期刊论文详细信息
Nutrition & Metabolism
Fructose in perspective
Eugene J Fine1  Richard D Feinman2 
[1] Albert Einstein College of Medicine, Bronx, NY, USA;State University of New York Downstate Medical Center, Brooklyn, NY, USA
关键词: Metabolic syndrome;    Low-carbohydrate diet;    Sugar;    Glucose;    Fructose;    Carbohydrate;   
Others  :  803362
DOI  :  10.1186/1743-7075-10-45
 received in 2013-04-19, accepted in 2013-06-23,  发布年份 2013
PDF
【 摘 要 】

Whether dietary fructose (as sucrose or high fructose corn syrup) has unique effects separate from its role as carbohydrate, or, in fact, whether it can be considered inherently harmful, even a toxin, has assumed prominence in nutrition. Much of the popular and scientific media have already decided against fructose and calls for regulation and taxation come from many quarters. There are conflicting data, however. Outcomes attributed to fructose — obesity, high triglycerides and other features of metabolic syndrome — are not found in every experimental test and may be more reliably caused by increased total carbohydrate. In this review, we try to put fructose in perspective by looking at the basic metabolic reactions. We conclude that fructose is best understood as part of carbohydrate metabolism. The pathways of fructose and glucose metabolism converge at the level of the triose-phosphates and, therefore, any downstream effects also occur with glucose. In addition, a substantial part of ingested fructose is turned to glucose. Regulation of fructose metabolism per se, is at the level of substrate control — the lower Km of fructokinase compared to glucokinase will affect the population of triose-phosphates. Generally deleterious effects of administering fructose alone suggest that fructose metabolism is normally controlled in part by glucose. Because the mechanisms of fructose effects are largely those of a carbohydrate, one has to ask what the proper control should be for experiments that compare fructose to glucose. In fact, there is a large literature showing benefits in replacing total carbohydrate with other nutrients, usually fat, and such experiments sensibly constitute the proper control for comparisons of the two sugars. In terms of public health, a rush to judgement analogous to the fat-cholesterol-heart story, is likely to have unpredictable outcome and unintended consequences. Popular opinion cannot be ignored in this problem and comparing fructose to ethanol, for example, is without biochemical correlates. Also, nothing in the biochemistry suggests that sugar is a toxin. Dietary carbohydrate restriction remains the best strategy for obesity, diabetes and metabolic syndrome. The specific contribution of the removal of fructose or sucrose to this effect remains unknown.

【 授权许可】

   
2013 Feinman and Fine; licensee BioMed Central Ltd.

【 预 览 】
附件列表
Files Size Format View
20140708040623207.pdf 2842KB PDF download
Figure 8. 53KB Image download
Figure 7. 81KB Image download
Figure 6. 119KB Image download
Figure 5. 103KB Image download
Figure 4. 85KB Image download
Figure 3. 61KB Image download
Figure 2. 53KB Image download
Figure 1. 79KB Image download
【 图 表 】

Figure 1.

Figure 2.

Figure 3.

Figure 4.

Figure 5.

Figure 6.

Figure 7.

Figure 8.

