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Team DO-IT : "Diet and food matrix in Obesity and metabolic diseases: role of Intestinal tract and innovative Therapeutics"

Our recent proof-of-concepts and discoveries revealed that:

Milk polar lipids can improve lipid metabolism via specific mechanisms of action in the intestine (Le Barz, Vors et al. JCI Insight 2021, Vors et al. Gut 2020, Milard et al. Mol Nutr Food Res 2019).
The health impact of nutrients depends on the food source and matrix that can affect digestion and absorption both for fats (Thorning et al. Am J Clin Nutr 2017; Astrup et al. BMJ 2019) and carbohydrates (Lambert-Porcheron et al. Mol Nutr Food Res 2017).
Intestine-derived mediators such as FGF19 (Benoit et al. Nature Medicine 2017) and postprandial LPS (Vors et al. JCEM 2015) can impact metabolism.
The techniques of bariatric surgery can have different metabolic consequences and complications (Robert et al. The Lancet 2019).
Adipose tissue stem cells are major mediators of nutrition mediated inflammation during obesity (Lefevre et al. FASEB J 2021, Eljaafari et al. Cells 2021).

Objectives

Decipher the role in health and diseases of complex nutrient structures (both in real foods and in formulated/processed foods) and of additives, ingredients or pollutants, via their impact in the gut (including absorption, barrier functions, microbiota),
Propose innovative strategies of metabolic disease prevention and cure focusing the gut (including microbiota modulation and bariatric surgery).

These processes will be explored in important pathophysiological situations where nutrition is critical (e.g. metabolic diseases, chronic kidney disease, GI diseases, management of aged patients, as well as pediatric nutritional diseases, …).

Our research includes:

Dietary polar lipids of animal (milk polar lipids, sphingolipids) and plant-based (lecithins, galactolipids, etc.) origin.
“Slow vs. Fast” lipids (more or less emulsified and/or rigid vs. liquid) in food matrices.
Prebiotics, slowly digestible starch, polyphenols, bioactive lipids and multifunctional synergistic strategies targeting different components of cardiometabolic risk
Probiotics for the treatment of type 2 diabetes and other metabolic diseases, chronic kidney disease, and for growth stimulation
Metabolic mediators of intestinal origin and their impacts and modulation through nutrition and metabolic status: FGF19 as prevention agent of sarcopenia, bile acids, metabolic endotoxemia, identification of new biomarkers of food-microbiota interactions.
Personalized bariatric medicine, surgical innovation and safety, dietary behaviour and nutritional management strategies.
Impacts on adipose tissue and stem cells: immunological and metabolic phenotyping, understanding of mechanisms and functional regulation.
Mathematical modelling of lipid absorption and postprandial response.

Biological resources & research models

Human intestinal cell lines: enterocytes (Caco-2/TC7), goblet cells/colon (HT29-MTX, HT29, LS-174).
Human breast cancer cell lines.
Mesenchymal, adipose or bone marrow stem cells, human or murine.
Peripheral blood mononuclear cells.
Mouse models of diet-induced obesity in adulthood or during perinatal life, T2D and NAFLD (male/female), intestinal inflammation (DSS) and derived tissues after different treatments (diets, pro-/prebiotics, pollutants, etc.).
PXR KO (liver, intestine) mouse models (male/female) and derived tissues after exposure to pollutants.
Mouse models of chronic kidney disease and tissues of these mice.
Human biological matrices (plasma, lipoproteins, urine, stool, expired air) from our biobanks and clinical studies.

Team DO-IT : "Diet and food matrix in Obesity and metabolic diseases: role of Intestinal tract and innovative Therapeutics"

Objectives

Biological resources & research models

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