Metabolic Fate of Fructose Ingested with and without Glucose in a Mixed Meal

Nutrients

Fanny Theytaz³  Sara de Giorgi³  Leanne Hodson¹  Nathalie Stefanoni³  Valentine Rey³  Philippe Schneiter³  Vittorio Giusti² 

[1] Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford OX3 7LE, UK; E-Mail:;Service of Endocrinology, Diabetes and Metabolism, Lausanne University Hospital, CH-1011 Lausanne, Switzerland; E-Mail:;Department of Physiology, University of Lausanne, rue du Bugnon 7, CH-1005 Lausanne, Switzerland; E-Mails:

关键词: fructose oxidation;    gluconeogenesis;    glucose production;    de novo lipogenesis;    hepatic;    intestinal;    sugar;   

DOI  :  10.3390/nu6072632

来源: mdpi

【 摘 要 】

Ingestion of pure fructose stimulates de novo lipogenesis and gluconeogenesis. This may however not be relevant to typical nutritional situations, where fructose is invariably ingested with glucose. We therefore assessed the metabolic fate of fructose incorporated in a mixed meal without or with glucose in eight healthy volunteers. Each participant was studied over six hours after the ingestion of liquid meals containing either ¹³C-labelled fructose, unlabeled glucose, lipids and protein (Fr + G) or ¹³C-labelled fructose, lipids and protein, but without glucose (Fr), or protein and lipids alone (ProLip). After Fr + G, plasma ¹³C-glucose production accounted for 19.0% ± 1.5% and ¹³CO2 production for 32.2% ± 1.3% of ¹³C-fructose carbons. After Fr, ¹³C-glucose production (26.5% ± 1.4%) and ¹³CO₂ production (36.6% ± 1.9%) were higher (p < 0.05) than with Fr + G. ¹³C-lactate concentration and very low density lipoprotein VLDL ¹³C-palmitate concentrations increased to the same extent with Fr + G and Fr, while chylomicron ¹³C-palmitate tended to increase more with Fr + G. These data indicate that gluconeogenesis, lactic acid production and both intestinal and hepatic de novo lipogenesis contributed to the disposal of fructose carbons ingested together with a mixed meal. Co-ingestion of glucose decreased fructose oxidation and gluconeogenesis and tended to increase ¹³C-pamitate concentration in gut-derived chylomicrons, but not in hepatic-borne VLDL-triacylglycerol (TG). This trial was approved by clinicaltrial. gov. Identifier is NCT01792089.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland.