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• General Description

  D-Fructose is present as a monosaccharide in fruits and vegetables^[1], as a disaccharide in sucrose (with D-glucose), and as oligoand polysaccharides (fructans) in many plants. It is also used as an added sweetener for food and drink, and as an excipient in pharmaceutical preparations, syrups, and solutions^[2].
  In equal amounts, it is sweeter than glucose or sucrose and is therefore commonly used as a bulk sweetener. An increase in high fructose corn syrup, as well as total fructose, consumption over the past 10 to 20 years has been linked to a rise in obesity and metabolic disorders^[3]. This raises concerns regarding the short and long-term effects of fructose in humans.
  Fructose is present more or less frequently than glucose in the juices of plants, fruits, and especially the honey, which is about half the solid matters^[4]. It leads to an equal amount of glucose by the hydrolysis of sugar cane and a smaller proportion than some other less common sugars. It is used, such as glucose, in the production of glycogen. It enters the body through either be eaten as such or as the result of digestion of sugar cane. It is mainly changed into glycogen or triglycerides after reaching the liver, so do not enter largely in the blood circulation. Glucose and fructose are partially inter-convertible under the influence of very dilute alkali. It is not surprising; therefore, that fructose must be converted to glycogen in the liver, which on hydrolysis yields of glucose^[5]. Dubois et al. reported that regular consumption of sugary drinks between meals increases risk of overweight among preschool children^[6].
  Fructose has been claimed to be of concern due to several factors: First, in the 1980’s, sucrose was replaced to a large extent, particularly in North America, by high fructose corn syrup (HFCS) in carbonated beverages. The intake of soft drinks containing HFCS has risen in parallel with the epidemic of obesity^[7]. Second, dietary fructose has been implicated in risk factors for cardiovascular disease (CVD): 1. Plasma triglycerides (TG) and VLDL-TG increased following the ingestion of large quantities of fructose; 2. Fructose intake has been found to predict LDL particle size in overweight schoolchildren^[8]. 3. A positive relationship has been demonstrated between fructose intake and uric acid levels^[9]. Third, the use of fructose as a sweetener has increased. The third National Health Examination Survey (NHANES) demonstrated that over 10% of Americans’ daily calories were from fructose^[10]. These studies suggest that the relationship between fructose and health needs re-evaluation. ;

• History of fructose consumption

  Before the development of the sugar industry, free fructose was found in relatively few foods.^[11] Relatively few unprocessed foods contain any significant amounts of free fructose monosaccharide. Historically, these foods have been relatively hard to obtain and they typically contain fructose in conjunction with glucose and/or fibre, which has significant implications for the absorption and metabolism of the former^{[12, 13]}. As a consequence, humans have historically had low dietary fructose intakes^[11] ;

• Rise of fructose consumption

  Fructose consumption has been escalating over the past several decades and is believed to play a role in the rising epidemic of metabolic disorders^[14]. Fructose is a simple monosaccharide that occurs naturally in fruit, though the two main sources of dietary fructose in the Western diet are sucrose (table sugar) and high-fructose corn syrup (HFCS)^[14]. Sucrose is cleaved enzymatically during digestion to produce one fructose molecule and one glucose molecule. HFCS, on the contrary, contains free fructose and glucose in varying ratios. A popular type of HFCS that is used to sweeten beverages in the United States – HFCS-55 – contains 55% fructose, 42% glucose and 3% oligosaccharides^[15]. The 1999–2004 data from the National Health and Nutrition Examination Survey (NHANES) show that the average daily intake of fructose in the United States is now approximately 49 g, which equates to 9.1% of total energy intake^[16]. In comparison, the average daily intake of fructose during 1977–1978 was 37 g^[16]. The highest consumers of fructose are 19–22-year-olds, largely due to excess consumption of sugar-sweetened beverages. Fructose consumption as a percentage of total energy intakes amongst male and female 19–22-year-olds in the 95th percentile is 17.5 and 17.9%, respectively^[16]. ;

• Source of fructose

  It is located in fruits and honey. Main source is sucrose; the sucrose is hydrolyzed by sucrase into fructose and glucose. It is absorbed through facilitated diffusion and can be obtained from the portal blood to the liver where it is converted to glucose^[17]. ;

• Biomedical importance of fructose

  This disease occurs due to deficiency of aldolase B. It has been observed in children, when children receive fructose in the diet. The vomiting and hypoglycemia is an important feature of this disease. Fructose 1 phosphate accumulates in the liver. Accumulation exhausts inorganic phosphate thereby inhibiting both glycogen phosphorylase and the synthesis of ATP. Inhibition of these reactions leads to hypoglycaemia. AMP also accumulates and metabolism leads to increased production of uric acid leading to hyperuricemia and gout^[18]. Treatment of this disease includes avoiding substances containing fructose^[19]. ;

