Abstract
OBJECTIVE Debate continues regarding the influence of dietary fats and sugars on the risk of developing metabolic diseases, including insulin resistance and nonalcoholic fatty liver disease (NAFLD). We investigated the effect of two eucaloric diets, one enriched with saturated fat (SFA) and the other enriched with free sugars (SUGAR), on intrahepatic triacylglycerol (IHTAG) content, hepatic de novo lipogenesis (DNL), and whole-body postprandial metabolism in overweight males. RESEARCH DESIGN AND METHODS Sixteen overweight males were randomized to consume the SFA or SUGAR diet for 4 weeks before consuming the alternate diet after a 7-week washout period. The metabolic effects of the respective diets on IHTAG content, hepatic DNL, and whole-body metabolism were investigated using imaging techniques and metabolic substrates labeled with stable-isotope tracers. RESULTS Consumption of the SFA diet significantly increased IHTAG by mean 6 SEM 39.0 6 10.0%, while after the SUGAR diet IHTAG was virtually unchanged. Consumption of the SFA diet induced an exaggerated postprandial glucose and insulin response to a standardized test meal compared with SUGAR. Although whole-body fat oxidation, lipolysis, and DNL were similar following the two diets, consumption of the SUGAR diet resulted in significant (P < 0.05) decreases in plasma total, HDL, and non-HDL cholesterol and fasting b-hydroxybutyrate plasma concentrations. CONCLUSIONS Consumption of an SFA diet had a potent effect, increasing IHTAG together with exaggerating postprandial glycemia. The SUGAR diet did not influence IHTAG and induced minor metabolic changes. Our findings indicate that a diet enriched in SFA is more harmful to metabolic health than a diet enriched in free sugars.
| Original language | English |
|---|---|
| Pages (from-to) | 1134-1141 |
| Number of pages | 8 |
| Journal | Diabetes Care |
| Volume | 43 |
| Issue number | 5 |
| Early online date | 12 Mar 2020 |
| DOIs | |
| Publication status | Published - 1 May 2020 |
Bibliographical note
Funding Information:Acknowledgments. The authors thank Louise Dennis and Rachel Craven-Todd (Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford) and all Clinical Research Unit staff for excellent nursing provision, Ruth Coleman (Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford) for helpful statistical advice and technical assistance, and Niall Dempster and Lia Anguelova (Oxford Centre for Diabetes, Endocrinology and Metabolism,UniversityofOxford) for providing medicalsupportduringstudydays.Theauthors thank Naira Beraza (Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford) of the Quadram Institute for assistance with the analysis of bile acids. The authors thank the volunteers from the Oxford BioBank (www.oxfordbiobank.org.uk) for their participation in this recall study. Funding. L.H. is a British Heart Foundation (BHF) Senior Fellow in Basic Science. This study was funded by the World Sugar Research Organisation and Biotechnology and Biological Sciences Research Council (BB/N005600/1) and the BHF FS/15/56/31645 (L.H.). F.R. is supported by Henning and Johan Throne-Holsts Foundation, Swedish Society for Medical Research, Swedish Society of Medicine, and The Foundation Blanceflor. M.-E.P. was the recipient of a fellowship grant from Fonds de Recherche du Québec-Santé and the Heart and Lung Institute Foundation. The Oxford BioBank and Oxford BioResource are funded by the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre. P.D. is a member (unpaid) of the joint Scientific Advisory Committee on Nutrition/NHS England/Diabetes UK working group to review the evidence on lower carbohydrate diets compared with current government advice for adults with T2D.
Funding Information:
The authors thank Louise Dennis and Rachel Craven-Todd (Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford) and all Clinical Research Unit staff for excellent nursing provision, Ruth Coleman (Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford) for helpful statistical advice and technical assistance, and Niall Dempster and Lia Anguelova (Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford) for providing medical support during study days. The authors thank Naira Beraza (Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford) of the Quadram Institute for assistance with the analysis of bile acids. The authors thank the volunteers from the Oxford BioBank (www.oxfordbiobank.org.uk) for their participation in this recall study. Senior Fellow in Basic Science. This study was funded by the World Sugar Research Organisation and Biotechnology and Biological Sciences Research Council (BB/N005600/1) and the BHF FS/15/56/31645 (L.H.). F.R. is supported by Henning and Johan Throne-Holsts Foundation, Swedish Society for Medical Research, Swedish Society of Medicine, and The Foundation Blanceflor. M.-E.P. was the recipient of a fellowship grant from Fonds de Recherche du Québec-Santé and the Heart and Lung Institute Foundation. The Oxford BioBank and Oxford BioResource are funded by the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre. P.D. is a member (unpaid) of the joint Scientific Advisory Committee on Nutrition/NHS England/Diabetes UK working group to review the evidence on lower carbohydrate diets compared with current government advice for adults with T2D. The conduct of the trial, data analyses, and writing of the manuscript were all undertaken by the authors and were completely independent from the World Sugar Research Organisation. The views expressed are those of the author(s) and not necessarily those of the NIHR or the Department of Health and Social Care.
Publisher Copyright:
© 2020 by the American Diabetes Association.