The Effect and Mechanism of Sucrose Consumption to Liver Disease – A Systematic Literature Review
Downloads
Introduction: One liver disease caused by excessive fat in the liver, called non-alcoholic liver disease (NAFLD), commonly occurs with obesity, diabetes, and other disorders. NAFLD is also associated with hepatic insulin resistance, steatosis, non-alcoholic steatohepatitis (NASH), and cirrhosis. Sucrose consumption has increased recently, and known can promotes NAFLD and will accelerate NAFLD development. This study aimed to discuss the effect and mechanism of sucrose intake on liver disease using a systematic literature review.
Methods: The author identified the articles from 6 online search engines, including PubMed, Science Direct, Sinta, Garuda, Google Scholar, and EBSCOHost. A total of 2271 retrieved articles were obtained from combined search strings in Indonesian and English from the search through online search engines. Excluded articles include title not relevant, duplicate articles, not open access, secondary study or review articles, research objective not appropriate, abstract not suitable, and the results/findings not relevant to the aims of this paper.
Results: A final of twenty-three articles were retrieved using the Mendeley reference manager. Studies included were published studies, types of experimental and observational studies, and their specific findings of sucrose effects on liver disease. Results reveal that most research was primarily conducted experimentally and in case-control study types on male rats.
Conclusion: The most common disease related to sucrose is NAFLD, fibrosis/cirrhosis with the indication of NASH, obesity, insulin resistance (IR), triglycerides (TG), hepatic steatosis, hepatocyte ballooning, and weight gain, which we will discuss further in this review.
Chhimwal J, Patial V, Padwad Y. Beverages and non-alcoholic fatty liver disease (NAFLD): Think before you drink. Clin Nutr. 2021;40:2508–2519.
Younossi Z, Anstee QM, Marietti M, et al. Global burden of NAFLD and NASH: Trends, predictions, risk factors and prevention. Nat Rev Gastroenterol Hepatol. 2018;15:11–20.
Basaranoglu M, Basaranoglu G, Sabuncu T, et al. Fructose as a key player in the development of fatty liver disease. World J Gastroenterol. 2013;19:1166–1172.
Vos MB, Lavine JE. Dietary fructose in non-alcoholic fatty liver disease. Hepatology. 2013;57:2525–2531.
Skenderian S, Park G, Jang C. Organismal fructose metabolism in health and non-alcoholic fatty liver disease shea. Biology (Basel). 2020;9:1–17.
Hydes T, Alam U, Cuthbertson DJ. The impact of macronutrient intake on non-alcoholic fatty liver disease (NAFLD): Too much fat, too much carbohydrate, or just too many calories? Front Nutr. 2021;8:1–16.
Zhou X, Han D, Xu R, et al. A Model of metabolic syndrome and related diseases with intestinal endotoxemia in rats fed a high fat and high sucrose diet. PLoS One. 2014;9:e115148.
Quintana-Castro R, Aguirre-Maldonado I, Soto-Rodríguez I, et al. Cd36 gene expression in adipose and hepatic tissue mediates the lipids accumulation in liver of obese rats with sucrose-induced hepatic steatosis. Prostaglandins Other Lipid Mediat. 2020;147:106404.
Lima MLRP, Leite LHR, Gioda CR, et al. A novel wistar rat model of obesity-related non-alcoholic fatty liver disease induced by sucrose-rich diet. J Diabetes Res. 2016;2016:1–10.
Nojima K, Sugimoto K, Ueda H, et al. Analysis of hepatic gene expression profile in a spontaneous mouse model of type 2 diabetes under a high sucrose diet. Endocr J. 2013;60:EJ12-0258.
Sekkarie A, Welsh JA, Northstone K, et al. Associations between free sugar and sugary beverage intake in early childhood and adult NAFLD in a population-based UK cohort. Children. 2021;8:1–12.
Zagorova M, Prasnicka A, Kadova Z, et al. Boldine attenuates cholestasis associated with non-alcoholic fatty liver disease in hereditary hypertriglyceridemic rats fed by high-sucrose diet. Physiol Res. 2015;64:467–476.
Torres-Villalobos G, Hamdan-Pérez N, Tovar AR, et al. Combined high-fat diet and sustained high sucrose consumption promotes NAFLD in a murine model. Ann Hepatol. 2015;14:540–546.
Sadowska J, Bruszkowska M. Comparing the effects of sucrose and high-fructose corn syrup on lipid metabolism and the risk of cardiovascular disease in male rats. Acta Sci Pol Technol Aliment. 2017;16:231–240.
