Effect of short-term carbohydrate overfeeding and long-term weight loss on liver fat in overweight humans
Open accessAbstract
Background Cross-sectional studies have identified a high intake of simple sugars as an important dietary factor predicting nonalcoholic fatty liver disease (NAFLD).Objective We examined whether overfeeding overweight subjects with simple sugars increases liver fat and de novo lipogenesis (DNL) and whether this is reversible by weight loss.Design Sixteen subjects [BMI (kg/m²): 30.6 ± 1.2] were placed on a hypercaloric diet (>1000 kcal simple carbohydrates/d) for 3 wk and, thereafter, on a hypocaloric diet for 6 mo. The subjects were genotyped for rs739409 in the PNPLA3 gene. Before and after overfeeding and after hypocaloric diet, metabolic variables and liver fat (measured by proton magnetic resonance spectroscopy) were measured. The ratio of palmitate (16:0) to linoleate (18:2n-6) in serum and VLDL triglycerides was used as an index of DNL.Results Carbohydrate overfeeding increased weight (±SEM) by 2% (1.8 ± 0.3 kg; P < 0.0001) and liver fat by 27% from 9.2 ± 1.9% to 11.7 ± 1.9% (P = 0.005). DNL increased in proportion to the increase in liver fat and serum triglycerides in subjects with PNPLA3-148IIbut not PNPLA3-148MM. During the hypocaloric diet, the subjects lost 4% of their weight (3.2 ± 0.6 kg; P < 0.0001) and 25% of their liver fat content (from 11.7 ± 1.9% to 8.8 ± 1.8%; P < 0.05).Conclusions Carbohydrate overfeeding for 3 wk induced a >10-fold greater relative change in liver fat (27%) than in body weight (2%). The increase in liver fat was proportional to that in DNL. Weight loss restores liver fat to normal. These data indicate that the human fatty liver avidly accumulates fat during carbohydrate overfeeding and support a role for DNL in the pathogenesis of NAFLD. This trial was registered at www.hus.fi as 235780.
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One of the more promising gene-diet interactions, notable in Hispanic populations, involves PNPLA3 and sugar consumption in relation to obesity and liver fat accumulation.
“One of the more promising gene-diet interactions, notable in Hispanic populations, involves PNPLA3 and sugar consumption in relation to obesity and liver fat accumulation;84-86”
From Dietary and Policy Priorities for Cardiovascular Disease, Diabetes, and Obesity: A Comprehensive Review (2016) · cites this paper as [85]
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“As an example, overfeeding for only 3 weeks can increase liver fat by 27 percent, while total body weight increases by only 2 percent (34).”
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“This effect was recently examined by measuring liver fat accumulation following 3 weeks of carbohydrate overfeeding (1000 extra kcal/day) in overweight individuals with the PNPLA3 geneotype rs738409 [43], which influences the prevalence of fatty liver [44].”
BackgroundTaskinen, M., Söderlund, S., Bogl, L. H., Hakkarainen, A., Matikainen, N., Pietiläinen, K. H., Räsänen, S., Lundbom, N. M. I., Björnson, E., Eliasson, B., et al. (2017) · Journal of Internal Medicine · doi:10.1111/joim.12632 · Cited by 118 · see citing works
Self-citationGenetics of nonalcoholic fatty liver disease
Dongiovanni, P., & Valenti, L. V. C. (2015) · Metabolism · doi:10.1016/j.metabol.2015.08.018 · Cited by 115 · see citing works
“[64] Sevastianova K, Santos A, Kotronen A, Hakkarainen A, Makkonen J, Silander K, et al.”
BackgroundVreman, R. A., Goodell, A. J., Rodríguez, L. A., Porco, T. C., Lustig, R. H., & Kahn, J. G. (2017) · BMJ Open · doi:10.1136/bmjopen-2016-013543 · Cited by 115 · see citing works
“48 For instance, added sugar is directly correlated with risk for metabolic syndrome in adolescents in the National Health and Nutrition Examination Survey (NHANES) even after controlling for total calories and BMI z-score.”
