Chemistry:Fructose

From HandWiki
Short description: Simple ketonic monosaccharide found in many plants
d-Fructose
Skeletal Structure of Cyclic D-Fructose.svg
d-Fructofuranose
D-Fructose.svg
d-Fructose (open-chain form)
β-d-fructose structure
Haworth projection of β-d-fructofuranose
Beta-D-fructofuranose-from-xtal-view-1-3D-bs-17.png
Beta-D-fructopyranose-from-xtal-view-2-3D-bs-17.png
Ball-and-stick model of β-d-fructopyranose
Names
IUPAC name
D-arabino-Hex-2-ulose[3]
Systematic IUPAC name
(3S,4R,5R)-1,3,4,5,6-Pentahydroxyhexan-2-one
Other names
Fruit sugar,[1] levulose,[2] d-fructofuranose, d-fructose, d-arabino-hexulose
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
EC Number
  • 200-333-3
KEGG
UNII
Properties
C6H12O6
Molar mass 180.156 g·mol−1
Density 1.694 g/cm3
Melting point 103 °C (217 °F; 376 K)
~4000 g/L (25 °C)
−102.60×10−6 cm3/mol
Thermochemistry
675.6 kcal/mol (2,827 kJ/mol)[4] (Higher heating value)
Pharmacology
1=ATC code }} V06DC02 (WHO)
Hazards
Lethal dose or concentration (LD, LC):
15000 mg/kg (intravenous, rabbit)[5]
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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Infobox references
Tracking categories (test):

Fructose (/ˈfrʌktoʊs, -oʊz/), or fruit sugar, is a ketonic simple sugar found in many plants, where it is often bonded to glucose to form the disaccharide sucrose. It is one of the three dietary monosaccharides, along with glucose and galactose, that are absorbed by the gut directly into the blood of the portal vein during digestion. The liver then converts both fructose and galactose into glucose, so that dissolved glucose, known as blood sugar, is the only monosaccharide present in circulating blood.

Fructose was discovered by French chemist Augustin-Pierre Dubrunfaut in 1847.[6][7] The name "fructose" was coined in 1857 by the English chemist William Allen Miller.[8] Pure, dry fructose is a sweet, white, odorless, crystalline solid, and is the most water-soluble of all the sugars.[9] Fructose is found in honey, tree and vine fruits, flowers, berries, and most root vegetables.

Commercially, fructose is derived from sugar cane, sugar beets, and maize. High-fructose corn syrup is a mixture of glucose and fructose as monosaccharides. Sucrose is a compound with one molecule of glucose covalently linked to one molecule of fructose. All forms of fructose, including those found in fruits and juices, are commonly added to foods and drinks for palatability and taste enhancement, and for browning of some foods, such as baked goods. As of 2004, about 240,000 tonnes of crystalline fructose were being produced annually.[10]

Excessive consumption of sugars, including fructose, (especially from sugar-sweetened beverages) may contribute to insulin resistance, obesity, elevated LDL cholesterol and triglycerides, leading to metabolic syndrome. The European Food Safety Authority (EFSA) stated in 2011 that fructose may be preferable over sucrose and glucose in sugar-sweetened foods and beverages because of its lower effect on postprandial blood sugar levels,[11] while also noting the potential downside that "high intakes of fructose may lead to metabolic complications such as dyslipidaemia, insulin resistance, and increased visceral adiposity".[11][12] The UK's Scientific Advisory Committee on Nutrition in 2015 disputed the claims of fructose causing metabolic disorders, stating that "there is insufficient evidence to demonstrate that fructose intake, at levels consumed in the normal UK diet, leads to adverse health outcomes independent of any effects related to its presence as a component of total and free sugars."[13]

Etymology

The word "fructose" was coined in 1857 from the Latin for fructus (fruit) and the generic chemical suffix for sugars, -ose.[8][14] It is also called fruit sugar and levulose or laevulose, due to its ability to rotate plane polarised light in a laevorotary fashion (anti-clockwise/to the left) when a beam is shone through it in solution. Likewise, dextrose (an isomer of glucose) is given its name due to its ability to rotate plane polarised light in a dextrorotary fashion (clockwise/to the right).[14]