Maj M, Harbottle B, Thomas PA, et al. Consumption of high-fructose corn syrup compared with sucrose promotes adiposity and increased triglyceridemia but comparable NAFLD severity in juvenile iberian pigs. J Nutr Dis. 2021;151:1139–1149.
Andayani PL, Santoso K, Kusumorini N, et al. Determinasi pemberian sukrosa terhadap kadar SGPT dan SGOT tikus galur wistar sebagai indikator fungsi hati. Bioma. 2016;12:60–68.
Castro RQ, Rodriguez IS, Lago RAD, et al. Dietary sucrose regulates the expression of the Cd36 gene in hepatic tissue of rats with obesity and non alcoholic fatty liver disease (NAFLD). Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2018;162:99–106.
Ragab SMM, Abd Elghaffar SK, El-Metwally TH, et al. Effect of a high fat, high sucrose diet on the promotion of non-alcoholic fatty liver disease in male rats: the ameliorative role of three natural compounds. Lipids Health Dis. 2015;14:1–11.
Plazas Guerrero CG, Acosta Cota SDJ, Castro Sánchez FH, et al. Evaluation of sucrose-enriched diet consumption in the development of risk factors associated to type 2 diabetes, atherosclerosis and non-alcoholic fatty liver disease in a murine model. Int J Environ Health Res. 2021;31:651–669.
Geidl-Flueck B, Hochuli M, Németh Á, et al. Fructose- and sucrose- but not glucose-sweetened beverages promote hepatic de novo lipogenesis: A randomized controlled trial. J Hepatol. 2021;75:46–54.
Baiges-Gaya G, Fernández-Arroyo S, Luciano-Mateo F, et al. Hepatic metabolic adaptation and adipose tissue expansion are altered in mice with steatohepatitis induced by high-fat high sucrose diet. J Nutr Biochem. 2021;89:108559.
Da Silva BS, Paulino AMB, Taffarel M, et al. High sucrose diet attenuates oxidative stress, inflammation and liver injury in thioacetamide-induced liver cirrhosis. Life Sci. 2021;267:118944.
Sun S, Araki Y, Hanzawa F, et al. High sucrose diet-induced dysbiosis of gut microbiota promotes fatty liver and hyperlipidemia in rats. J Nutr Biochem. 2021;93:108621.
Corona-Pérez A, Díaz-Muñoz M, Cuevas-Romero E, et al. Interactive effects of chronic stress and a high-sucrose diet on nonalcoholic fatty liver in young adult male rats. Int J Biol Stress. 2017;20:608–617.
Souza Cruz EM, Bitencourt de Morais JM, Dalto da Rosa CV, et al. Long-term sucrose solution consumption causes metabolic alterations and affects hepatic oxidative stress in Wistar rats Ellen. Biol Open. 2020;9:1–8.
Tallino S, Duffy M, Ralle M, et al. Nutrigenomics analysis reveals that copper deficiency and dietary sucrose up-regulate inflammation, fibrosis and lipogenic pathways in a mature rat model of non-alcoholic fatty liver disease. J Nutr Biochem. 2015;26:996–1006.
Fernandes-Lima F, Monte TLRG, Nascimento FADM, et al. Short Exposure to a high-sucrose diet and the first ‘hit' of non-alcoholic fatty liver disease in mice. Cells Tissues Organs. 2016;201:464–472.
Oliveira LSC, Santos DA, Barbosa-da-Silva S, et al. The inflammatory profile and liver damage of a sucrose-rich diet in mice. J Nutr Biochem. 2014;25:193–200.
Sun S, Hanzawa F, Umeki M, et al. Time-restricted feeding suppresses excess sucrose-induced plasma and liver lipid accumulation in rats. PLoS One. 2018;13:1–18.
Tappy L. Metabolism of sugars: A window to the regulation of glucose and lipid homeostasis by splanchnic organs. Clin Nutr. 2021;40:1691–1698.
Chao HW, Chao SW, Lin H, et al. Homeostasis of glucose and lipid in non-alcoholic fatty liver disease. Int J Mol Sci. 2019;20:1–18.
Stanhope KL. Sugar consumption, metabolic disease and obesity: The state of the controversy. Crit Rev Clin Lab Sci. 2016;53:52–67.
Kanuri G, Bergheim I. In vitro and in vivo models of non-alcoholic fatty liver disease (NAFLD). Int J Mol Sci. 2013;14:11963–11980.
Copyright (c) 2022 Sim Hellene Anjani Sigma
This work is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License.
1. The journal allows the author to hold the copyright of the article without restrictions.
2. The journal allows the author(s) to retain publishing rights without restrictions
3. The legal formal aspect of journal publication accessibility refers to Creative Commons Attribution Share-Alike (CC BY-SA).
