Nutrition

Ingestion of a high-fructose meal increases blood uric acid (UA) concentration in healthy humans. Individuals presenting with homozygous mutation of ALDOB gene coding for Aldolase B, one of the key enzyme in fructose metabolism, develop acute, life-threatening disorders when exposed to fructose due to ATP depletion in hepatocytes and proximal kidney tubule cells. Clinically individuals develop acute hypoglycaemia, renal tubular acidosis and hyperuricemia. Deficiency of aldolase B due to homozygous mutation of ALDOB gene (Hereditary Fructose Intolerance or HFI) is observed in 1: 20 000 birth in Europe, but the incidence of carriers of one mutated allele of the gene is relatively frequent in the general population (ca 1 in 70). Although carriers have no reported metabolic defects it was reported that they had enhanced uric acid response for iv fructose. We therefore hypothesized that carriers of ALDOB mutations may have higher sensitivity to adverse effects of fructose than the general population. In a first study we investigated 8 heterozygous subjects for HFI. UA response to oral fructose was significantly increased in heterozygous subjects for HFI and this study was recently published in the American Journal of Clinical Nutrition [1]. It is well known that stimulation of de novo lipogenesis occurs during prolonged exposure to dietary fructose, and an experimental design including an exposure to dietary fructose over several days may be needed to document differences between HFI and Controls. In order to look for the potentiation of the adverse effects of fructose on cardiometabolic risk factors, we currently realize a 2nd study. The purpose of this study is to evaluate whether consumption of a fructose-enriched 7 days controlled diet could reveal 1) the occurrence of hyperuricemia, dyslipidemia and glucose intolerance, and 2) renal functional impairment and increased intermediate metabolism (energetic) in HFI subjects.

[1] Are heterozygous carriers for hereditary fructose intolerance predisposed to metabolic disturbances when exposed to fructose? Debray FG, Damjanovic K, Rosset R, Mittaz-Crettol L, Roux C, Braissant O, Barbey F, Bonafé L, De Bandt JP, Tappy L, Paquot N, and Tran C. Am J Clin Nutr. 2018, 108:1–8.

We are also involved in several collaborative studies in the field of human nutrition. The project untitled Food4Gut is granted by the Walloon Region as part of a research program of general interest in novel nutritional approach to obesity, based on colonic nutrient supply, investigating biological, behavioral and societal aspects. In our department, we tested the hypothesis that the modification of the microbiota via colonic nutrient supplementation accompanied by dietary advice provided to encourage the consumption of vegetables rich in these colonic nutrients, could modulate the feeding behavior, the body composition, inflammation and comorbidities associated with obesity. The experiments are already done (> 40 obese subjects with colonic nutrient supplementation during 3 months) and analyzes are ongoing.

Another collaboration is developed with the Public Health department of Liege University. Nutrition is an important life-style factor contributing to health and functional disability in elderly people. Malnutrition can result from insufficient energetic intake and / or increased energetic expenditure. We performed some studies in order to investigate these aspects. The Measurement of food intake of elderly individuals in geriatric institutions gave important informations, for clinical or research purposes, to assess the effect of diet on health. The assessment of energy expenditure is also important and we investigated also this problem in nursing home residents using indirect calorimetry and compared the energy expenditure with energy intake. Others studies are currently underway.