Chemical properties

Figure 1: Relationship between the acyclic and the cyclic (hemiketal) isomers of fructose
d- and l-isomers of fructose (open-chain form)

Fructose is a 6-carbon polyhydroxyketone.[15] Crystalline fructose adopts a cyclic six-membered structure, called β-d-fructopyranose, owing to the stability of its hemiketal and internal hydrogen-bonding. In solution, fructose exists as an equilibrium mixture of the tautomers β-d-fructopyranose, β-d-fructofuranose, α-d-fructofuranose, α-d-fructopyranose and keto-d-fructose (the non-cyclic form).[16]

The distribution of d-fructose tautomers in solution is related to several variables, such as solvent and temperature.[17] d-Fructopyranose and d-fructofuranose distributions in water have been identified multiple times as roughly 70% fructopyranose and 22% fructofuranose.[18]

Reactions

Fructose and fermentation

Fructose may be anaerobically fermented by yeast and bacteria.[19] Yeast enzymes convert sugar (sucrose, glucose, and fructose, but not lactose) to ethanol and carbon dioxide.[20] Some of the carbon dioxide produced during fermentation will remain dissolved in water, where it will reach equilibrium with carbonic acid. The dissolved carbon dioxide and carbonic acid produce the carbonation in some fermented beverages, such as champagne.

Fructose and Maillard reaction

Fructose undergoes the Maillard reaction, non-enzymatic browning, with amino acids. Because fructose exists to a greater extent in the open-chain form than does glucose, the initial stages of the Maillard reaction occur more rapidly than with glucose. Therefore, fructose has potential to contribute to changes in food palatability, as well as other nutritional effects, such as excessive browning, volume and tenderness reduction during cake preparation, and formation of mutagenic compounds.[21]

Dehydration

Fructose readily dehydrates to give hydroxymethylfurfural ("HMF", C6H6O3), which can be processed into liquid dimethylfuran (C6H8O). This process, in the future, may become part of a low-cost, carbon-neutral system to produce replacements for petrol and diesel from plants.[22]

Physical and functional properties

Sweetness of fructose

The primary reason that fructose is used commercially in foods and beverages, besides its low cost, is its high relative sweetness. It is the sweetest of all naturally occurring carbohydrates. The relative sweetness of fructose has been reported in the range of 1.2–1.8 times that of sucrose.[23][24][25][26] However, it is the 6-membered ring form of fructose that is sweeter; the 5-membered ring form tastes about the same as usual table sugar. Warming fructose leads to formation of the 5-membered ring form.[27] Therefore, the relative sweetness decreases with increasing temperature. However, it has been observed that the absolute sweetness of fructose is identical at 5 °C as 50 °C and thus the relative sweetness to sucrose is not due to anomeric distribution but a decrease in the absolute sweetness of sucrose at higher temperatures.[25]

Figure 2: Relative sweetness of sugars and sweeteners

The sweetness of fructose is perceived earlier than that of sucrose or glucose, and the taste sensation reaches a peak (higher than that of sucrose), and diminishes more quickly than that of sucrose. Fructose can also enhance other flavors in the system.[23][25]

Fructose exhibits a sweetness synergy effect when used in combination with other sweeteners. The relative sweetness of fructose blended with sucrose, aspartame, or saccharin is perceived to be greater than the sweetness calculated from individual components.[28][25]

Fructose solubility and crystallization

Fructose has higher water solubility than other sugars, as well as other sugar alcohols. Fructose is, therefore, difficult to crystallize from an aqueous solution.[23] Sugar mixes containing fructose, such as candies, are softer than those containing other sugars because of the greater solubility of fructose.[29]

Fructose hygroscopicity and humectancy

Fructose is quicker to absorb moisture and slower to release it to the environment than sucrose, glucose, or other nutritive sweeteners.[28] Fructose is an excellent humectant and retains moisture for a long period of time even at low relative humidity (RH). Therefore, fructose can contribute a more palatable texture, and longer shelf life to the food products in which it is used.[23]

Freezing point

Fructose has a greater effect on freezing point depression than disaccharides or oligosaccharides, which may protect the integrity of cell walls of fruit by reducing ice crystal formation. However, this characteristic may be undesirable in soft-serve or hard-frozen dairy desserts.[23]

