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Consumption of fructose-sweetened beverages for 10 weeks reduces net fat oxidation and energy expenditure in overweight/obese men and women
Open accessAbstract
Background/objectives The results of short-term studies in humans suggest that, compared with glucose, acute consumption of fructose leads to increased postprandial energy expenditure and carbohydrate oxidation and decreased postprandial fat oxidation. The objective of this study was to determine the potential effects of increased fructose consumption compared with isocaloric glucose consumption on substrate utilization and energy expenditure following sustained consumption and under energy-balanced conditions.Subjects/methods As part of a parallel arm study, overweight/obese male and female subjects, 40-72 years, consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Energy expenditure and substrate utilization were assessed using indirect calorimetry at baseline and during the 10th week of intervention.Results Consumption of fructose, but not glucose, led to significant decreases of net postprandial fat oxidation and significant increases of net postprandial carbohydrate oxidation (P<0.0001 for both). Resting energy expenditure (REE) decreased significantly from baseline values in subjects consuming fructose (P=0.031) but not in those consuming glucose.Conclusions Increased consumption of fructose for 10 weeks leads to marked changes of postprandial substrate utilization including a significant reduction of net fat oxidation. In addition, we report that REE is reduced compared with baseline values in subjects consuming fructose-sweetened beverages for 10 weeks.
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“fructose contained in sugar sweetened beverages is suggested to likely induce the onset of obesity by reducing resting energy expenditure and promoting leptin resistance.102 103”
From Dietary sugar consumption and health: umbrella review (2023) · cites this paper as [102]
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Dietary treatment of nonalcoholic steatohepatitis
Perito, E. R., Rodríguez, L. A., & Lustig, R. H. (2012) · Current Opinion in Gastroenterology · doi:10.1097/mog.0b013e32835ca11d · Cited by 20
“The largest decreases in postprandial fat oxidation rates were in individuals with metabolic syndrome.[59] In adults, high-fructose diets exacerbate dyslipidemia and insulin resistance more than isocaloric highglucose diets, with effects most pronounced on adults who already have metabolic syndrome.”
BackgroundChronic arsenic exposure impairs adaptive thermogenesis in male C57BL/6J mice
Castriota, F., Zushin, P. H., Sanchez, S. S., Phillips, R. V., Hubbard, A., Stahl, A., Smith, M. T., Wang, J.-C., & Merrill, M. A. L. (2020) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00282.2019 · Cited by 18
Sugar and Dyslipidemia: A Double-Hit, Perfect Storm
Gugliucci, A. (2023) · Journal of Clinical Medicine · doi:10.3390/jcm12175660 · Cited by 19
“The main solid ingredient in fruit juices is also free sugar, which can range in concentration from 100 to 120 g/L, depending on the type and quality of the fruit [20,41,48,49].”
BackgroundSigala, D. M., Hieronimus, B., Medici, V., Lee, V., Nuñez, M. V., Bremer, A. A., Cox, C. L., Price, C. A., Benyam, Y., Abdelhafez, Y. G., et al. (2022) · Nutrients · doi:10.3390/nu14081648 · Cited by 17
“Fructose and/or its metabolites induce expression of sterol regulatory element binding protein 1c (SREBP-1c) and carbohydrate response element binding protein (ChREBP) and lead to increased de novo lipogenesis (DNL) [37,38] and apolipoprotein CIII (apoCIII) production [38,39], and decreased fat oxidation [10,40].”
BackgroundSelf-citationQuintana‐Castro, R., Aguirre-Maldonado, I., Soto-Rodríguez, I., Lago, R. A. D., Gruber-Pagola, P., de Larrea, Y. K. U., Juárez-Rivera, V. E., Ramos-Manuel, L. E., & Alexander-Aguilera, A. (2019) · Prostaglandins & Other Lipid Mediators · doi:10.1016/j.prostaglandins.2019.106404 · Cited by 18
Eekelen, E. W.-V., Beulens, J. W. J., Geelen, A., Schrauwen‐Hinderling, V. B., Lamb, H. J., Roos, A., Rosendaal, F. R., & de Mutsert, R. (2018) · Journal of Nutrition · doi:10.1093/jn/nxy313 · Cited by 17
“Moreover, chronic fructose consumption has been shown to decrease resting energy expenditure in a 10-wk trial (59).”
BackgroundStookey, J. D., Hamer, J., Espinoza, G., Higa, A., Ng, V., Tinajero-Deck, L., Havel, P. J., & King, J. C. (2012) · Advances in Nutrition · doi:10.3945/an.112.001990 · Cited by 18
“The significantly lower fat oxidation 30 min after breakfast with orange juice in the adults may therefore reflect noninsulinmediated effects of fructose availability (50) or other factors such as gastric emptying, nutrient absorption, insulin sensitivity, glycogen stores, acid/base balance, cortisol, and hydration st…”
BackgroundSelf-citationImpact of dietary glycemic challenge on fuel partitioning
Bosy‐Westphal, A., Hägele, F. A., & Nas, A. (2016) · European Journal of Clinical Nutrition · doi:10.1038/ejcn.2016.230 · Cited by 16
Thompson, Z., Kolb, E. M., & Garland, T. (2017) · Behavioural Processes · doi:10.1016/j.beproc.2017.11.004 · Cited by 15
“Recent studies have shown that fructose can suppress home-cage activity in rodents (Rendeiro et al., 2015) and decrease energy expenditure in humans (Cox et al., 2012).”
