The metabolic effect of fructose on normal rats in a mild dose with glucose and saccharose as control

  • Ge Song Institute of Grain Quality and Nutrition Research, Academy of National Food and Strategic Reserves Administration, Beijing; and Department of Nutrition and Food Hygiene, School of Public Health, Peking University, Beijing, People’s Republic of China
  • Wentao Qi Institute of Grain Quality and Nutrition Research, Academy of National Food and Strategic Reserves Administration, Beijing, People’s Republic of China
  • Yong Wang Institute of Grain Quality and Nutrition Research, Academy of National Food and Strategic Reserves Administration, Beijing, People’s Republic of China
  • Shaojie Pang Institute of Grain Quality and Nutrition Research, Academy of National Food and Strategic Reserves Administration, Beijing, People’s Republic of China
  • Yong Li Department of Nutrition and Food Hygiene, School of Public Health, Peking University, Beijing, People’s Republic of China
DOI: https://doi.org/10.29219/fnr.v65.5589
Keywords: Fructose, Glucose, Sarccharose, Mild dose, Metabolic effect, Intestinal microbiota

Abstract

Aims: To study the metabolic effects of fructose, glucose and saccharose in a moderate dose by analyzing changes of blood indicators, pancreas inflammation, liver fat accumulation and intestinal microbiota in normal Sprague-Dawley (SD) rats.

Subjects and methods: Six-week-old rats were assigned to four groups (n = 10), which were gavaged with normalsaline (Con), glucose dissolved in normal saline (Glu), saccharose-glucose dissolved in normal saline (Sac), and fructose dissolved in normal saline (Fru) for 20 weeks.

Results: No significant differences in body weight and blood parameters including total cholesterol (TC), total triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), lipase (LPS) and free fatty acid (FFA) among the Con, Glu, Sac and the Fru group. The fructose can significantly (P < 0.05) decrease fasting and postprandial blood glucose increase compared to glucose, and the risk of pancreas inflammation and liver fat accumulation induced by fructose is lower than glucose in rats. We found there were no significant differences in intestinal microbial diversity. At the family level, rats in the Glu group had a relatively higher abundance of Peptostreptococcaceae and rats in the Fru group had a relatively higher abundance of Bacteroidaceae. Moreover, the proportions of Peptostreptococcaceae romboutsia and Staphylococcus lentus in the Glu group were significantly higher than in the Fru group, while the proportions of Lachnospira; Lachnospiraceae blautia, Bacteroides and Cellulosilyticus in the Fru group were significantly higher than in the Glu group. The concentration of isobutyric acid was relatively lower in all the sugar treated groups than in the Con. A significant decrease in isobutyric acid was found on comparing the Fru group to the Con group (P < 0.05).

Conclusion: Fructose, glucose and sucrose made no significant changes on rats in body weight, blood indicators, organ index and bacterial diversity. Moreover, fructose can potentially attenuate fasting and postprandial blood-glucose increase, pancreas inflammation and liver-fat accumulation when compared to glucose in mild doses. The relative abundance of six kinds of bacterial genera was found significantly different between rats fed on fructose and glucose.

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References


  1. Tran LT, Yuen VG, McNeill JH. The fructose-fed rat: a review on the mechanisms of fructose-induced insulin resistance and hypertension. Molecular and cellular biochemistry. 2009; 332(1–2): 145–59. doi: 10.1007/s11010-009-0184-4

  2. Ter Horst KW, Serlie MJ. Fructose Consumption, Lipogenesis, and Non-Alcoholic Fatty Liver Disease. Nutrients. 2017; 9(9). doi: 10.3390/nu9090981

  3. Tappy L, Lê KA. Metabolic effects of fructose and the worldwide increase in obesity. Physiological reviews. 2010; 90(1): 23–46. doi: 10.1152/physrev.00019.2009

  4. Lanaspa MA, Tapia E, Soto V, Sautin Y, Sánchez-Lozada LG. Uric acid and fructose: potential biological mechanisms. Seminars in nephrology. 2011; 31(5): 426–32. doi: 10.1016/j.semnephrol.2011.08.006

  5. Hannou SA, Haslam DE, McKeown NM, Herman MA. Fructose metabolism and metabolic disease. The Journal of clinical investigation. 2018; 128(2): 545–55. doi: 10.1172/jci96702

  6. Stanhope KL. Sugar consumption, metabolic disease and obesity: The state of the controversy. Critical reviews in clinical laboratory sciences. 2016; 53(1): 52–67. doi: 10.3109/10408363.2015.1084990

