that the insulin resistance of obesity and DM2 is characterized by the increased expression of a catalytically impaired PTP-1B in adipose tissue and that impaired PTFE activity may be pathogenic for insulin resistance in these conditions.
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Bis(maltolato)Oxovanadium(IV) Attenuates Hyperinsulinemia and Hypertension in Spontaneously Hypertensive Rats
TL;DR: SH rats are hyperinsulinemic but not insulin resistant compared with WKY rats; and chronic oral BMOV caused concurrent decreases in plasma insulin and BP in SH rats, which suggests that hyperinsulinemia may contribute toward the development of high BP in the SH rat.
54
Feedback regulation of glucose-dependent insulinotropic polypeptide (GIP) secretion by insulin in conscious rats
TL;DR: Feedback regulation of glucose-dependent insulinotropic polypeptide was studied in a conscious rat model and the GIP rise was blunted and the peak occurred at 10 min, while in HH GIP peaked at 192 +/- 32 pM 10 min after oral glucose (a 92% increase over basal).
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Regulation of rat insulin-receptor kinase by glucose in vivo.
TL;DR: It is suggested that acute hyperglycemia may increase insulin-receptor kinase activity in vivo, possibly augmenting glucose disposal thereby, whereas the chronic hyper glycemia of diabetes mellitus results in metabolic derangements that nullify this effect.
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