BackgroundStiede, K., Miao, W., Blanchette, H., Beysen, C., Harriman, G. C. B., Harwood, H. J., Kelley, H., Kapeller, R., Schmalbach, T., & Westlin, W. (2017) · Hepatology · doi:10.1002/hep.29246 · Cited by 114 · see citing works
“There exists both indirect and direct evidence that elevated lipogenesis provides a significant source of the fatty acids accumulating in the livers of patients with NAFLD.”
BackgroundMondo-Mlx Mediates Organismal Sugar Sensing through the Gli-Similar Transcription Factor Sugarbabe
Mattila, J., Havula, E., Suominen, E., Teesalu, M., Surakka, I. L., Hynynen, R., Kilpinen, H., Väänänen, J., Hovatta, I., Käkelä, R., et al. (2015) · Cell Reports · doi:10.1016/j.celrep.2015.08.081 · Cited by 109 · see citing works
“While genetic variants are known to interact with diet in this setting (Sevastianova et al., 2012), our understanding of the underlying mechanisms remains limited.”
BackgroundFatty acid metabolism is altered in non-alcoholic steatohepatitis independent of obesity
Walle, P., Takkunen, M. J., Männistö, V., Vaittinen, M., Lankinen, M. A., Kärjä, V. J., Käkelä, P., Ågren, J., Tiainen, M., Schwab, U., et al. (2016) · Metabolism · doi:10.1016/j.metabol.2016.01.011 · Cited by 108 · see citing works
“Abbreviations: NAFLD, non-alcoholic fatty liver disease; NASH, non-alcoholic steatohepatitis; FA, fatty acid; VLCD, very low calorie diet; CE, cholesteryl esters; TG, triglycerides; PL, phospholipids; METSIM, Metabolic Syndrome in Men; ALT, alanine aminotransferase; KOBS, Kuopio Obesity Surgery Study; SCD1, stearoyl-C…”
BackgroundInfluentialBanting Memorial Lecture 2012 Reversing the twin cycles of Type 2 diabetes
Taylor, R. (2012) · Diabetic Medicine · doi:10.1111/dme.12039 · Cited by 107 · see citing works
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“Keywords: non-alcoholic fatty liver disease, carbohydrate, saturated fat, over-feeding, de novo lipogenesis (DNL), adipose tissue expandability, fructose, randomized study Hydes et al. NAFLD: Fat, Carbohydrate or Calories”
BackgroundInfluentialEffects of exercise training on intrahepatic lipid content in humans
Brouwers, B., Hesselink, M. K. C., Schrauwen, P., & Schrauwen-Hinderling, V. B. (2016) · Diabetologia · doi:10.1007/s00125-016-4037-x · Cited by 94 · see citing works
“Sevastianova et al [25] found that DNL increased in proportion to the increase in IHL content after 3 weeks of carbohydrate overfeeding, directly supporting a role for DNL in hepatic lipid accumulation.”
BackgroundAre Fruit Juices Healthier Than Sugar-Sweetened Beverages? A Review
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A Low-Glycemic-Load versus Low-Fat Diet in the Treatment of Fatty Liver in Obese Children
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“In a nonrandomized study of 16 adults, liver fat increased during 3 weeks of high-GI carbohydrate overfeeding, and then decreased with weight loss.(18) Furthermore, randomized controlled trials of lowcarbohydrate and low-GI diets have shown preliminary evidence of efficacy in the treatment of fatty liver and related m…”
BackgroundCarbohydrate intake and nonalcoholic fatty liver disease
Neuschwander‐Tetri, B. A. (2013) · Current Opinion in Clinical Nutrition & Metabolic Care · doi:10.1097/mco.0b013e328361c4d1 · Cited by 89 · see citing works
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Tang, Y., Huang, J., Zhang, W. Y., Qin, S., Yang, Y. X., Ren, H., Yang, Q.-B., & Hu, H. (2019) · Therapeutic Advances in Gastroenterology · doi:10.1177/1756284819878046 · Cited by 85 · see citing works
“1 10 (4); 10 (4) 14 (14) WHR, FM, weight, BMI, TC, LDL-C, HDL-C, TG, Glu, insulin, HOMA-IR, TNF-α, IL-6”
Hydes, T., Ravi, S., Loomba, R. S., & Gray, M. E. (2020) · Clinical and Molecular Hepatology · doi:10.3350/cmh.2020.0067 · Cited by 84 · see citing works
“After overfeeding overweight adults with 1,000 kcal/day of candy or SSBs for 3 weeks, body weight increased by 2% accompanied by 27% increase in IHLC.(94) IHLC returned to baseline once baseline weight was achieved over the following 6 months.”
