Team 2 : «Mitochondria-ER Interactions and Signalling in Metabolic health and diseases»

Diapositive1Our team was initially created in 2011 (team 3 of CarMeN: gluco-lipotoxicity, metabolic stress and diabetes). It involved basic researchers and clinicians with complementary skills in the field of insulin action and secretion. Our aim was to identify common molecular mechanisms by which glucolipotoxicity-associated metabolic stress affects hepatic/muscle insulin action and pancreatic insulin secretion, thus contributing to the two components of type 2 diabetes (T2DM). In recent years, we focused on the involvement of mitochondria and ER in the functional alterations of these tissues, highlighting for the first time a key role of structural and functional interactions between the two organelles in the alterations of insulin action and secretion in T2DM. Therefore, our team has evolved and is now called “organelle communication and diabetes” (OrCaDia, 2016-2020). Our goal is to clarify the mechanisms by which ER-mitochondria interactions are involved in the pathogenesis of T2DM and whether the control of these interactions could be a new target to improve both insulin action and secretion in T2DM (Figure 1).


Scientific research

The communication between intracellular organelles allows the cell to adapt its metabolism according to its environment in order to maintain cellular homeostasis. More specifically, endoplasmic reticulum (ER) and mitochondria interact at contact points, called MAMs (mitochondria-associated endoplasmic reticulum membranes), in order to exchange lipids and calcium, 2 signalling molecules that play a key role in metabolic homeostasis. Indeed, lipids and calcium homeostasis control both insulin action and secretion, explaining why these two organelles play an important role in the pathogenesis of type 2 diabetes (T2DM).

We recently demonstrated a new role of ER-mitochondria cross-talk in the control of insulin action both in the liver and skeletal muscle, as well as a role of disrupted ER-mitochondria interactions in the development of hepatic and muscular insulin resistance (Tubbs E et al. Diabetes 2014, Rieusset J et al. Diabetologia 2016, Tubbs E et al. Diabetes 2018) (Figure 2). Altered structural communications between ER and mitochondria are also associated with altered insulin secretion in beta cells of pancreas of type 2 diabetic patients (Thivolet C et al. PLoS One 2017). Altogether, these data reveal a new mechanism common to both peripheral insulin resistance and beta cell dysfunction, highlighting new preventive and/or therapeutic strategies for the two features of T2DM.

In parallel, we analysed the dynamic regulations of MAM in health and diseases, in order to identify new intracellular targets to modulate ER-mitochondria interactions, and subsequently to regulate glucose homeostasis. We recently demonstrated that ER-mitochondria interactions are regulated by nutritional transitions, and more particularly are reduced at postprandial state, in the presence of high concentrations of glucose, in order to adapt mitochondria dynamics and metabolism and orientate glucose flux towards stockage (Theurey P et al. J Mol Cell Biol 2016) (Figure 3). Interestingly, this regulation is lost in liver of obese and diabetic mice. Therefore, MAMs are a new glucose sensing platform which allow hepatocytes to adapt its metabolism to nutritional transition, and disruption of this regulation could participate to metabolic inflexibility in obesity and T2DM.

The general goal of our research is to better characterize the nature and the physiological significance of MAMs in glucose homeostasis and their roles in the pathogenesis of T2DM. For that, we combine investigations in cellular models, in mouse models of T2DM and in humans. More specifically, our specific aims are:

  • To identify the molecular nature of MAM actors and their functional roles,
  • To characterize the physiological significance of MAMs in the control of insulin action and secretion,
  • To identify the regulators of MAMs and their functional impacts,
  • To validate if the MAMs could be a new target for the treatment of T2DM.

Ultimately, the combination of cellular and integrated approaches, both in animals and humans, coupled with innovative imaging tools, should allow us to clarify the role of communication between the ER and mitochondria in the T2DM physiopathology and to open new avenues for the treatment of this pathology.


  • Preclinical mouse models of T2DM
  • Human and mouse primary cells in culture (hepatocytes, myotubes and islets)
  • Structural and functional analysis of ER-mitochondria communication. Particularly, we developed and validated a new method to detect and quantify ER-mitochondria interactions by in situ proximity ligation assay (PLA), via the visualization of the VDAC1/IP3R1, Grp75/IP3R1 or CypD/IP3R1 interactions in both fixed cells and paraffin-embedded tissues (Figure 4).


  • We also performed subcellular fractionation, electronic microscopy analysis and co-immunoprecipitation analysis to access ER-mitochondria interactions, and analyse calcium transfer from ER to mitochondria by confocal microscopy using Cameleon probes.
  • Analysis of insulin action and secretion
  • Proteomic analysis
  • Lipidomic analysis
  • Strong complementarity between basic research and clinical investigations favouring translational research

Biological resources:

  • Tissues from obese and diabetic mice
  • Human and mouse primary cells in culture (hepatocytes, myotubes and islets)
  • Mitochondria, ER and MAM fractions from liver and skeletal muscle of obese and diabetic mice
  • nPOD human pancreas sections

Key words:

  • Diabetes
  • Insulin resistance
  • Insulin secretion
  • Mitochondria
  • Endoplasmic reticulum
  • MAM
  • Calcium


National and international collaborations / Poxel / Fondation de France / Activ’inside

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Team 2 Leader
RIEUSSET  Jennifer DR2


BERGERs Marie-Agnès AI
CAUSSY Cyrielle IE
CHARCOSSET/DiFilipo Mathilde PH
DURAND Christine TR
GODET Murielle CR
HUMBERT Alexandre PhD
JI Jingwei IR
MADEC Anne-Marie MCU
MORIO Béatrice DR2


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