Welcome to Marion Bonnet






Marion Bonnet performed her PhD in the lab “Physiology and Physiopathology of the Nervous System” in Marseille. She investigated the central regulation of feeding behavior and  glucose homeostasis.

Welcome to Marion who joined, in January, Professor Thorens’ lab for a post-doc, she will work on the central detection of glucose.

MON, 02.09.2013 12:15 5022 Susanna R. Keller, M.D. Invited Professor


Susanna R. Keller, M.D.
Associate Professor of Medicine and Cell Biology
Director Diabetes Center Animal Characterization Core
University of Virginia


  “Regulation of glucose and energy homeostasis by the Rab GAPs AS160 and Tbc1d1”

Monday, 2nd September 2013    At 12:15

 Room 5022   Génopode Building

Host : Prof. Bernard Thorens

Abstract: Regulation of Glucose and Energy homeostasis by the Rab GAPs AS160 and Tbc1d1.

Insulin increases glucose uptake in skeletal muscle and adipocytes and thus facilitates the disposal of ~90% of glucose after a meal. The increased glucose uptake is achieved through the translocation of the glucose transporter GLUT4 from an intracellular compartment to the cell surface. Recent studies have implicated two Rab GTPase-activating proteins (Rab GAPs), AS160 and Tbc1d1, in the regulation of glucose uptake and GLUT4 subcellular distribution. To determine the roles of the two Rab GAPs in GLUT4 subcellular distribution, glucose uptake, and whole body glucose and energy homeostasis, we characterized single AS160 and Tbc1d1 and double AS160/Tbc1d1 knockout (KO) mice. Our results with isolated skeletal muscles and adipocytes demonstrate that AS160 but not Tbc1d1 regulates glucose uptake in adipocytes, while AS160 and Tbc1d1 each regulate glucose uptake in specific skeletal muscles. Our results further show that AS160 or Tbc1d1 deletions lead to similar changes in glucose uptake, total GLUT4 and GLUT4 cell surface expression in the specific skeletal muscles, but AS160 deletion leads to different changes in glucose uptake and GLUT4 cell surface expression between skeletal muscle and adipocytes. At the whole body level glucose homeostasis is prominently regulated by AS160, while energy expenditure is primarily controlled by Tbc1d1. Our observations further show that the two Rab GAPs do not compensate for each other in the single knockout mice, and the double AS160/Tbc1d1 knockout mice combine the defects of the single knockout mice at both the cellular and the whole body level. In conclusion, our results suggest that AS160 and Tbc1d1, consistent with their differential tissue distribution, have distinct roles with regard to where they regulate glucose uptake. However, they may have similar functions with regard to how they regulate GLUT4 expression and translocation. Lastly, the two Rab GAPs differentially regulate whole body glucose and energy homeostasis.


Welcome to Alexandre Picard

After two years of medical studies, Alexandre continued his studies at the University of Paris 7 and received a Bachelor of cell biology and physiology and a master cell biology, physiology and pathology.

He did then a thesis in the field of metabolic diseases on the study of the role of hippocampal lipoprotein lipase in the nervous regulation of energy homeostasis. Welcome to Alexandre, who will join Thorens’ lab on 01.05.2013.


Welcome to Sabrina Vollers Thorens’Group

Welcome to Sabrina who will join Thorens’ group on 01.03.2013.

After having completed her Bachelor’s degree in biology at Mount Holyoke College in 2002. She contributed, as a research assistant, to biochemical and biophysical characterization of the amyloid-beta protein in the laboratory of Dr. David Teplow at Brigham and Women’s hospital in Boston.

After this, she joined the Bioanalytical Development group at Genzyme Corporation.

From 2006 to 2013, Sabrina performed her doctoral research at the University of Massachusetts Medical School, in the laboratory of Dr. Anthony Carruthers. Her dissertation focused on identification and kinetic characterization of the domain controlling accelerated exchange in human glucose transporters.