BackgroundType 2 diabetes and remission: practical management guided by pathophysiology
Taylor, R. (2020) · Journal of Internal Medicine · doi:10.1111/joim.13214 · Cited by 84 · see citing works
Truong, X. T., & Lee, D. H. (2025) · Diabetes & Metabolism Journal · doi:10.4093/dmj.2025.0644 · Cited by 84 · see citing works
“3) [13,50,60,67,73].”
Hepatocyte-specific, PPARγ-regulated mechanisms to promote steatosis in adult mice
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Gunn, P. J., Green, C., Pramfalk, C., & Hodson, L. (2017) · Physiological Reports · doi:10.14814/phy2.13532 · Cited by 74 · see citing works
“…PNPLA3 I148M variant are suggested to have lower DNLderived intrahepatic fat and to secrete poorly-lipidated apoB particles (Pirazzi et al. 2012; Sevastianova et al. 2012), which may explain the consistently lower rate of DNL and the tendency (in FBS but not HS) to secrete less TAG in HepG2…”
BackgroundSimons, N., Veeraiah, P., Simons, P. I., Schaper, N. C., Kooi, M. E., Schrauwen-Hinderling, V. B., Feskens, E. J., van der Ploeg, E. (., Van den Eynde, M. D., Schalkwijk, C. G., et al. (2021) · The American Journal of Clinical Nutrition · doi:10.1093/ajcn/nqaa332 · Cited by 74 · see citing works
Maestri, M., Santopaolo, F., Pompili, M., Gasbarrini, A., & Ponziani, F. R. (2023) · Frontiers in Nutrition · doi:10.3389/fnut.2023.1110536 · Cited by 76 · see citing works
Lambert, J. E., Parnell, J. A., Eksteen, B., Raman, M., Bomhof, M. R., Rioux, K. P., Madsen, K. L., & Reimer, R. A. (2015) · BMC Gastroenterology · doi:10.1186/s12876-015-0400-5 · Cited by 73 · see citing works
“Energy reduction and weight loss significantly reduces lipogenesis, contributing to reduction in steatosis [102–106].”
BackgroundSteven, S., Hollingsworth, K. G., Small, P. K., Woodcock, S. A., Pucci, A., Aribasala, B., Al‐Mrabeh, A., Batterham, R. L., & Taylor, R. (2016) · Diabetic Medicine · doi:10.1111/dme.13257 · Cited by 71 · see citing works
Vilar‐Gómez, E., Pirola, C. J., Sookoian, S. C., Wilson, L., Belt, P. H., Liang, T., Liu, W., & Chalasani, N. (2020) · The American Journal of Gastroenterology · doi:10.14309/ajg.0000000000001072 · Cited by 69 · see citing works
A Comprehensive Updated Review of Pharmaceutical and Nonpharmaceutical Treatment for NAFLD
Hossain, N., Kanwar, P., & Mohanty, S. R. (2016) · Gastroenterology Research and Practice · doi:10.1155/2016/7109270 · Cited by 68 · see citing works
PNPLA3 I148M variant and hepatocellular carcinoma: A common genetic variant for a rare disease
Valenti, L. V. C., Dongiovanni, P., Corradini, S. G., Burza, M. A., & Romeo, S. (2013) · Digestive and Liver Disease · doi:10.1016/j.dld.2012.12.006 · Cited by 67 · see citing works
Self-citationTriose Kinase Controls the Lipogenic Potential of Fructose and Dietary Tolerance
Liu, L., Li, T., Liao, Y., Wang, Y., Gao, Y., Hu, H., Huang, H., Wu, F., Chen, Y., Xu, S., et al. (2020) · Cell Metabolism · doi:10.1016/j.cmet.2020.07.018 · Cited by 65 · see citing works
Sugar-sweetened beverages and cardio-metabolic disease risks
Richelsen, B. (2013) · Current Opinion in Clinical Nutrition & Metabolic Care · doi:10.1097/mco.0b013e328361c53e · Cited by 65 · see citing works
Imamura, F., Sharp, S. J., Koulman, A., Schulze, M. B., Kröger, J., Griffin, J. L., Huerta, J. M., Guevara, M., Sluijs, I., Agudo, A., et al. (2017) · PLoS Medicine · doi:10.1371/journal.pmed.1002409 · Cited by 65 · see citing works
“PLOS Medicine | https://doi.org/10.1371/journal.pmed.1002409 October 11, 2017 12 / 19 This could reflect their diverse roles in eicosanoid pathways and pro- and anti-inflammatory pathways, and their associations with dietary intakes (e.g., fish) independent of DNL-driving dietary factors [5].”