• Fructose metabolism

  Sugar is present in fruits. Sucrose is hydrolyzed by sucrase to glucose and fructose. Dietary fructose is transferred from the intestine to the liver for metabolism. Fructose is converted to fructose 1 phosphate that further converted to acetone and glyceraldehyde dihydroxy, which is further converted to glyceraldehyde 3 phosphate to enter glycolysis. In the well-fed state, fructose is converted to glycogen^[20] or triglycerides^[21]. Hyperlipidemia, diabetes mellitus and obesity are interlinked. Consumption of fructose is increasing and is considered responsible for overweight. Several studies show that fructose increases incidence of obesity, dyslipidemia, insulin resistance, and hypertension. Metabolism of fructose takes place mainly in the liver and high fructose stream leads to accumulation of triglycerides in the liver (hepatic steatosis). This results in impairment of lipid metabolism and enhancement of expression of proinflammatory cytokine. Fructose alters glucose-induced expression of activated acetyl CoA carboxylase (ACC), pSer hormone sensitive lipase (pSerHSL) and adipose triglyceride lipase (ATGL) in HepG2 liver or primary liver cell cultures in vitro. This relates to the increased de novo synthesis of triglycerides in vitro and in vivo hepatic steatosis in fructose-fed versus glucose-and standard-diet mice fed. These studies provide new understanding of the mechanisms involved in fructose-mediated hepatic hypertriglyceridemia^[22].
  Rate of metabolism of fructose is more rapid than glucose, because triose formed from fructose 1-phosphate by pass phosphofructokinase, the primary rate-limiting step in glycolysis. Elevated levels of dietary fructose significantly elevate the rate of lipogenesis in the liver, because of the rapid production of acetyl-coenzyme A^[23]. ;

• Fructose and diseases

  Fructose and hyperuricemia
  Increased intake of fructose is associated with hyperuricemia. Various studies indicate that that increased intake of sugar sweetened soft drinks and fructose is associated with risk of hyperuricemia in men^[24].
  Fructose and metabolic syndrome
  It is hypothesized that fructose induces metabolic syndrome in health individuals. Study was carried out to investigate the role of uric acid in the hypertensive response. In this study, allopurinol was given to patients to lower the serum uric acid level. Ultimately it was found that excessive intake of fructose can increase the blood pressure and is responsible of metabolic syndrome but the lowering of serum uric acid level by allopurinol prevents the increase in mean arterial blood pressure^[25].
  Fructose and obesity
  Fructose is almost similar to glucose because they are isomers to each other. Difference is in their metabolic pathway due to its almost complete hepatic extraction and rapid hepatic conversion into glucose, glycogen, lactate, and fat. In initial period when science was not so progressed, the diabetics patients were using fructose due to its low glycemic index. It has been observed now that obesity, diabetes mellitus, insulin resistance and hypertension are associated with chronic consumption of fructose. Dyslipidemia and impairment in hepatic insulin resistance are also due to increase intake of fructose in the diet. Adverse metabolic effects of fructose are responsible for hepatic de novo lipogenesis, hyperuricemia, oxidative stress and lipotoxicity. Epidemiological studies show that obesity, metabolic and cardiovascular disorders are also due to consumption of sweetened beverages (containing either sucrose or a mixture of glucose and fructose). Adverse metabolic effects of fructose are usually on high consumption and there is lack of evidence of adverse effect on moderate consumption of fructose. Study shows that free fructose is more dangerous than consumption of fructose consumed with sucrose^[26].
  Fructose and hypertension
  The rise in fructose intake has been paralleled by a rise in hypertension. A study of the US population during 2007–2008 found that 29% of adults were hypertensive, compared to 11–13% in 1939 and 24% during 1988–1994^[27,28]. Epidemiological studies have hinted at a link between fructose consumption and hypertension. Jalal et al.^[29] reported that excess dietary fructose (>74 g/day) in the form of added sugar was associated with higher blood pressure (BP) values in US adults who did not have a history of hypertension. Similarly, a study of 4867 adolescents found that SBP rose by 2mmHg from the lowest to the highest category of sugar-sweetened beverage intake^[30]. In a prospective study of US adults, Chen et al.^[31] found that drinking one less sugar-sweetened beverage per day was associated with a 1.8mmHg reduction in SBP and a 1.1mmHg reduction in DBP over 18 months. ;