Fructose and starch functionality in food systems

Fructose increases starch viscosity more rapidly and achieves a higher final viscosity than sucrose because fructose lowers the temperature required during gelatinizing of starch, causing a greater final viscosity.[30]

Although some artificial sweeteners are not suitable for home baking, many traditional recipes use fructose.[31]

Food sources

Crystalline fructose

Natural sources of fructose include fruits, vegetables (including sugar cane), and honey.[32] Fructose is often further concentrated from these sources. The highest dietary sources of fructose, besides pure crystalline fructose, are foods containing white sugar (sucrose), high-fructose corn syrup, agave nectar, honey, molasses, maple syrup, fruit and fruit juices, as these have the highest percentages of fructose (including fructose in sucrose) per serving compared to other common foods and ingredients. Fructose exists in foods either as a free monosaccharide or bound to glucose as sucrose, a disaccharide. Fructose, glucose, and sucrose may all be present in food; however, different foods will have varying levels of each of these three sugars.

The sugar contents of common fruits and vegetables are presented in Table 1. In general, in foods that contain free fructose, the ratio of fructose to glucose is approximately 1:1; that is, foods with fructose usually contain about an equal amount of free glucose. A value that is above 1 indicates a higher proportion of fructose to glucose and below 1 a lower proportion. Some fruits have larger proportions of fructose to glucose compared to others. For example, apples and pears contain more than twice as much free fructose as glucose, while for apricots the proportion is less than half as much fructose as glucose.

Apple and pear juices are of particular interest to pediatricians because the high concentrations of free fructose in these juices can cause diarrhea in children. The cells (enterocytes) that line children's small intestines have less affinity for fructose absorption than for glucose and sucrose.[33] Unabsorbed fructose creates higher osmolarity in the small intestine, which draws water into the gastrointestinal tract, resulting in osmotic diarrhea. This phenomenon is discussed in greater detail in the Health Effects section.

Table 1 also shows the amount of sucrose found in common fruits and vegetables. Sugarcane and sugar beet have a high concentration of sucrose, and are used for commercial preparation of pure sucrose. Extracted cane or beet juice is clarified, removing impurities; and concentrated by removing excess water. The end product is 99.9%-pure sucrose. Sucrose-containing sugars include common white sugar and powdered sugar, as well as brown sugar.[34]

Table 1. Sugar content of selected common plant foods (g/100g)[35]
Food Item Total
CarbohydrateA
including
"dietary fiber" 		Total
Sugars 		Free
Fructose 		Free
Glucose 		Sucrose Fructose/
Glucose
Ratio 		Sucrose
as a % of
Total Sugars

Free Fructose as a % of Total Sugars

Fruits              
Apple 13.8 10.4 5.9 2.4 2.1 2.0 19.9 57
Apricot 11.1 9.2 0.9 2.4 5.9 0.7 63.5 10
Banana 22.8 12.2 4.9 5.0 2.4 1.0 20.0 40
Fig, dried 63.9 47.9 22.9 24.8 0.9 0.93 1.9 47.8
Grapes 18.1 15.5 8.1 7.2 0.2 1.1 1 52
Navel orange 12.5 8.5 2.25 2.0 4.3 1.1 50.4 26
Peach 9.5 8.4 1.5 2.0 4.8 0.9 56.7 18
Pear 15.5 9.8 6.2 2.8 0.8 2.1 8.0 63
Pineapple 13.1 9.9 2.1 1.7 6.0 1.1 60.8 21
Plum 11.4 9.9 3.1 5.1 1.6 0.66 16.2 31
Vegetables              
Beet, Red 9.6 6.8 0.1 0.1 6.5 1.0 96.2 1.5
Carrot 9.6 4.7 0.6 0.6 3.6 1.0 77 13
Red Pepper, Sweet 6.0 4.2 2.3 1.9 0.0 1.2 0.0 55
Onion, Sweet 7.6 5.0 2.0 2.3 0.7 0.9 14.3 40
Sweet Potato 20.1 4.2 0.7 1.0 2.5 0.9 60.3 17
Yam 27.9 0.5 tr tr tr na tr
Sugar Cane 13–18 0.2 – 1.0 0.2 – 1.0 11–16 1.0 high 1.5-5.6
Sugar Beet 17–18 0.1 – 0.5 0.1 – 0.5 16–17 1.0 high 0.59-2.8
Grains              
Maize, Sweet 19.0 6.2 1.9 3.4 0.9 0.61 15.0 31
^A The carbohydrate figure is calculated in FoodData Central and does not always correspond to the sum of the sugars, the starch, and the "dietary fiber".