BackgroundInfluentialA “systems medicine” approach to the study of non-alcoholic fatty liver disease
Petta, S., Valenti, L. V. C., Bugianesi, E., Targher, G., Bellentani, S., Bonino, F., Ferrannini, E., Loguercio, C., Lonardo, A., Marra, F., et al. (2015) · Digestive and Liver Disease · doi:10.1016/j.dld.2015.10.027 · Cited by 64 · see citing works
“Preliminary data suggest that I148M-homozygous subjects might benefit from weight loss after a short-term low-carbohydrate diet [68,78]; however, disease progression is modulated by multiple environmental and genetic factors [48,79–82].”
BackgroundUnderstanding Dietary Intervention-Mediated Epigenetic Modifications in Metabolic Diseases
Asif, S., Morrow, N. M., Mulvihill, E. E., & Kim, K.-H. (2020) · Frontiers in Genetics · doi:10.3389/fgene.2020.590369 · Cited by 69 · see citing works
Lipidomes in health and disease: Analytical strategies and considerations
Wei, F., Lamichhane, S., Orešič, M., & Hyötyläinen, T. (2019) · TrAC Trends in Analytical Chemistry · doi:10.1016/j.trac.2019.115664 · Cited by 60 · see citing works
Nutrition and Nonalcoholic Fatty Liver Disease
Chakravarthy, M. V., Waddell, T. K., Banerjee, R., & Guess, N. D. (2019) · Gastroenterology Clinics of North America · doi:10.1016/j.gtc.2019.09.003 · Cited by 59 · see citing works
Insights from Genome-Wide Association Analyses of Nonalcoholic Fatty Liver Disease
Kahali, B., Halligan, B. D., & Speliotes, E. K. (2015) · Seminars in Liver Disease · doi:10.1055/s-0035-1567870 · Cited by 53 · see citing works
Lallukka, S., Sevastianova, K., Perttilä, J., Hakkarainen, A., Orho‐Melander, M., Lundbom, N. M. I., Olkkonen, V. M., & Yki-Järvinen, H. (2013) · Diabetologia · doi:10.1007/s00125-013-2829-9 · Cited by 53 · see citing works
“The latter is in keeping with our previous studies, in which we showed, by direct measurement of glycerol turnover using stable isotopes [39] and insulin action on serum NEFA [40], that lipolysis is not increased in individuals with increased liver fat due to the PNPLA3-I148M variant.”
ResultSelf-citationReversal of type 2 diabetes in youth who adhere to a very-low-energy diet: a pilot study
Gow, M. L., Baur, L. A., Johnson, N. A., Cowell, C. T., & Garnett, S. P. (2016) · Diabetologia · doi:10.1007/s00125-016-4163-5 · Cited by 52 · see citing works
Janssen, J. A. M. J. L. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25105488 · Cited by 57 · see citing works
“These liver changes may reduce hepatic insulin clearance and increase peripheral insulin levels (see further below paragraphs Hepatic Insulin clearance and hyperinsulinemia and The personal fat threshold hypothesis and the development of type 2 diabetes for more details) [66].”
BackgroundManaging NAFLD in Type 2 Diabetes: The Effect of Lifestyle Interventions, a Narrative Review
Parry, S. A., & Hodson, L. (2020) · Advances in Therapy · doi:10.1007/s12325-020-01281-6 · Cited by 50 · see citing works
Effects of dietary interventions on liver volume in humans
Bian, H., Hakkarainen, A., Lundbom, N. M. I., & Yki‐Järvinen, H. (2013) · Obesity · doi:10.1002/oby.20623 · Cited by 48 · see citing works
“The increase in liver fat volume could be due to de novo lipogenesis, which increased in the overfeeding study (17).”