Jurado‐Fasoli, L., Amaro‐Gahete, F. J., Merchán-Ramírez, E., Labayen, I., & Ruiz, J. R. (2020) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2020.11.021 · Cited by 15
Monar, G. V. F., Cruz, C. S., & Martinez, E. C. (2025) · Journal of Nutrition and Metabolism · doi:10.1155/jnme/5571686 · Cited by 14
Comparison of aspartame- and sugar-sweetened soft drinks on postprandial metabolism
Pearson, R. C., Green, E. S., Olenick, A. A., & Jenkins, N. T. (2023) · Nutrition and Health · doi:10.1177/02601060211057415 · Cited by 12
Butcko, A. J., Putman, A. K., & Mottillo, E. P. (2024) · Antioxidants · doi:10.3390/antiox13010087 · Cited by 12
“…through decreased expression of fatty acid oxidation genes (i.e., PPAR α ) as well as direct effects on modifying the mitochondrial proteome [64,65]. fructose reduces fa tt y acid oxidation through decreased expression of fa tt y acid oxidation genes (i.e., PPAR α ) as well as direct e ff…”
BackgroundFructose: metabolic signal and modern hazard
Johnson, R. J., Lanaspa, M. A., Tolan, D. R., Goncalves, M. D., Softic, S., Stanhope, K. L., Sánchez‐Lozada, L. G., Herman, M. A., & Rabinowitz, J. D. (2026) · Nature Metabolism · doi:10.1038/s42255-026-01506-y · Cited by 13
“The decrease in fatty acid oxidation following fructose ingestion is distinct from glucose and is greatest in the postprandial period 37,38 , and may be mediated, in part, by fructose’s ability to increase hepatocellular malonyl-CoA, which drives fatty acid synthesis and inhibits fat oxidation…”
InfluentialSelf-citationSmeraglio, A., Kennedy, E. K., Horgan, A., Purnell, J. Q., & Gillingham, M. B. (2013) · Nutrition Research · doi:10.1016/j.nutres.2013.03.007 · Cited by 11
“Recently, fructose consumption has also been shown to decrease fat oxidation in obese subjects fed a high fructose diet over a tenweek period [20].”
BackgroundLiu, Z., Huang, H., Xie, J., Hou, L., & Xu, C. (2023) · Nutrition Journal · doi:10.1186/s12937-023-00897-y · Cited by 10
“Studies in humans and animals have reported that fructose promotes de novo lipogenesis and inhibits 𝛽 -fatty acid oxidation in the liver [30–32].”
BackgroundWu, H., Li, S., Chen, L., Yang, X., & Tan, X. W. (2024) · Food & Function · doi:10.1039/d3fo04602h · Cited by 11
Gugliucci, A. (2024) · Journal of Clinical Medicine · doi:10.3390/jcm13175229 · Cited by 10
Precision nutrition for obesity management: A gut microbiota–centered weight-loss approach
Carvalho, L. M., da Mota, J. C. N. L., Ribeiro, A., Carvalho, B. G., Martínez, J. A., & Nicoletti, C. F. (2025) · Nutrition · doi:10.1016/j.nut.2025.112892 · Cited by 10
Ibrahim, M. A., Bonfiglio, S. M., Schlögl, M., Vinales, K. L., Piaggi, P., Venti, C. A., Walter, M. F., Krakoff, J. A., & Thearle, M. S. (2017) · Obesity · doi:10.1002/oby.22068 · Cited by 9
“Contrary to our findings, a study assessing EE responses to long-term consumption of glucose- versus fructose-sweetened beverages in subjects with overweight found that consuming fructose was associated with reductions in resting EE over a 10-week period (26), so it is possible that longer-term feeding with our diets…”
ResultChan, W., Smith, B. H., Stegall, M. D., & Borrows, R. (2018) · Transplantation · doi:10.1097/tp.0000000000002424 · Cited by 8
Macedo, R. C. O., Vieira, A., Moritz, C. E. J., & Reischak-Oliveira, Á. (2018) · British Journal Of Nutrition · doi:10.1017/s0007114518001538 · Cited by 10
“Moreover, it is associated with the reduction of liver sensitivity to insulin (49) , even at moderate doses (40g/d) (19) , and decrease of fat oxidation (50) .”