All data with a unit of g (gram) are based on 100 g of a food item. The fructose/glucose ratio is calculated by dividing the sum of free fructose plus half sucrose by the sum of free glucose plus half sucrose.

Fructose is also found in the manufactured sweetener, high-fructose corn syrup (HFCS), which is produced by treating corn syrup with enzymes, converting glucose into fructose.[36] The common designations for fructose content, HFCS-42 and HFCS-55, indicate the percentage of fructose present in HFCS.[36] HFCS-55 is commonly used as a sweetener for soft drinks, whereas HFCS-42 is used to sweeten processed foods, breakfast cereals, bakery foods, and some soft drinks.[36]

Carbohydrate content of commercial sweeteners (percent on dry basis)

Sugar Fructose Glucose Sucrose
(Fructose+Glucose) 		Other
sugars
Granulated sugar 0 0 100 0
Caramel 1 1 97 1
HFCS-42 42 53 0 5
HFCS-55 55 41 0 4
HFCS-90 90 5 0 5
Honey 50 44 1 5
Maple syrup 1 4 95 0
Molasses 23 21 53 3
Tapioca Syrup 55 45 0 0
Corn syrup 0 98 0 2

[34] for HFCS, and USDA for fruits and vegetables and the other refined sugars.[35]

Cane and beet sugars have been used as the major sweetener in food manufacturing for centuries. However, with the development of HFCS, a significant shift occurred in the type of sweetener consumption in certain countries, particularly the United States.[37] Contrary to the popular belief, however, with the increase of HFCS consumption, the total fructose intake relative to the total glucose intake has not dramatically changed. Granulated sugar is 99.9%-pure sucrose, which means that it has equal ratio of fructose to glucose. The most commonly used forms of HFCS, HFCS-42, and HFCS-55, have a roughly equal ratio of fructose to glucose, with minor differences. HFCS has simply replaced sucrose as a sweetener. Therefore, despite the changes in the sweetener consumption, the ratio of glucose to fructose intake has remained relatively constant.[38]

Figure 3: Adjusted consumption of refined sugar per capita in the US

Nutritional information

Providing 368 kcal per 100 grams of dry powder (table), fructose has 95% the caloric value of sucrose by weight.[39][40] Fructose powder is 100% carbohydrates and supplies no other nutrients in significant amount (table).

Fructose, dry powdered
Nutritional value per 100 g (3.5 oz)
Energy368 kcal (1,540 kJ)
100 g
0 g
0 g
MineralsQuantity %DV†
Calcium
0%
0 mg
Iron
1%
0.1 mg
Phosphorus
0%
0 mg
Potassium
0%
0 mg
Sodium
1%
12 mg
Full Link to USDA Database entry
†Percentages are roughly approximated using US recommendations for adults.
Source: USDA Nutrient Database

Fructose digestion and absorption in humans

Figure 4: Hydrolysis of sucrose to glucose and fructose by sucrase
Figure 5: Intestinal sugar transport proteins

Fructose exists in foods either as a monosaccharide (free fructose) or as a unit of a disaccharide (sucrose). Free fructose is absorbed directly by the intestine. When fructose is consumed in the form of sucrose, it is digested (broken down) and then absorbed as free fructose. As sucrose comes into contact with the membrane of the small intestine, the enzyme sucrase catalyzes the cleavage of sucrose to yield one glucose unit and one fructose unit, which are then each absorbed. After absorption, it enters the hepatic portal vein and is directed toward the liver.