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Added fructose as a principal driver of non-alcoholic fatty liver disease: a public health crisis
DiNicolantonio, J. J., Subramonian, A. M., & O’Keefe, J. H. (2017) · Open Heart · doi:10.1136/openhrt-2017-000631 · Cited by 46 · see citing works
Lombardi, R., Iuculano, F., Pallini, G., Fargion, S. R., & Fracanzani, A. L. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21228761 · Cited by 44 · see citing works
“[27] who demonstrated that a 3-week hypercaloric (+1000 kcal/day) diet enriched with sugars (i.”
BackgroundFrankó, A., Merkel, D., Kovářová, M., Hoene, M., Jaghutriz, B. A., Heni, M., Königsrainer, A., Papan, C., Lehr, S., Häring, H., et al. (2018) · Nutrients · doi:10.3390/nu10091314 · Cited by 41 · see citing works
“Carbohydrate overfeeding led to an increased de-novo lipogenesis in proportion to the increase in liver fat and serum triglycerides in subjects with I148I carriers, which however, was not observed in M148M carriers [12].”
BackgroundBeverages and Non-alcoholic fatty liver disease (NAFLD): Think before you drink
Chhimwal, J., Patial, V., & Padwad, Y. S. (2021) · Clinical Nutrition · doi:10.1016/j.clnu.2021.04.011 · Cited by 41 · see citing works
Fuente-Martín, E., García‐Cáceres, C., Díaz, F., Argente-Arizón, P., Granado, M., Barrios, V., Argente, J., & Chowen, J. A. (2013) · Endocrinology · doi:10.1210/en.2012-2196 · Cited by 39 · see citing works
Dietary approach in the treatment of nonalcoholic fatty liver disease
Ferolla, S. M. (2015) · World Journal of Hepatology · doi:10.4254/wjh.v7.i24.2522 · Cited by 38 · see citing works
Umpleby, A. M., Shojaee‐Moradie, F., Fielding, B. A., Li, X., Marino, A., Jawad, N. M. M., Isherwood, C., Jackson, N., Ahmad, A., Stolinski, M., et al. (2017) · Clinical Science · doi:10.1042/cs20171208 · Cited by 38 · see citing works
Self-citationRuuth, M. K., Lahelma, M., Luukkonen, P. K., Lorey, M. B., Qadri, S. U., Sädevirta, S., Hyötyläinen, T., Kovanen, P. T., Hodson, L., Yki‐Järvinen, H., et al. (2021) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.120.315766 · Cited by 38 · see citing works
Self-citationThe PNPLA3 Ile148Met interacts with overweight and dietary intakes on fasting triglyceride levels
Stojkovic, I. A., Ericson, U., Rukh, G., Riddestråle, M., Romeo, S., & Orho‐Melander, M. (2014) · Genes & Nutrition · doi:10.1007/s12263-014-0388-4 · Cited by 37 · see citing works
“Dietary CHOs and especially sucrose intake has been proposed as a key player in liver fat deposition due to the high lipogenic potential of fructose, which stimulates hepatic de novo lipogenesis (Polson and Thompson 2003; Le et al. 2009; Maersk et al. 2012; Abdemalek et al. 2010; Sevastinova et al. 2012).”
BackgroundSelf-citationNutrition, nonalcoholic fatty liver disease and the microbiome
Vos, M. B. (2013) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000043 · Cited by 36 · see citing works
Fructose and metabolic health: governed by hepatic glycogen status?
Hengist, A., Koumanov, F., & Gonzalez, J. T. (2019) · The Journal of Physiology · doi:10.1113/jp277767 · Cited by 35 · see citing works
“…by a disproportional increase in de novo lipogenesis (DNL) and liver fat accumulation with more prolonged (i.e. 3 weeks) fructose overfeeding (Sevastianova et al. 2012), and liver fat correlates strongly with hepatic very-low-density lipoprotein (VLDL) production and serum TAG concentrations…”
BackgroundSigala, D. M., Hieronimus, B., Medici, V., Lee, V., Nuñez, M. V., Bremer, A. A., Cox, C. L., Price, C. A., Benyam, Y., Chaudhari, A. J., et al. (2021) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgab508 · Cited by 36 · see citing works
“The majority of the studies reporting fructose, sucrose, or candy and soda consumption increased liver fat utilized these types of hypercaloric feeding protocols (44-47).”