• References

  1. Wang, Y.M.; van Eys, J. Nutritional significance of fructose and sugar alcohols. Annu. Rev. Nutr. 1981, 1, 437–475.
  2. Hanover, L.M.; White, J.S. Manufacturing, composition, and applications of fructose. Am. J. Clin. Nutr. 1993, 58 (Suppl. S5), 724S–732S.
  3. Bray GA, Nielsen SJ, Popkin BM: Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. Am J Clin Nutr 2004, 79:537-543.
  4. Ischayek JI, Kern M. US honeys varying in glucose and fructose content elicit similar glycemic indexes. J Am Diet Assoc 2006; 106(8):1260—2.
  5. Faiq A. Carbohydrate metabolism. In: Biochemistry review. 1st ed. Karachi: Urdu Bazar; 2004. p. 1—100.
  6. Dubois L, Farmer A, Girard M, Peterson K. J Am Diet Assoc 2007;107:924—34.
  7. Bray G: How bad is fructose? Am J Clin Nutr 2007, 86:895-896 .
  8. Aeberli I, Zimmermann MB, Molinari L, et al: Am J Clin Nutr 2007, 86:1174-1178.
  9. Nakagawa T, Hu H, Zharikov S, et al: A causal role for uric acid in fructose-induced metabolic syndrome. Am J Physiol Renal Physiol 2006, 290: F625-631.
  10. Vos M, Kimmons J, Gillespie C, Welsh J, Blanck H: Medscape J Med 2008, 10(7):160.
  11. Bray GA. How bad is fructose? Am J Clin Nutr 2007; 86: 895–6.
  12. Lustig RH. Fructose: it’s ‘alcohol without the buzz’. Adv Nutr 2013; 4: 226–35.
  13. Lustig RH. Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc 2010; 110: 1307–21.
  14. Johnson RJ, Segal MS, Sautin Y, Nakagawa T, Feig DI, Kang D-H, et al. Am J Clin Nutr 2007; 86:899–906.
  15. Hanover LM, White JS. Manufacturing, composition, and applications of fructose. Am J Clin Nutr 1993; 58:724S–732S.
  16. Marriott BP, Cole N, Lee E. National estimates of dietary fructose intake increased from 1977 to 2004 in the United States. J Nutr 2009; 139:1228S–1235S.
  17. Park YK, Yetley EA. Intakes and food sources of fructose in the United States. Am J Clin Nutr 1993;58(5):737—47.
  18. Choi HK, Willett W, Curhan G. Fructose-rich beverages and risk of gout in women. J Am Med Assoc 2010;24304(20):2270—8.
  19. Ali M, Rellos P, Cox TM. Hereditary fructose intolerance. J Med Genet 1998;35(5):353—565.
  20. Segebarth C, Grivegnée AR, Longo R, Luyten PR, den Hollander JA. Biochimie 1991;73(1):105—8.
  21. Angelopoulos TJ, Lowndes J, Zukley L, Melanson KJ, Nguyen V, Huffman A, et al. J Nutr 2009;139(6):1242—5.
  22. Huang D, Dhawan T, Young S, Yong WH, Boros LG, Lipids Health Dis 2011;24:10—20.
  23. Van der Meulen R, Makras L, Verbrugghe K, Adriany T, De Vuyst L. Appl Environ Microbiol 2006;72(2):1006—12.
  24. Akram M. Management of acute gout. Inter J Fam Med 2010;3(4):233—4.
  25. Perez S, Schold J. Int J Obes 2009;34:454—61.
  26. Tappy L, Lê KA. Metabolic effects of fructose and the worldwide increase in obesity. Physiol Rev 2010;90(1): 23—46.
  27. Egan BM, Zhao Y, Axon RN. Us trends in prevalence, awareness, treatment, and control of hypertension, 1988–2008. JAMA 2010; 303:2043–2050.
  28. Robinson SC, Brucer M. Range of normal blood pressure. A statistical and clinical study of 11,383 persons. Arch Intern Med 1939; 64:409–444.
  29. Jalal DI, Smits G, Johnson RJ, Chonchol M. J Am Soc Nephrol 2010; 21:1543–1549.
  30. Nguyen S, Choi HK, Lustig RH, Hsu C-y. J Pediatr 2009;154:807–813.
  31. Chen L, Caballero B, Mitchell DC, Loria C, Lin P-H, Champagne CM, et al. Circulation 2010; 121:2398–2406.
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