The FFRD is proud to allocate over 80% of its expenses to research and is pleased to support high-quality research in francophone diabetology for over a decade.
The basic research projects funded by the FFRD have addressed major themes related to both type 1 diabetes and type 2 diabetes, such as:
The protection and replacement of pancreatic beta cells,
Molecular mechanisms contributing to insulin resistance,
Implications of other key organs: the liver, adipose tissue, intestine,
The contribution of the microbiota to metabolic diseases.
The clinical research projects, on the other hand, have addressed themes related to type 1 and type 2 diabetes, as well as gestational diabetes. They involve large multicenter cohort clinical studies, and their investigations are more mechanistic and/or interventional.
Several of the projects funded by the FFRD have specifically studied:
The role of the intestine and the microbiota
The role of epigenetics
The research projects supported by the FFRD complement the projects led by the SFD (French Society of Diabetes). These are large-scale, internationally oriented projects that primarily meet five criteria: scientific originality, feasibility, financial adequacy, scientific relevance of the project and international competitiveness.
Call for Projects
📌 A new call for proposals FFRD will be launched in 2026!
The Fondation Francophone pour la Recherche sur le Diabète planned to support 2 research projects with a total funding of €500.000.
All kinds of research: clinical, basic and translational
All kinds of diabetes: type 1, type 2 and gestational
From its mechanisms, its prevention and management, its comorbidities and complications
This call for proposals is intended for FRENCH-SPEAKING researchers only (multi laboratories possible)
Save the dates:
Candidates preliminary selection: Thursday 9th July 2026
Hearings and awardees election: Tuesday 8th September 2026 (at the FFRD office, in Paris)
Submiting a project
‼️ NEXT CALL FOR PROJECTS IN 2026 ‼️
📆 See you next year to discover the new FFRD call for projects, its terms and conditions, as well as the lastest news from the Foundation… 👀
⚠️ opening of the call for projects in the first quarter of 2026…
Recipients
This year two candidates are recipients of the FFRD 2025 Research Grants :
Clinical Research Project
Jean-François GAUTIER
Paris Cité University, Diabetes and Endocrinology at Lariboisière Hospital in Paris
Projet :
“Deciphering the natural history of severe liver injury in people with type 2 diabetes and MASLD: the QUID-NASH Follow Up study”.
Cardiovascular and Metabolic diseases Institute, Inserm, CHU in Toulouse
Projet :
” Characterizing adipose tissue dysfunction associated with obesity in patients with type 1 diabetes: towards an improved prediction of cardiovascular risk “.
« Evaluation of the effects of tight glycemic control on cognitive functions in children living with type 1 diabetes: comparison between open loop and closed loop insulin administration ».
Montreal Clinical Research Institute – IRCM (Canada)
Projet :
« Identification of dysglycemia with continuous glucose monitoring: A prospective study to assess the relationship with clinical evolution in cystic fibrosis ».
« Characterization of the intestinal mucosal immune system in patients with visceral adiposity and type 2 diabetic: causal role of the corresponding microbiota ».
The recipients supported by the FFRD speak about it…
Jacques BELTRAND
Professeur of Pediatric Diabetology, Necker Enfants Malades Institute, Paris
Study of the effects of strict glycemic control on cognitive functions in children with newly diagnosed Type 1 Diabetes
Brain imaging data have highlighted the impact that glycemic variability can have on the development of gray and white matter in children’s brains. While fluctuations between hypo- and hyperglycemia do not affect a child’s psychomotor and intellectual development, significant glycemic variability could influence the acquisition of highly specific brain functions. New automated insulin delivery systems help reduce this variability. In adolescents, a study has shown that these systems can correct the neuropsychological impact of glycemic variability. Their use from the onset of the disease in children could therefore prevent delays in brain growth.
The study we are conducting in Île-de-France aims to determine the best treatment approach in the months following diagnosis to ensure that brain growth is comparable to that of children without type 1 diabetes. Study participants will be treated within weeks of diagnosis either with an insulin pump and glucose sensor or with new automated insulin delivery systems. Brain MRIs will be performed on patients at the beginning of the study and after 18 months of treatment, as well as on children of the same age without diabetes. This study, the first pediatric study supported by the FFRD, will provide important insights into the best care pathway for children in the months following diagnosis.
Rémi RABASA-LHORET
MD, PhD, Directeur de recherche, Institut de Recherches Cliniques de Montréal (ICRM)
Identify dysglycemia in patients with cystic fibrosis (cystic fibrosis) with continuous blood glucose reading
Patients with cystic fibrosis exhibit a broad spectrum of dysglycemia associated with an increased risk of accelerated clinical decline (weight loss and/or lung function decline) and the risk of cystic fibrosis-related diabetes (CFRD). However, the current screening test, oral glucose tolerance test (OGTT), is associated with multiple issues, including patient and healthcare team acceptance, costs, etc. The support of the FFRD will enable us to conduct a study to determine whether continuous glucose monitoring simplifies the screening of DAFK and helps predict whether patients are at higher risk of weight loss and/or lung function decline. These findings will provide better answers regarding the use and interpretation of continuous glucose monitoring in clinical practice .
Soazig LE LAY
INSERM, l’Institut du Thorax de Nantes
Extracellular vesicles enriched in adiponectin: an innovative biotherapeutic approach for diabetes treatment
Adiponectin (Adpn), an insulin-sensitizing adipokine, represents a promising target for treating cardiometabolic complications of type 2 diabetes (T2D). However, the development of Adpn-mimicking drugs has been hindered by challenges in obtaining its active oligomerized form (conversion of monomers into oligomers). Our research on extracellular vesicles (EVs) derived from adipose tissue has shown that they are naturally enriched with active Adpn. These vesicles enhance the bioavailability and prolong the stability of Adpn in circulation while preserving its insulin-sensitizing properties. Thanks to the support of the FFRD, we will study the use of extracellular vesicles (EVs) enriched in adiponectin (Adpn) as “molecular taxis” to deliver active forms of this adipokine and restore insulin sensitivity. This project paves the way for using extracellular vesicles (EVs) as biotherapeutics to better understand and treat complications of type 2 diabetes.
Mariana IGOILLO-ESTEVE
Université Libre de Bruxelles, UCDR, Belgium
Study of the Contribution of TRMT10A Protein Deficiency and Small Non-Coding RNAs to the Pathogenesis of Type 1 Diabetes
Type 1 diabetes (T1D) is an autoimmune disease that targets pancreatic beta cells. Its onset results from a complex interaction between genetic, immunological, and environmental factors, including enterovirus infections. Individuals with T1D require lifelong insulin therapy and face an increased risk of complications. To date, no treatment exists to cure or prevent the development of T1D.
In our previous research, we demonstrated that mutations leading to a loss of function of the TRMT10A protein are responsible for juvenile diabetes, associated with microcephaly. We also found that the absence of TRMT10A causes the death of pancreatic beta cells, partly explained by an increase in the quantity of certain small non-coding RNAs in the cell. We now know that enterovirus infections also reduce the levels of TRMT10A. Thanks to the invaluable support of the FFRDwe have been able to establish various human cellular models of T1D and TRMT10A deficiency. These models will allow us to assess the extent to which the reduction in TRMT10A and the production of small non-coding RNAs contribute to the development of T1D, and to unravel the mechanisms leading to beta cell destruction. These findings could pave the way for new therapeutic approaches for this disease.
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