The mechanism of fructose absorption in the small intestine is not completely understood. Some evidence suggests active transport, because fructose uptake has been shown to occur against a concentration gradient.[41] However, the majority of research supports the claim that fructose absorption occurs on the mucosal membrane via facilitated transport involving GLUT5 transport proteins.[42] Since the concentration of fructose is higher in the lumen, fructose is able to flow down a concentration gradient into the enterocytes, assisted by transport proteins. Fructose may be transported out of the enterocyte across the basolateral membrane by either GLUT2 or GLUT5, although the GLUT2 transporter has a greater capacity for transporting fructose, and, therefore, the majority of fructose is transported out of the enterocyte through GLUT2.[42]

Capacity and rate of absorption

The absorption capacity for fructose in monosaccharide form ranges from less than 5 g to 50 g (per individual serving) and adapts with changes in dietary fructose intake.[43] Studies show the greatest absorption rate occurs when glucose and fructose are administered in equal quantities.[43] When fructose is ingested as part of the disaccharide sucrose, absorption capacity is much higher because fructose exists in a 1:1 ratio with glucose. It appears that the GLUT5 transfer rate may be saturated at low levels, and absorption is increased through joint absorption with glucose.[44] One proposed mechanism for this phenomenon is a glucose-dependent cotransport of fructose. In addition, fructose transfer activity increases with dietary fructose intake. The presence of fructose in the lumen causes increased mRNA transcription of GLUT5, leading to increased transport proteins. High-fructose diets (>2.4 g/kg body wt) increase the transport proteins within three days of intake.[45]

Malabsorption

Several studies have measured the intestinal absorption of fructose using the hydrogen breath test.[46][47][48][49] These studies indicate that fructose is not completely absorbed in the small intestine. When fructose is not absorbed in the small intestine, it is transported into the large intestine, where it is fermented by the colonic flora. Hydrogen is produced during the fermentation process and dissolves into the blood of the portal vein. This hydrogen is transported to the lungs, where it is exchanged across the lungs and is measurable by the hydrogen breath test. The colonic flora also produces carbon dioxide, short-chain fatty acids, organic acids, and trace gases in the presence of unabsorbed fructose.[50] The presence of gases and organic acids in the large intestine causes gastrointestinal symptoms such as bloating, diarrhea, flatulence, and gastrointestinal pain.[46] Exercise immediately after consumption can exacerbate these symptoms by decreasing transit time in the small intestine, resulting in a greater amount of fructose emptied into the large intestine.[51]

Fructose metabolism

All three dietary monosaccharides are transported into the liver by the GLUT2 transporter.[52] Fructose and galactose are phosphorylated in the liver by fructokinase (Km= 0.5 mM) and galactokinase (Km = 0.8 mM), respectively. By contrast, glucose tends to pass through the liver (Km of hepatic glucokinase = 10 mM) and can be metabolised anywhere in the body. Uptake of fructose by the liver is not regulated by insulin. However, insulin is capable of increasing the abundance and functional activity of GLUT5, fructose transporter, in skeletal muscle cells.[53]

Fructolysis

Main page: Biology:Fructolysis

The initial catabolism of fructose is sometimes referred to as fructolysis, in analogy with glycolysis, the catabolism of glucose. In fructolysis, the enzyme fructokinase initially produces fructose 1-phosphate, which is split by aldolase B to produce the trioses dihydroxyacetone phosphate (DHAP) and glyceraldehyde. Unlike glycolysis, in fructolysis the triose glyceraldehyde lacks a phosphate group. A third enzyme, triokinase, is therefore required to phosphorylate glyceraldehyde, producing glyceraldehyde 3-phosphate. The resulting trioses are identical to those obtained in glycolysis and can enter the gluconeogenic pathway for glucose or glycogen synthesis, or be further catabolized through the lower glycolytic pathway to pyruvate.

Metabolism of fructose to DHAP and glyceraldehyde

The first step in the metabolism of fructose is the phosphorylation of fructose to fructose 1-phosphate by fructokinase, thus trapping fructose for metabolism in the liver. Fructose 1-phosphate then undergoes hydrolysis by aldolase B to form DHAP and glyceraldehydes; DHAP can either be isomerized to glyceraldehyde 3-phosphate by triosephosphate isomerase or undergo reduction to glycerol 3-phosphate by glycerol 3-phosphate dehydrogenase. The glyceraldehyde produced may also be converted to glyceraldehyde 3-phosphate by glyceraldehyde kinase or further converted to glycerol 3-phosphate by glycerol 3-phosphate dehydrogenase. The metabolism of fructose at this point yields intermediates in the gluconeogenic pathway leading to glycogen synthesis as well as fatty acid and triglyceride synthesis.

