Malnutrition

La malnutrition est un état physiopathologique résultant de l'influence combinée de la sur- ou sous-nutrition (déficience ou excès de calories ou d’un ou plusieurs nutriments) et d'autres facteurs (génétiques, inflammatoires…) sur la composition du corps et sur ses fonctions biologiques. Son origine peut être une quantité de nourriture inadaptée au besoin (apport calorique insuffisant ou excessif) ou l'ingestion d'aliments de mauvaise qualité (carences nutritionnelles ou excès de sucre, de protéines, de sel, de graisses…) ; d'autres facteurs, notamment psychologiques et pathologiques, interviennent également. La maigreur squelettique, symbole habituel de la malnutrition, illustre les effets de la sous-nutrition, mais la malnutrition prend bien d'autres formes, dont l'obésité. Quels que soient la forme et le poids du corps, une personne peut être malnutrie. Et, qu'une personne ait une allure maigre, normale ou obèse n'indique pas l'état de malnutrition. La malnutrition n'est pas la

Gut physiology mediates a trade-off between adaptation to malnutrition and susceptibility to food-borne pathogens

Sveta Chakrabarti, Sylvain Kolly, Bruno Lemaitre

The animal gut plays a central role in tackling two common ecological challenges, nutrient shortage and food-borne parasites, the former by efficient digestion and nutrient absorption, the latter by acting as an immune organ and a barrier. It remains unknown whether these functions can be independently optimised by evolution, or whether they interfere with each other. We report that Drosophila melanogaster populations adapted during 160 generations of experimental evolution to chronic larval malnutrition became more susceptible to intestinal infection with the opportunistic bacterial pathogen Pseudomonas entomophila. However, they do not show suppressed immune response or higher bacterial loads. Rather, their increased susceptibility to P.entomophila is largely mediated by an elevated predisposition to loss of intestinal barrier integrity upon infection. These results may reflect a trade-off between the efficiency of nutrient extraction from poor food and the protective function of the gut, in particular its tolerance to pathogen-induced damage.

Wiley-Blackwell2015

Vitamin B12 deficiency and impaired expression of amnionless during aging

Laurence Goulet, Sonia Karaz, Alice Pannerec

Background Physical frailty and loss of mobility in elderly individuals lead to reduced independence, quality of life, and increased mortality. Vitamin B12 deficiency has been linked to several age-related chronic diseases, including in the musculo-skeletal system, where vitamin B12 deficiency is generally believed to be linked to poor nutritional intake. In the present study, we asked whether aging and frailty associate with altered vitamin B12 homeostasis in humans and investigated the underlying molecular mechanisms using preclinical models. Methods We analysed a subset of the Singapore Longitudinal Aging Study and stratified 238 participants based on age and Fried frailty criteria. Levels of methyl-malonic acid (MMA), a marker for vitamin B12 deficiency, and amnionless, the vitamin B12 co-receptor that anchors the vitamin B12 transport complex to the membrane of epithelial cells, were measured in plasma. In addition, vitamin B12 levels and the molecular mechanisms of vitamin B12 uptake and excretion were analysed in ileum, kidney, liver, and blood using a rat model of natural aging where nutritional intake is fully controlled. Results We demonstrate that aging and frailty are associated with a higher prevalence of functional vitamin B12 deficiency that can be detected by increased levels of MMA in blood (rho = 0.25; P = 0.00013). The decline in circulating vitamin B12 levels is recapitulated in a rat model of natural aging where food composition and intake are stable. At the molecular level, these perturbations involve altered expression of amnionless in the ileum and kidney. Interestingly, we demonstrate that amnionless can be detected in serum where its levels increase during aging in both rodents and human (P = 3.3e-07 and 9.2e-07, respectively). Blood amnionless levels negatively correlate with vitamin B12 in rats (r(2) = 0.305; P = 0.0042) and positively correlate with the vitamin B12 deficiency marker MMA in humans (rho = 0.22; P = 0.00068). Conclusions Our results demonstrate that aging and frailty cause intrinsic vitamin B12 deficiencies, which can occur independently of nutritional intake. Mechanistically, vitamin B12 deficiency involves the physio-pathological decline of both the intestinal uptake and the renal reabsorption system for vitamin B12. Finally, amnionless is a novel biomarker which can detect perturbed vitamin B12 bioavailability during aging and physical frailty.

2018

Vitamin B12 deficiency and impaired expression of amnionless during aging

Laurence Goulet, Sonia Karaz, Alice Pannerec

2018

Effects of chronic undernutrition on insulin and on the insulin-like growth factor system during ovarian folliculogenesis in mares

Gut physiology mediates a trade-off between adaptation to malnutrition and susceptibility to food-borne pathogens

Vitamin B12 deficiency and impaired expression of amnionless during aging

Gut physiology mediates a trade-off between adaptation to malnutrition and susceptibility to food-borne pathogens

Effects of chronic undernutrition on insulin and on the insulin-like growth factor system during ovarian folliculogenesis in mares

Vitamin B12 deficiency and impaired expression of amnionless during aging