  7. Crescenzo R, Bianco F, Coppola P, Mazzoli A, Valiante S, Liverini G, et al. Adipose tissue remodeling in rats exhibiting fructose-induced obesity. European journal of nutrition. 2014; 53(2): 413–9. doi: 10.1007/s00394-013-0538-2

  8. Lee WC, Chien CT, Yu HJ, Lee SW. Bladder dysfunction in rats with metabolic syndrome induced by long-term fructose feeding. The Journal of urology. 2008; 179(6): 2470–6. doi: 10.1016/j.juro.2008.01.086

  9. Kovačević S, Nestorov J, Matić G, Elaković I. Fructose-enriched diet induces inflammation and reduces antioxidative defense in visceral adipose tissue of young female rats. European journal of nutrition. 2017; 56(1): 151–60. doi: 10.1007/s00394-015-1065-0

  10. Girard A, Madani S, Boukortt F, Cherkaoui-Malki M, Belleville J, Prost J. Fructose-enriched diet modifies antioxidant status and lipid metabolism in spontaneously hypertensive rats. Nutrition (Burbank, Los Angeles County, Calif). 2006; 22(7–8): 758–66. doi: 10.1016/j.nut.2006.05.006

  11. D’Angelo G, Elmarakby AA, Pollock DM, Stepp DW. Fructose feeding increases insulin resistance but not blood pressure in Sprague-Dawley rats. Hypertension (Dallas, Tex : 1979). 2005; 46(4): 806–11. doi: 10.1161/01.Hyp.0000182697.39687.34

  12. Maier IB, Stricker L, Ozel Y, Wagnerberger S, Bischoff SC, Bergheim I. A low fructose diet in the treatment of pediatric obesity: a pilot study. Pediatrics international: official journal of the Japan Pediatric Society. 2011; 53(3): 303–8. doi: 10.1111/j.1442-200X.2010.03248.x

  13. Bass EF, Baile CA, Lewis RD, Giraudo SQ. Bone quality and strength are greater in growing male rats fed fructose compared with glucose. Nutrition research (New York, NY). 2013; 33(12): 1063–71. doi: 10.1016/j.nutres.2013.08.006

  14. Stanhope KL, Havel PJ. Fructose consumption: recent results and their potential implications. Annals of the New York Academy of Sciences. 2010; 1190: 15–24. doi: 10.1111/j.1749-6632.2009.05266.x

  15. Do MH, Lee E, Oh MJ, Kim Y, Park HY. High-Glucose or -Fructose Diet Cause Changes of the Gut Microbiota and Metabolic Disorders in Mice without Body Weight Change. Nutrients. 2018; 10(6). doi: 10.3390/nu10060761

  16. Boursier J, Mueller O, Barret M, Machado M, Fizanne L, Araujo-Perez F, et al. The severity of nonalcoholic fatty liver disease is associated with gut dysbiosis and shift in the metabolic function of the gut microbiota. Hepatology (Baltimore, Md). 2016; 63(3): 764–75. doi: 10.1002/hep.28356

  17. Silva JCP, Mota M, Martins FO, Nogueira C, Gonçalves T, Carneiro T, et al. Intestinal Microbial and Metabolic Profiling of Mice Fed with High-Glucose and High-Fructose Diets. Journal of proteome research. 2018; 17(8): 2880–91. doi: 10.1021/acs.jproteome.8b00354

  18. Payne AN, Chassard C, Lacroix C. Gut microbial adaptation to dietary consumption of fructose, artificial sweeteners and sugar alcohols: implications for host-microbe interactions contributing to obesity. Obesity reviews : an official journal of the International Association for the Study of Obesity. 2012; 13(9): 799–809. doi: 10.1111/j.1467-789X.2012.01009.x

  19. Lim SM, Jeong JJ, Woo KH, Han MJ, Kim DH. Lactobacillus sakei OK67 ameliorates high-fat diet-induced blood glucose intolerance and obesity in mice by inhibiting gut microbiota lipopolysaccharide production and inducing colon tight junction protein expression. Nutrition research (New York, NY). 2016; 36(4): 337–48. doi: 10.1016/j.nutres.2015.12.001

  20. Organization WHJWHO. Guideline : Sugars intake for adults and children. Geneva: World Health Organization; 2015.

  21. Reagan-Shaw S, Nihal M, Ahmad N. Dose translation from animal to human studies revisited. FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 2008; 22(3): 659–61. doi: 10.1096/fj.07-9574LSF