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Dietary macro and micronutrients associated with MASLD: Analysis of a national US cohort database
Nemer, M., Osman, F., & Said, A. (2024) · Annals of Hepatology · doi:10.1016/j.aohep.2024.101491 · Cited by 32 · see citing works
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“Comparable with our findings, 4 d to 3 wk of overfeeding with simple CHO increased fasting serum TGs (18,21,22,27) and liver fat (21,22,28) in healthy participants.”
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Genetic and Epigenetic Culprits in the Pathogenesis of Nonalcoholic Fatty Liver Disease
Kovalic, A. J., Banerjee, P., Tran, Q. T., Singal, A. K., & Satapathy, S. K. (2018) · Journal of Clinical and Experimental Hepatology · doi:10.1016/j.jceh.2018.04.001 · Cited by 32 · see citing works
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Kaliora, A. C., Kokkinos, A. D., Diolintzi, A., Stoupaki, M. G., Gioxari, A., Kanellos, P. T., Dedoussis, G. V., Vlachogiannakos, J., Revenas, C., Ladas, S. D., et al. (2016) · Food & Function · doi:10.1039/c6fo01040g · Cited by 31 · see citing works
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Crosstalk between dietary patterns, obesity and nonalcoholic fatty liver disease
Ristić-Medić, D., Bajerska, J., & Vučić, V. (2022) · World Journal of Gastroenterology · doi:10.3748/wjg.v28.i27.3314 · Cited by 27 · see citing works
Hepatic Steatosis and Steatohepatitis: Are they Really Two Distinct Entities?
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- Authors
- Sevastianova, K., Santos, A., Kotronen, A., Hakkarainen, A., Makkonen, J., Silander, K., Peltonen, M., Romeo, S., Lundbom, J., Lundbom, N., Olkkonen, V. M., Gylling, H., Fielding, B. A., Rissanen, A., & Yki-Järvinen, H.
- Affiliations
- Minerva Foundation (FI)
- Institute for Molecular Medicine Finland (FI)
- Corresponding author
- Sevastianova, Ksenia
- ORCID
- Venue
- The American Journal of Clinical Nutrition
- Publisher
- Elsevier BV
- Published
- 2012-10
- Volume
- 96
- Issue
- 4
- Pages
- 727-734
- ISSN
- 0002-9165 (ISSN-L)
- OpenAlex
- W2144702146
- Cited by
- 211
- References
- 51
- Citations by year
- 2026: 2 · 2025: 11 · 2024: 9 · 2023: 17 · 2022: 10 · 2021: 13 · 2020: 21 · 2019: 20 · 2018: 9 · 2017: 17 · 2016: 20 · 2015: 24 · 2014: 9 · 2013: 25 · 2012: 4
- FWCI
- 14.85
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- American Journal of Clinical Nutrition (publishedVersion)
- PubMed (publishedVersion)
- Surrey Research Insight Open Access (The University of Surrey) (submittedVersion)
- STM:n Hallinnonalan avoin julkaisuarkisto (Julkari) (submittedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Keywords
- non-alcoholic fatty liver disease, liver fat, monosaccharides, de novo lipogenesis, weight loss, hypocaloric diet, hypercaloric diet, PNPLA3, VLDL triglycerides, overweight, serum triglycerides
- MeSH terms
- Acyltransferases, Adult, Diet, Reducing, Dietary Carbohydrates, Fatty Liver, Female, Humans, Lipase, Lipoproteins, VLDL, Liver, Male, Membrane Proteins, Triglycerides, Hypertriglyceridemia, Weight Gain, Weight Loss, Body Mass Index, Dietary Sucrose, Polymorphism, Single Nucleotide, Lipogenesis, Overweight, Lipid Metabolism, Phospholipases A2, Calcium-Independent, Genetic Association Studies, Non-alcoholic Fatty Liver Disease
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