【 参考文献 】
  • [1]Johnson RK, Appel LJ, Brands M, Howard BV, Lefevre M, Lustig RH, Sacks F, Steffen LM, Wylie-Rosett J: Dietary sugars intake and cardiovascular health: a scientific statement from the American Heart Association. Circulation 2009, 120(11):1011-1020.
  • [2]Taubes G, Couzens CK: Big Sugar’s Sweet Little Lies. In: Mother Jones; 2012.
  • [3]Lustig RH: Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc 2010, 110(9):1307-1321.
  • [4]Lustig RH, Schmidt LA, Brindis CD: Public health: The toxic truth about sugar. Nature 2012, 482(7383):27-29.
  • [5]Bray GA: Fructose: pure, white, and deadly? Fructose, by any other name, is a health hazard. J Diabetes Sci Technol 2010, 4(4):1003-1007.
  • [6]Livesey G, Taylor R: Fructose consumption and consequences for glycation, plasma triacylglycerol, and body weight: meta-analyses and meta-regression models of intervention studies. Am J Clin Nutr 2008, 88(5):1419-1437.
  • [7]Mayes PA: Intermediary metabolism of fructose. Am J Clin Nutr 1993, 58(5 Suppl):754S-765S.
  • [8]Sun SZ, Empie MW: Fructose metabolism in humans - what isotopic tracer studies tell us. Nutr Metab (Lond) 2012, 9(1):89. BioMed Central Full Text
  • [9]Basciano H, Federico L, Adeli K: Fructose, insulin resistance, and metabolic dyslipidemia. Nutr Metab (Lond) 2005, 2(1):5. BioMed Central Full Text
  • [10]Rizkalla SW: Health implications of fructose consumption: A review of recent data. Nutr Metab (Lond) 2010, 7:82. BioMed Central Full Text
  • [11]Accurso A, Bernstein RK, Dahlqvist A, Draznin B, Feinman RD, Fine EJ, Gleed A, Jacobs DB, Larson G, Lustig RH, et al.: Dietary carbohydrate restriction in type 2 diabetes mellitus and metabolic syndrome: time for a critical appraisal. Nutr Metab (Lond) 2008, 5(1):9. BioMed Central Full Text
  • [12]Forsythe CE, Phinney SD, Fernandez ML, Quann EE, Wood RJ, Bibus DM, Kraemer WJ, Feinman RD, Volek JS: Comparison of low fat and low carbohydrate diets on circulating Fatty Acid composition and markers of inflammation. Lipids 2008, 43(1):65-77.
  • [13]Volek JS, Feinman RD: Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction. Nutr Metab (Lond) 2005, 2:31. BioMed Central Full Text
  • [14]Volek JS, Fernandez ML, Feinman RD, Phinney SD: Dietary carbohydrate restriction induces a unique metabolic state positively affecting atherogenic dyslipidemia, fatty acid partitioning, and metabolic syndrome. Prog Lipid Res 2008, 47(5):307-318.
  • [15]Westman EC, Yancy WS, Mavropoulos JC, Marquart M, McDuffie JR: The Effect of a Low-Carbohydrate, Ketogenic Diet Versus a Low-Glycemic Index Diet on Glycemic Control in Type 2 Diabetes Mellitus. Nutr Metab (Lond) 2005, 5:36.
  • [16]Yancy WS Jr, Olsen MK, Guyton JR, Bakst RP, Westman EC: A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Ann Intern Med 2004, 140(10):769-777.
  • [17]Gannon MC, Hoover H, Nuttall FQ: Further decrease in glycated hemoglobin following ingestion of a LoBAG30 diet for 10 weeks compared to 5 weeks in people with untreated type 2 diabetes. Nutr Metab (Lond) 2010, 7:64. BioMed Central Full Text
  • [18]Gannon MC, Nuttall FQ: Effect of a high-protein, low-carbohydrate diet on blood glucose control in people with type 2 diabetes. Diabetes 2004, 53(9):2375-2382.
  • [19]Parniak MA, Kalant N: Enhancement of glycogen concentrations in primary cultures of rat hepatocytes exposed to glucose and fructose. Biochem J 1988, 251(3):795-802.
  • [20]Petersen KF, Laurent D, Yu C, Cline GW, Shulman GI: Stimulating effects of low-dose fructose on insulin-stimulated hepatic glycogen synthesis in humans. Diabetes 2001, 50(6):1263-1268.
  • [21]McDevitt RM, Bott SJ, Harding M, Coward WA, Bluck LJ, Prentice AM: De novo lipogenesis during controlled overfeeding with sucrose or glucose in lean and obese women. Am J Clin Nutr 2001, 74(6):737-746.
  • [22]Teff KL, Grudziak J, Townsend RR, Dunn TN, Grant RW, Adams SH, Keim NL, Cummings BP, Stanhope KL, Havel PJ: Endocrine and metabolic effects of consuming fructose- and glucose-sweetened beverages with meals in obese men and women: influence of insulin resistance on plasma triglyceride responses. J Clin Endocrinol Metab 2009, 94(5):1562-1569.
  • [23]Cox CL, Stanhope KL, Schwarz JM, Graham JL, Hatcher B, Griffen SC, Bremer AA, Berglund L, McGahan JP, Keim NL, et al.: Consumption of fructose- but not glucose-sweetened beverages for 10 weeks increases circulating concentrations of uric acid, retinol binding protein- 4, and gamma-glutamyl transferase activity in overweight/obese humans. Nutr Metab (Lond) 2012, 9(1):68. BioMed Central Full Text
