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Thierry Alquier

Researcher at Université de Montréal

Publications -  58
Citations -  7159

Thierry Alquier is an academic researcher from Université de Montréal. The author has contributed to research in topics: Insulin & Free fatty acid receptor 1. The author has an hindex of 29, co-authored 52 publications receiving 6563 citations. Previous affiliations of Thierry Alquier include Beth Israel Deaconess Medical Center & Harvard University.

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AMP-activated protein kinase: Ancient energy gauge provides clues to modern understanding of metabolism

TL;DR: Through signaling, metabolic, and gene expression effects, AMPK enhances insulin sensitivity and fosters a metabolic milieu that may reduce the risk for obesity and type 2 diabetes.
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AMP-kinase regulates food intake by responding to hormonal and nutrient signals in the hypothalamus

TL;DR: Hypothalamic AMPK plays a critical role in hormonal and nutrient-derived anorexigenic and orexigenic signals and in energy balance, and inhibition of hypothalamic AM PK is necessary for leptin's effects on food intake and body weight, as constitutively active AMPK blocks these effects.
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Diet-induced Obesity Alters AMP Kinase Activity in Hypothalamus and Skeletal Muscle *

TL;DR: DIO in FVB mice alters α2-AMPK in muscle and hypothalamus and STAT3 in hypothalamic and impairs further effects of leptin on these signaling pathways and may contribute to resistance to leptin action on food intake and energy expenditure in obese states.
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GPR40 Is Necessary but Not Sufficient for Fatty Acid Stimulation of Insulin Secretion In Vivo

TL;DR: It is concluded that GPR40 contributes approximately half of the full acute insulin secretory response to fatty acids in mice but does not play a role in the mechanisms by which fatty acids chronically impair insulin secretion.
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The Fatty Acid Receptor GPR40 Plays a Role in Insulin Secretion In Vivo After High-Fat Feeding

TL;DR: GPR40 plays a role not only in fatty acid modulation of insulin secretion, but also in GSIS after high-fat feeding, which raises doubts on the validity of a therapeutic approach based on GPR40 antagonism for the treatment of type 2 diabetes.