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Françoise Assimacopoulos-Jeannet

Researcher at University of Geneva

Publications -  61
Citations -  3728

Françoise Assimacopoulos-Jeannet is an academic researcher from University of Geneva. The author has contributed to research in topics: Insulin & Brown adipose tissue. The author has an hindex of 35, co-authored 61 publications receiving 3642 citations. Previous affiliations of Françoise Assimacopoulos-Jeannet include Centre national de la recherche scientifique & Catholic University of Leuven.

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IL-1 receptor antagonist serum levels are increased in human obesity: a possible link to the resistance to leptin?

TL;DR: It is demonstrated that IL-1Ra levels are highly elevated in human obesity and that its concentrations decrease after weight loss from bypass surgery, and LBM and insulin resistance are better predictors of serum IL- 1Ra concentrations than are leptin levels, suggesting that additional metabolic factors control the secretion of this cytokine antagonist.
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Uncoupling protein-3 expression in rodent skeletal muscle is modulated by food intake but not by changes in environmental temperature

TL;DR: The results show that the increase in UCP3 expression induced by fasting is associated with the maintenance of thermogenesis measured in muscle in vitro and is not modulated by environmental temperature.
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Uncoupling Protein 2: A Possible Link Between Fatty Acid Excess and Impaired Glucose-Induced Insulin Secretion?

TL;DR: The data are compatible with a role of UCP2 and partial mitochondrial uncoupling in the decreased secretory response to glucose observed after chronic exposure of the beta-cell to elevated fatty acids, and suggest that the expression and/or activity of the protein may modulate insulin secretion in response to fructose.
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Glucose Down-regulates the Expression of the Peroxisome Proliferator-activated Receptor-α Gene in the Pancreatic β-Cell *

TL;DR: The results suggest that a reduction in PPARα gene expression together with a rise in malonyl-CoA plays a role in the coordinated adaptation ofβ-cell glucose and lipid metabolism to hyperglycemia and may be implicated in the mechanism of β-cell “glucolipotoxicity.”
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Long-term exposure of beta-INS cells to high glucose concentrations increases anaplerosis, lipogenesis, and lipogenic gene expression.

TL;DR: The results suggest that a coordinated induction of glycolytic and lipogenic genes in conjunction with glycogen and triglyceride deposition, as well as increased anaplerosis and altered lipid partitioning, contribute to the adaptive process to hyperglycemia and glucose sensitization of the beta-cell.