Synthesis of glycogen from DHAP and glyceraldehyde 3-phosphate

The resultant glyceraldehyde formed by aldolase B then undergoes phosphorylation to glyceraldehyde 3-phosphate. Increased concentrations of DHAP and glyceraldehyde 3-phosphate in the liver drive the gluconeogenic pathway toward glucose and subsequent glycogen synthesis.[54] It appears that fructose is a better substrate for glycogen synthesis than glucose and that glycogen replenishment takes precedence over triglyceride formation.[55] Once liver glycogen is replenished, the intermediates of fructose metabolism are primarily directed toward triglyceride synthesis.[56]

Figure 6: Metabolic conversion of fructose to glycogen in the liver

Synthesis of triglyceride from DHAP and glyceraldehyde 3-phosphate

Carbons from dietary fructose are found in both the free fatty acid and glycerol moieties of plasma triglycerides. High fructose consumption can lead to excess pyruvate production, causing a buildup of Krebs cycle intermediates.[57] Accumulated citrate can be transported from the mitochondria into the cytosol of hepatocytes, converted to acetyl CoA by citrate lyase and directed toward fatty acid synthesis.[57][58] In addition, DHAP can be converted to glycerol 3-phosphate, providing the glycerol backbone for the triglyceride molecule.[58] Triglycerides are incorporated into very-low-density lipoproteins (VLDL), which are released from the liver destined toward peripheral tissues for storage in both fat and muscle cells.

Figure 7: Metabolic conversion of fructose to triglyceride in the liver

Potential health effects

In 2022, the European Food Safety Authority stated that there is research evidence that fructose and other added free sugars may be associated with increased risk of several chronic diseases:[11][12] the risk is moderate for obesity and dyslipidemia (more than 50%), and low for non-alcoholic fatty liver disease, type 2 diabetes (from 15% to 50%) and hypertension. EFSA further stated that clinical research did "not support a positive relationship between the intake of dietary sugars, in isocaloric exchange with other macronutrients, and any of the chronic metabolic diseases or pregnancy-related endpoints assessed" but advised "the intake of added and free sugars should be as low as possible in the context of a nutritionally adequate diet."[12]

Cardiometabolic diseases

When fructose is consumed in excess as a sweetening agent in foods or beverages, it may be associated with increased risk of obesity, diabetes, and cardiovascular disorders that are part of metabolic syndrome.[12]

Compared with sucrose

Fructose was found to increase triglycerides in type-2 but not type-1 diabetes and moderate use of it has previously been considered acceptable as a sweetener for diabetics,[59] possibly because it does not trigger the production of insulin by pancreatic β cells.[60] For a 50 gram reference amount, fructose has a glycemic index of 23, compared with 100 for glucose and 60 for sucrose.[61] Fructose is also 73% sweeter than sucrose at room temperature, allowing diabetics to use less of it per serving. Fructose consumed before a meal may reduce the glycemic response of the meal.[62] Fructose-sweetened food and beverage products cause less of a rise in blood glucose levels than do those manufactured with either sucrose or glucose.[11]

