Claude Knauf4
Elodie Luche4
Patrice D. Cani4
Wifredo Ricart3
4Claude Knauf
4Elodie Luche
4Patrice D. Cani
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  • José Manuel Fernández-Real, Sofia Pérez del Pulgar, Elodie Luche, José Maria Moreno-Navarrete, Aurelie Waget, Matteo Serino +8 others
  • 2011
OBJECTIVE The study objective was to evaluate the possible role of the macrophage molecule CD14 in insulin resistance. RESEARCH DESIGN AND METHODS The effects of recombinant human soluble CD14 (rh-sCD14) on insulin sensitivity (clamp procedure) and adipose tissue gene expression were evaluated in wild-type (WT) mice, high fat-fed mice, ob/ob mice, and(More)
  • J. Andrew Pospisilik, Claude Knauf, Nicholas Joza, Paule Benit, Michael Orthofer, Patrice D. Cani +11 others
  • 2007
Type-2 diabetes results from the development of insulin resistance and a concomitant impairment of insulin secretion. Recent studies place altered mitochondrial oxidative phosphorylation (OxPhos) as an underlying genetic element of insulin resistance. However, the causative or compensatory nature of these OxPhos changes has yet to be proven. Here, we show(More)
  • Matteo Serino, Elodie Luche, Sandra Gres, Audrey Baylac, Mathieu Bergé, Claire Cenac +15 others
  • 2012
OBJECTIVE The gut microbiota, which is considered a causal factor in metabolic diseases as shown best in animals, is under the dual influence of the host genome and nutritional environment. This study investigated whether the gut microbiota per se, aside from changes in genetic background and diet, could sign different metabolic phenotypes in mice. (More)
  • Vanessa Deveaux, Thomas Cadoudal, Yasukatsu Ichigotani, Fatima Teixeira-Clerc, Alexandre Louvet, Sylvie Manin +12 others
  • 2009
BACKGROUND Obesity-associated inflammation is of critical importance in the development of insulin resistance and non-alcoholic fatty liver disease. Since the cannabinoid receptor CB2 regulates innate immunity, the aim of the present study was to investigate its role in obesity-induced inflammation, insulin resistance and fatty liver. METHODOLOGY Murine(More)
  • Claude Knauf, Patrice D. Cani, Dong-Hoon Kim, Miguel A. Iglesias, Chantal Chabo, Aurélie Waget +6 others
  • 2008
OBJECTIVE Ingested glucose is detected by specialized sensors in the enteric/hepatoportal vein, which send neural signals to the brain, which in turn regulates key peripheral tissues. Hence, impairment in the control of enteric-neural glucose sensing could contribute to disordered glucose homeostasis. The aim of this study was to determine the cells in the(More)
OBJECTIVE AMP-activated protein kinase (AMPK) signaling acts as a sensor of nutrients and hormones in the hypothalamus, thereby regulating whole-body energy homeostasis. Deletion of Ampkα2 in pro-opiomelanocortin (POMC) neurons causes obesity and defective neuronal glucose sensing. LKB1, the Peutz-Jeghers syndrome gene product, and(More)
Calgranulin B (S100A9) was recognized as a candidate type 2 diabetes (T2D) gene in the genomic profiling of muscle from a rodent model of T2D and identifying the human orthologs of genes localized in T2D susceptibility regions. Circulating and S100A9 expressions in muscle and adipose tissue, isolated fat cells, and mouse models were evaluated. A common(More)
These days, the gut microbiota is universally recognized as an active organ that can modulate the overall host metabolism by promoting multiple functions, from digestion to the systemic maintenance of overall host physiology. Dysbiosis, the alteration of the complex ecologic system of gut microbes, is associated with and causally responsible for multiple(More)
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