  22. Yan M, Ye L, Yin S, Lu X, Liu X, Lu S, et al. Glycycoumarin protects mice against acetaminophen-induced liver injury predominantly via activating sustained autophagy. British journal of pharmacology. 2018; 175(19): 3747–57. doi: 10.1111/bph.14444

  23. Guo XX, Zeng Z, Qian YZ, Qiu J, Wang K, Wang Y, et al. Wheat Flour, Enriched with γ-Oryzanol, Phytosterol, and Ferulic Acid, Alleviates Lipid and Glucose Metabolism in High-Fat-Fructose-Fed Rats. Nutrients. 2019; 11(7). doi: 10.3390/nu11071697

  24. Carran EL, White SJ, Reynolds AN, Haszard JJ, Venn BJ. Acute effect of fructose intake from sugar-sweetened beverages on plasma uric acid: a randomised controlled trial. European journal of clinical nutrition. 2016; 70(9): 1034–8. doi: 10.1038/ejcn.2016.112

  25. DiNicolantonio JJ, O’Keefe JH, Lucan SC. Added fructose: a principal driver of type 2 diabetes mellitus and its consequences. Mayo Clinic proceedings. 2015; 90(3): 372–81. doi: 10.1016/j.mayocp.2014.12.019

  26. Tsilas CS, de Souza RJ, Mejia SB, Mirrahimi A, Cozma AI, Jayalath VH, et al. Relation of total sugars, fructose and sucrose with incident type 2 diabetes: a systematic review and meta-analysis of prospective cohort studies. CMAJ : Canadian Medical Association journal = journal de l’Association medicale canadienne. 2017; 189(20): E711–e20. doi: 10.1503/cmaj.160706

  27. Johnson RJ, Perez-Pozo SE, Sautin YY, Manitius J, Sanchez-Lozada LG, Feig DI, et al. Hypothesis: could excessive fructose intake and uric acid cause type 2 diabetes? Endocrine reviews. 2009; 30(1): 96–116. doi: 10.1210/er.2008-0033

  28. Milutinović DV, Brkljačić J, Teofilović A, Bursać B, Nikolić M, Gligorovska L, et al. Chronic Stress Potentiates High Fructose-Induced Lipogenesis in Rat Liver and Kidney. Molecular nutrition & food research. 2020: e1901141. doi: 10.1002/mnfr.201901141

  29. Bickel PE, Tansey JT, Welte MA. PAT proteins, an ancient family of lipid droplet proteins that regulate cellular lipid stores. Biochimica et biophysica acta. 2009; 1791(6): 419–40. doi: 10.1016/j.bbalip.2009.04.002

  30. Smith PM, Howitt MR, Panikov N, Michaud M, Gallini CA, Bohlooly YM, et al. The microbial metabolites, short-chain fatty acids, regulate colonic Treg cell homeostasis. Science (New York, NY). 2013; 341(6145): 569–73. doi: 10.1126/science.1241165

  31. Liu YJ, Tang B, Wang FC, Tang L, Lei YY, Luo Y, et al. Parthenolide ameliorates colon inflammation through regulating Treg/Th17 balance in a gut microbiota-dependent manner. Theranostics. 2020; 10(12): 5225–41. doi: 10.7150/thno.43716

  32. Machiels K, Joossens M, Sabino J, De Preter V, Arijs I, Eeckhaut V, et al. A decrease of the butyrate-producing species Roseburia hominis and Faecalibacterium prausnitzii defines dysbiosis in patients with ulcerative colitis. Gut. 2014; 63(8): 1275–83. doi: 10.1136/gutjnl-2013-304833

  33. Lavelle A, Sokol H. Gut microbiota-derived metabolites as key actors in inflammatory bowel disease. Nature reviews Gastroenterology & hepatology. 2020; 17(4): 223–37. doi: 10.1038/s41575-019-0258-z

  34. Laffin M, Fedorak R, Zalasky A, Park H, Gill A, Agrawal A, et al. A high-sugar diet rapidly enhances susceptibility to colitis via depletion of luminal short-chain fatty acids in mice. Scientific reports. 2019; 9(1): 12294. doi: 10.1038/s41598-019-48749-2

Published
2021-05-18
How to Cite
Song G., Qi W., Wang Y., Pang S., & Li Y. (2021). The metabolic effect of fructose on normal rats in a mild dose with glucose and saccharose as control. Food & Nutrition Research, 65. https://doi.org/10.29219/fnr.v65.5589
Issue
Vol 65 (2021)
Section
Original Articles
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