  • [24]Volek JS, Phinney SD, Forsythe CE, Quann EE, Wood RJ, Puglisi MJ, Kraemer WJ, Bibus DM, Fernandez ML, Feinman RD: Carbohydrate Restriction has a More Favorable Impact on the Metabolic Syndrome than a Low Fat Diet. Lipids 2009, 44(4):297-309.
  • [25]Ishimoto T, Lanaspa MA, Le MT, Garcia GE, Diggle CP, Maclean PS, Jackman MR, Asipu A, Roncal-Jimenez CA, Kosugi T, et al.: Opposing effects of fructokinase C and A isoforms on fructose-induced metabolic syndrome in mice. Proc Natl Acad Sci USA 2012, 109(11):4320-4325.
  • [26]Lanaspa MA, Sanchez-Lozada LG, Cicerchi C, Li N, Roncal-Jimenez CA, Ishimoto T, Le M, Garcia GE, Thomas JB, Rivard CJ, et al.: Uric acid stimulates fructokinase and accelerates fructose metabolism in the development of fatty liver. PLoS One 2012, 7(10):e47948.
  • [27]Stefanovski D, Youn JH, Rees M, Watanabe RM, Ader M, Ionut V, Jackson AU, Boehnke M, Collins FS, Bergman RN: Estimating hepatic glucokinase activity using a simple model of lactate kinetics. Diabetes Care 2012, 35(5):1015-1020.
  • [28]Chu CA, Fujimoto Y, Igawa K, Grimsby J, Grippo JF, Magnuson MA, Cherrington AD, Shiota M: Rapid translocation of hepatic glucokinase in response to intraduodenal glucose infusion and changes in plasma glucose and insulin in conscious rats. Am J Physiol Gastrointest Liver Physiol 2004, 286(4):G627-634.
  • [29]Delarue J, Normand S, Pachiaudi C, Beylot M, Lamisse F, Riou JP: The contribution of naturally labelled 13C fructose to glucose appearance in humans. Diabetologia 1993, 36(4):338-345.
  • [30]Lecoultre V, Egli L, Carrel G, Theytaz F, Kreis R, Schneiter P, Boss A, Zwygart K, Le KA, Bortolotti M, et al.: Effects of fructose and glucose overfeeding on hepatic insulin sensitivity and intrahepatic lipids in healthy humans. Obesity (Silver Spring) 2013, 21:782-785.
  • [31]Dirlewanger M, Schneiter P, Jequier E, Tappy L: Effects of fructose on hepatic glucose metabolism in humans. Am J Physiol Endocrinol Metab 2000, 279(4):E907-911.
  • [32]Kahn R: Metabolic syndrome–what is the clinical usefulness? Lancet 2008, 371(9628):1892-1893.
  • [33]Swarbrick MM, Stanhope KL, Elliott SS, Graham JL, Krauss RM, Christiansen MP, Griffen SC, Keim NL, Havel PJ: Consumption of fructose-sweetened beverages for 10 weeks increases postprandial triacylglycerol and apolipoprotein-B concentrations in overweight and obese women. Br J Nutr 2008, 100(5):947-952.
  • [34]Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, Hatcher B, Cox CL, Dyachenko A, Zhang W, et al.: Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest 2009, 119(5):1322-1334.
  • [35]Chong MF, Fielding BA, Frayn KN: Mechanisms for the acute effect of fructose on postprandial lipemia. Am J Clin Nutr 2007, 85(6):1511-1520.
  • [36]Hollenbeck CB: Dietary fructose effects on lipoprotein metabolism and risk for coronary artery disease. Am J Clin Nutr 1993, 58(5 Suppl):800S-809S.
  • [37]Chong MF, Fielding BA, Frayn KN: Metabolic interaction of dietary sugars and plasma lipids with a focus on mechanisms and de novo lipogenesis. Proc Nutr Soc 2007, 66(1):52-59.
  • [38]Hudgins LC, Parker TS, Levine DM, Hellerstein MK: A dual sugar challenge test for lipogenic sensitivity to dietary fructose. J Clin Endocrinol Metab 2011, 96(3):861-868.
  • [39]Woods HF, Alberti KG: Dangers of intravenous fructose. Lancet 1972, 2(7791):1354-1357.
  • [40]Jentjens RL, Underwood K, Achten J, Currell K, Mann CH, Jeukendrup AE: Exogenous carbohydrate oxidation rates are elevated after combined ingestion of glucose and fructose during exercise in the heat. J Appl Physiol 2006, 100(3):807-816.
  • [41]Veech RL, Raijman L, Krebs HA: Equilibrium relations between the cytoplasmic adenine nucleotide system and nicotinamide-adenine nucleotide system in rat liver. Biochem J 1970, 117(3):499-503.
  • [42]Abdelmalek MF, Lazo M, Horska A, Bonekamp S, Lipkin EW, Balasubramanyam A, Bantle JP, Johnson RJ, Diehl AM, Clark JM: Higher dietary fructose is associated with impaired hepatic adenosine triphosphate homeostasis in obese individuals with type 2 diabetes. Hepatology 2012, 56(3):952-960.
  • [43]Jentjens RL, Shaw C, Birtles T, Waring RH, Harding LK, Jeukendrup AE: Oxidation of combined ingestion of glucose and sucrose during exercise. Metabolism 2005, 54(5):610-618.
  • [44]Gannon MC, Nuttall FQ, Westphal SA, Fang S, Ercan-Fang N: Acute metabolic response to high-carbohydrate, high-starch meals compared with moderate-carbohydrate, low-starch meals in subjects with type 2 diabetes. Diabetes Care 1998, 21(10):1619-1626.
  • [45]Nuttall FQ, Gannon MC: The metabolic response to a high-protein, low-carbohydrate diet in men with type 2 diabetes mellitus. Metabolism 2006, 55(2):243-251.
  文献评价指标  
  下载次数:103次 浏览次数:34次