Comparison of free fructose and glucose to sucrose in the ability to cause fatty liver
- First Online:
- 502 Downloads
There is evidence that disaccharide sucrose produce a greater increase in serum fructose and triglycerides (TGs) than the effect produced by their equivalent monosaccharides, suggesting that long-term exposure to sucrose or fructose + glucose could potentially result in different effects.
Aim of the study
We studied the chronic effects of a combination of free fructose and glucose relative to sucrose on rat liver.
Rats were fed either a combination of 30% fructose and 30% glucose (FG) or 60% sucrose (S). Control rats were fed normal rat chow (C). All rats were pair fed and were followed for 4 months. After killing, blood chemistries and liver tissue were examined.
Both FG-fed- and S-fed rats developed early features of metabolic syndrome when compared with C. In addition, both diets induced hepatic alterations, including variable increases in hepatic TG accumulation and fatty liver, an increase in uric acid content in the liver, as well as an increase in hepatic levels of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-α) measured in liver homogenates.
Diets containing 30% of fructose either as free fructose and glucose, or as sucrose, induce metabolic syndrome, intrahepatic accumulation of uric acid and TGs, increased MCP-1 and TNF-α as well as fatty liver in rats. It will be relevant to determine clinically whether pharmacological reduction in uric acid levels might have a therapeutic advantage in the treatment of non-alcoholic fatty liver disease.
KeywordsNon-alcoholic steatosis Metabolic syndrome Sucrose Fructose
- 1.Abdelmalek MF, Suzuki A, Guy C, Johnson RJ (2007) Fructose induced hyperuricemia as a causal mechanism of nonalcoholic liver disease. Hepatology 46(Suppl 1):293AGoogle Scholar
- 3.Beck-Nielsen H, Pedersen O, Lindskov HO (1980) Impaired cellular insulin binding and insulin sensitivity induced by high-fructose feeding in normal subjects. Am J Clin Nutr 33:273–278Google Scholar
- 4.Blakely SR, Hallfrisch J, Reiser S, Prather ES (1981) Long-term effects of moderate fructose feeding on glucose tolerance parameters in rats. J Nutr 111:307–314Google Scholar
- 5.Brown CM, Dulloo AG, Yepuri G, Montani JP (2008) Fructose ingestion acutely elevates blood pressure in healthy young humans. Am J Physiol Regul Integr Comp Physiol 294:R730–R737Google Scholar
- 10.Donnelly KL, Smith CI, Schwarzenberg SJ, Jessurun J, Boldt MD, Parks EJ (2005) Sources of fatty acids stored in liver and secreted via lipoproteins in patients with nonalcoholic fatty liver disease. J Clin Invest 115:1343–1351Google Scholar
- 13.Hallfrisch J (1990) Metabolic effects of dietary fructose. FASEB J 4:2652–2660Google Scholar
- 14.Hallfrisch J, Ellwood KC, Michaelis OE, Reiser S, O’Dorisio TM, Prather ES (1983) Effects of dietary fructose on plasma glucose and hormone responses in normal and hyperinsulinemic men. J Nutr 113:1819–1826Google Scholar
- 16.Johnson RJ, Segal MS, Sautin Y, Nakagawa T, Feig DI, Kang DH, Gersch MS, Benner S, Sanchez-Lozada LG (2007) Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr 86:899–906Google Scholar
- 17.Kanellis J, Watanabe S, Li JH, Kang DH, Li P, Nakagawa T, Wamsley A, Sheikh-Hamad D, Lan HY, Feng L, Johnson RJ (2003) Uric acid stimulates monocyte chemoattractant protein-1 production in vascular smooth muscle cells via mitogen-activated protein kinase and cyclooxygenase-2. Hypertension 41:1287–1293CrossRefGoogle Scholar
- 21.Lonardo A, Loria P, Leonardi F, Borsatti A, Neri P, Pulvirenti M, Verrone AM, Bagni A, Bertolotti M, Ganazzi D, Carulli N (2002) Fasting insulin and uric acid levels but not indices of iron metabolism are independent predictors of non-alcoholic fatty liver disease. A case–control study. Dig Liver Dis 34:204–211CrossRefGoogle Scholar
- 24.Marchesini G, Babini M (2006) Nonalcoholic fatty liver disease and the metabolic syndrome. Minerva Cardioangiol 54:229–239Google Scholar
- 27.Monsivais P, Perrigue MM, Drewnowski A (2007) Sugars and satiety: does the type of sweetener make a difference? Am J Clin Nutr 86:116–123Google Scholar
- 36.Sanchez-Lozada LG, Tapia E, Bautista-Garcia P, Soto V, Ávila-Casado C, Vega-Campos IP, Nakagawa T, Zhao L, Franco M, Johnson RJ (2008) Effects of febuxostat on metabolic and renal alterations in rats with fructose-induced metabolic syndrome. Am J Physiol Renal Physiol 294:F710–F718CrossRefGoogle Scholar
- 39.Stanhope KL, Griffen SC, Bair BR, Swarbrick MM, Keim NL, Havel PJ (2008) Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals. Am J Clin Nutr 87:1194–1203Google Scholar
- 41.Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, Hatcher B, Cox CL, Dyachenko A, Zhang W, McGahan JP, Seibert A, Krauss RM, Chiu S, Schaefer EJ, Ai M, Otokozawa S, Nakajima K, Nakano T, Beysen C, Hellerstein MK, Berglund L, Havel PJ (2009) Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest 119:1322–1334CrossRefGoogle Scholar
- 42.Swarbrick MM, Stanhope KL, Elliott SS, Graham JL, Krauss RM, Christiansen MP, Griffen SC, Keim NL, Havel PJ (2008) Consumption of fructose-sweetened beverages for 10 weeks increases postprandial triacylglycerol and apolipoprotein-B concentrations in overweight and obese women. Br J Nutr 100:947–952CrossRefGoogle Scholar
- 43.Teff KL, Elliott SS, Tschop M, Kieffer TJ, Rader D, Heiman M, Townsend RR, Keim NL, D’Alessio D, Havel PJ (2004) Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. J Clin Endocrinol Metab 89:2963–2972CrossRefGoogle Scholar
- 45.Wexler BC (1982) Allantoxanamide-induced myocardial necrosis in Sprague-Dawley vs spontaneously hypertensive rats. Proc Soc Exp Biol Med 170:476–485Google Scholar