See also

References

  1. ↑ "Fructose". Merriam-Webster. http://mw4.m-w.com/dictionary/fructose. 
  2. ↑ Levulose comes from the Latin word laevus, "left"; levulose is the old word for the most occurring isomer of fructose. D-fructose rotates plane-polarised light to the left, hence the name."Levulose". http://www.monashscientific.com.au/Levulose.htm. .
  3. ↑ "2-Carb-10". https://iupac.qmul.ac.uk/2carb/10.html. 
  4. ↑ CRC Handbook of Chemistry and Physics (49th ed.). 1968–69. p. D-186. 
  5. ↑ Chambers, Michael. "ChemIDplus – 57-48-7 – BJHIKXHVCXFQLS-UYFOZJQFSA-N – Fructose [USP:JAN – Similar structures search, synonyms, formulas, resource links, and other chemical information."]. US National Institutes of Health. https://chem.nlm.nih.gov/chemidplus/rn/57-48-7. 
  6. ↑ Dubrunfaut (1847). "Sur une propriété analytique des fermentations alcoolique et lactique, et sur leur application à l'étude des sucres" (in fr). Annales de Chimie et de Physique 21: 169–178. https://books.google.com/books?id=PJ45AAAAcAAJ&pg=PA169.  On page 174, Dubrunfaut relates the discovery and properties of fructose.
  7. ↑ Fruton, J. S. (1974). "Molecules and Life – Historical Essays on the Interplay of Chemistry and Biology". Molecular Nutrition & Food Research (New York: Wiley‐Interscience) 18 (4). doi:10.1002/food.19740180423. https://onlinelibrary.wiley.com/doi/abs/10.1002/food.19740180423. Retrieved 2021-02-05. 
  8. ↑ 8.0 8.1 Miller, William Allen (1857). "Part III. Organic Chemistry". Elements of Chemistry: Theoretical and Practical. London: John W. Parker and son. pp. 52, 57. https://archive.org/details/elementschemist03millgoog. 
  9. ↑ Hyvonen, L.; Koivistoinen, P (1982). "Fructose in Food Systems". Nutritive Sweeteners. London & New Jersey: Applied Science Publishers. pp. 133–144. ISBN 978-0-85334-997-6. 
  10. ↑ Wach, Wolfgang (2004). "fructose". Ullmann’s Encyclopedia of Industrial Chemistry. Weinheim: Wiley-VCH. doi:10.1002/14356007.a12_047.pub2. ISBN 9783527303854. 
  11. ↑ 11.0 11.1 11.2 11.3 "Scientific Opinion on the substantiation of health claims related to fructose and reduction of post-prandial glycaemic responses (ID 558) pursuant to Article 13(1) of Regulation (EC) No 1924/2006". EFSA Journal (EFSA Panel on Dietetic Products, Nutrition and Allergies) 9 (6): 2223. 2011. doi:10.2903/j.efsa.2011.2223. "The Panel notes that these values support a significant decrease in post-prandial blood glucose responses when fructose replaces either sucrose or glucose.". 
  12. ↑ 12.0 12.1 12.2 12.3 EFSA Panel on Nutrition, Novel Foods and Food Allergens (28 February 2022). "Tolerable upper intake level for dietary sugars". EFSA Journal 20 (2): 337. doi:10.2903/j.efsa.2022.7074. ISSN 1831-4732. PMID 35251356. PMC 8884083. https://doi.org/10.2903/j.efsa.2022.7074. Retrieved 3 October 2022. 
  13. ↑ "Carbohydrates and Health". UK Scientific Advisory Committee on Nutrition, Public Health England, TSO. 2015. https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/445503/SACN_Carbohydrates_and_Health.pdf. 
  14. ↑ 14.0 14.1 "Fructose. Origin and meaning of fructose" (in en). Online Etymology Dictionary, Douglas Harper. 2017. https://www.etymonline.com/word/fructose. 
  15. ↑ "D-Fructose". PubChem, US National Library of Medicine. 20 February 2021. https://pubchem.ncbi.nlm.nih.gov/compound/2723872. 
  16. ↑ Shi, Kemeng; Pedersen, Christian Marcus; Guo, Zhaohui; Li, Yanqiu; Zheng, Hongyan; Qiao, Yan; Hu, Tuoping; Wang, Yingxiong (1 December 2018). "NMR studies of the tautomer distributions of d‑fructose in lower alcohols/DMSO‑d6". Journal of Molecular Liquids 271: 926–932. doi:10.1016/j.molliq.2018.09.067. https://doi.org/10.1016/j.molliq.2018.09.067. Retrieved 24 February 2021. 
