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Vincent Poitout

Researcher at Université de Montréal

Publications -  151
Citations -  11950

Vincent Poitout is an academic researcher from Université de Montréal. The author has contributed to research in topics: Insulin & Glucose homeostasis. The author has an hindex of 57, co-authored 142 publications receiving 11054 citations. Previous affiliations of Vincent Poitout include University of Minnesota & Pacific Northwest Diabetes Research Institute.

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Glucolipotoxicity: Fuel Excess and β-Cell Dysfunction

TL;DR: The role of glucolipotoxicity and lipotoxicity in the natural history of β-cell compensation, decompensation, and failure during the course of type 2 diabetes is defined.
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β-Cell Glucose Toxicity, Lipotoxicity, and Chronic Oxidative Stress in Type 2 Diabetes

TL;DR: Evidence is reviewed that patients with type 2 diabetes continually undergo oxidative stress, that elevated glucose concentrations increase levels of reactive oxygen species inβ-cells, that islets have intrinsically low antioxidant enzyme defenses, and that antioxidant drugs and overexpression of antioxidant enzymes protect β-cells from glucose toxicity.
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Minireview: Secondary β-Cell Failure in Type 2 Diabetes—A Convergence of Glucotoxicity and Lipotoxicity

TL;DR: It is proposed that chronic hyperglycemia, independent of hyperlipidemia, is toxic for -cell function, whereas chronic hyper Lipotoxicity is deleterious only in the context of concomitant hyper glycemia.
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A glucose monitoring system for on line estimation in man of blood glucose concentration using a miniaturized glucose sensor implanted in the subcutaneous tissue and a wearable control unit.

TL;DR: This glucose monitoring system, based on subcutaneous sensing of glucose, is able to provide a direct on line estimation of blood glucose concentration, using a novel calibration procedure and a monitoring unit designed for this purpose.
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Glucolipotoxicity of the pancreatic beta cell

TL;DR: It is likely that glucolipotoxicity contributes to beta-cell failure in type 2 diabetes as well as to the decline in beta- cell function observed after the onset of the disease.