Understanding the Impact of Added Sugar Consumption on Risk for Type 2 Diabetes
Price, C. A., & Stanhope, K. L. (2016) · Journal of the California Dental Association · doi:10.1080/19424396.2016.12221068 · Cited by 9
Self-citationDietary Fructose: A Literature Review of Current Evidence and Implications on Metabolic Health
Agarwal, V., Das, S., Kapoor, N., Prusty, B., & Das, B. (2024) · Cureus · doi:10.7759/cureus.74143 · Cited by 9
Fructose and Nonalcoholic Fatty Liver Disease
Lustig, R. H. (2016) · Journal of the California Dental Association · doi:10.1080/19424396.2016.12221067 · Cited by 7
What should we advise MAFLD patients to eat and drink?
Machado, M. V. (2021) · Metabolism and Target Organ Damage · doi:10.20517/mtod.2021.11 · Cited by 7
Fructose-containing sugars and metabolic risk: a systematic review and meta-analysis
Prasetya, G., Astina, J., Palupi, E., Namkieat, P., Jiamjarasrangsi, W., & Sapwarobol, S. (2025) · Food & Nutrition Research · doi:10.29219/fnr.v69.11062 · Cited by 7
“These results are inconsistent with prior research suggesting that free fructose may pose a greater risk for metabolic syndrome components than sucrose (29).”
Cohen, C. C., Dabelea, D., Michelotti, G. A., Tang, L., Shankar, K., Goran, M. I., & Perng, W. (2022) · Metabolites · doi:10.3390/metabo12060559 · Cited by 6
“Fructose intake may also alter hepatic lipid metabolism by stimulating lipogenic gene expression via the activation of several transcriptional activator families, including carbohydrateresponsive element-binding protein (ChREBP), sterol regulatory element-binding protein (SREBP), and peroxisome proliferator-activated…”
BackgroundHyer, M. M., Dyer, S. K., Kovalchick, L. V., Targett, I. L., Burns, C. M., Kloster, A., Wegener, A. J., Salome-Sanchez, C., & Neigh, G. N. (2022) · Psychoneuroimmunology Journal · doi:10.32371/pnij/246142 · Cited by 6
Brown, M., & Matveyenko, A. V. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.842603 · Cited by 7
“Despite differing perspectives on the dietary etiology of T2DM, long-term ingestion of a diet rich in saturated fatty acids and/or refined sugars has been clearly demonstrated to lead to increased visceral adiposity (57, 58), reduced energy expenditure (59, 60), peripheral insulin resistance (61, 62), and pancreatic i…”
Background
Metadata
- Authors
- Cox, C. L., Stanhope, K. L., Schwarz, J. M., Graham, J. L., Hatcher, B., Griffen, S. C., Bremer, A. A., Berglund, L., McGahan, J. P., Havel, P. J., & Keim, N. L.
- Affiliations
- University of California, Davis (US)
- Touro University California (US)
- Vanderbilt University (US)
- United States Department of Agriculture (US)
- Corresponding author
- Keim, N L
- Venue
- European Journal of Clinical Nutrition
- Published
- 2011-09-28
- Volume
- 66
- Issue
- 2
- Pages
- 201-208
- ISSN
- 0954-3007 (ISSN-L)
- 1476-5640
- PMC
- PMC3252467
- OpenAlex
- W2121517321
- Cited by
- 132
- References
- 30
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 5 · 2023: 11 · 2022: 13 · 2021: 5 · 2020: 9 · 2019: 12 · 2018: 11 · 2017: 7 · 2016: 6 · 2015: 14 · 2014: 10 · 2013: 11 · 2012: 6
- FWCI
- 7.34
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- European Journal of Clinical Nutrition (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- American Diabetes Association (UL1 RR024146)
- U.S. Department of Agriculture (5306‐51530‐019‐00D, UL1 RR024146, 5306‐51530‐019)
- National Institutes of Health (5r01hl075675-05, 5r01hl091333-02, HL‐091333, RR024146)
- University of California, Davis (RR024146, UL1 RR024146)
- Agricultural Research Service
- National Heart, Lung, and Blood Institute (R01 HL-075675, R01 HL-091333, HL-091333, R01HL107256)
- National Center for Research Resources (UL1RR024146)
- National Center for Complementary and Integrative Health (AT0-02993, AT0-03545, AT 002599, R21AT002993, R21AT002599)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Nursing › Nutrition and Dietetics › Muscle metabolism and nutrition
- Keywords
- fructose, glucose, fat oxidation, energy expenditure, resting energy expenditure, substrate utilization, carbohydrate oxidation, overweight, obesity, energy balance, postprandial metabolism
- MeSH terms
- Aged, Basal Metabolism, Beverages, Energy Intake, Energy Metabolism, Female, Fructose, Glucose, Humans, Male, Middle Aged, Obesity, Oxidation-Reduction, Sweetening Agents, Dietary Sucrose, Carbohydrate Metabolism, Lipid Metabolism
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