Lactose and sucrose each stimulate hepatic de novo lipogenesis: A randomized crossover trial

Résumé fourni par la source

ABSTRACT Background Fructose-containing sugars can exaggerate postprandial lipaemia and stimulate hepatic de novo lipogenesis (DNL) relative to glucose-based carbohydrates. Despite being consumed by most of the global population, the effects of galactose-containing sugars on hepatic DNL are currently unknown. Objective To assess the effects of lactose ingestion on lipaemia and DNL. Methods Twenty-four adults without obesity (12 male and 12 female) completed three laboratory visits in a randomised, crossover design (33±14-day washout; mean±SD). During laboratory visits, participants consumed beverages containing 50g fat with 100g of carbohydrate. The control carbohydrate was a glucose polymer (maltodextrin), the experimental carbohydrate was galactose-containing carbohydrate (lactose) and the active comparator was fructose-containing carbohydrate (sucrose). Hepatic DNL was assessed by the 2 H 2 O method and [U- 13 C]-palmitate was added to the test drink to trace the fate of the ingested fat. Blood and breath samples were taken to determine plasma metabolite and hormone concentrations, in addition to plasma and breath 2 H and 13 C enrichments. Summary statistics were analysed by one-way ANOVA, and time series data by two-way (time x treatment) ANOVA or linear mixed models when data were missing. Results The plasma triacylglycerol iAUC (mean±SD) in response to maltodextrin was 0.85±1.13mmol·L -1 ·360 min and peak hepatic DNL was 11±3%. Following lactose ingestion, plasma triacylglycerol iAUC increased to 1.63±1.47mmol·L -1 ·360 min ( p <0.001 versus maltodextrin), and hepatic DNL increased to 22±4% ( p <0.001 versus maltodextrin), to a degree statistically indistinguishable from following sucrose ingestion [1.50±1.58mmol/L -1 ·360 min ( p =0.41 versus lactose); and 23±4% ( p =0.54 versus lactose)]. Contributions of dietary fat to VLDL- and Chylomicron-TG-palmitate were both higher following ingestion of lactose versus maltodextrin (both p <0.05), and were statistiscally indistinguishable following lactose ingestion versus sucrose (both p >0.05). Conclusions Lactose ingestion stimulates hepatic DNL by a magnitude that is not statistically different from fructose. This challenges the prevailing view that galactose-containing sugars are metabolically equivalent to glucose-based carbohydrates. Clinical Trials Registration: NCT04924530 ( https://clinicaltrials.gov/study/NCT04924530 ).

Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.