  17. ↑ Schneider, Bernd; Lichtenthaler, Frieder W.; Steinle, Georg; Schiweck, Hubert (22 December 1985). "Studies on Ketoses, 1 Distribution of Furanoid and Pyranoid Tautomers of D-Fructose in Water, Dimethyl Sulfoxide, and Pyridinevia1H NMR Intensities of Anomeric Hydroxy Groups in [D6DMSO"]. Liebigs Annalen der Chemie 1985 (12): 2443–2453. doi:10.1002/jlac.198519851213. https://doi.org/10.1002/jlac.198519851213. Retrieved 24 February 2021. 
  18. ↑ Funcke, Werner; von Sonntag, Clemens; Triantaphylides, Christian (October 1979). "Detection of the open-chain forms of d-fructose and L-sorbose in aqueous solution by using 13C-n.m.r. spectroscopy". Carbohydrate Research 75: 305–309. doi:10.1016/S0008-6215(00)84649-2. https://doi.org/10.1016/S0008-6215(00)84649-2. Retrieved 24 February 2021. 
  19. ↑ McWilliams, Margaret (2001). Foods: Experimental Perspectives, 4th Edition. Prentice Hall. ISBN 978-0-13-021282-5. https://archive.org/details/foodsexperimenta00mcwi. 
  20. ↑ Keusch, P. "Yeast and Sugar- the Chemistry must be right". http://www.chemie.uni-regensburg.de/Organische_Chemie/Didaktik/Keusch/D-fermentation_sugar-e.htm. 
  21. ↑ Dills, WL (1993). "Protein fructosylation: Fructose and the Maillard reaction". Journal of Clinical Nutrition 58 (5 Suppl): 779–787. doi:10.1093/ajcn/58.5.779S. PMID 8213610. 
  22. ↑ Huber, GW; Iborra, S; Corma, A (September 2006). "Synthesis of transportation fuels from biomass: chemistry, catalysts, and engineering". Chem. Rev. 106 (9): 4044–98. doi:10.1021/cr068360d. PMID 16967928. https://works.bepress.com/cgi/viewcontent.cgi?article=1058&context=george_huber. Retrieved 2020-08-28. 
  23. ↑ 23.0 23.1 23.2 23.3 23.4 Hanover, L. M.; White, J. S. (1 November 1993). "Manufacturing, composition, and applications of fructose" (in en). The American Journal of Clinical Nutrition 58 (5): 724S–732S. doi:10.1093/ajcn/58.5.724S. ISSN 0002-9165. PMID 8213603. http://ajcn.nutrition.org/content/58/5/724S.abstract. Retrieved 7 February 2017. 
  24. ↑ "Sugar Sweetness". Oregon State University. Archived from the original on May 16, 2008. https://web.archive.org/web/20080516050325/http://food.oregonstate.edu/sugar/sweet.html. Retrieved 7 February 2017. 
  25. ↑ 25.0 25.1 25.2 25.3 Lee, Thomas D. (1 January 2000). "Sweeteners" (in en). Kirk-Othmer Encyclopedia of Chemical Technology. doi:10.1002/0471238961.19230505120505.a01.pub2. ISBN 978-0471238966. 
  26. ↑ Jana, A.H.; Joshi, N.S.S. (November 1994). "Sweeteners for frozen [desserts success – a review"]. Australian Journal of Dairy Technology 49. http://agris.fao.org/agris-search/search.do?recordID=AU9500465. Retrieved 7 February 2017. 
  27. ↑ Shallenberger, R.S. (1994). Taste Chemistry. Chapman and Hall. ISBN 978-0-7514-0150-9. 
  28. ↑ 28.0 28.1 Nabors, LO (2001). American Sweeteners. pp. 374–375. 
  29. ↑ McWilliams, Margaret (2001). Foods: Experimental Perspectives, 4th Edition. Upper Saddle River, NJ : Prentice Hall. ISBN 978-0-13-021282-5. https://archive.org/details/foodsexperimenta00mcwi. 
  30. ↑ White, DC; Lauer GN (1990). "Predicting gelatinization temperature of starch/sweetener system for cake formulation by differential scanning calorimetry I. Development of a model". Cereal Foods World 35: 728–731. 
  31. ↑ Margaret M. Wittenberg (2007). New Good Food: Essential Ingredients for Cooking and Eating Well. Diet and Nutrition Series; pages 249–51. Ten Speed Press. p. 249. ISBN 978-1580087506. https://archive.org/details/isbn_9781580087506. "fructose traditional baking." 
  32. ↑ Park, KY; Yetley AE (1993). "Intakes and food sources of fructose in the United States". American Journal of Clinical Nutrition 58 (5 Suppl): 737S–747S. doi:10.1093/ajcn/58.5.737S. PMID 8213605. 
  33. ↑ Riby, JE; Fujisawa T; Kretchmer N (1993). "Fructose absorption". American Journal of Clinical Nutrition 58 (5 Suppl): 748S–753S. doi:10.1093/ajcn/58.5.748S. PMID 8213606. 
  34. ↑ 34.0 34.1 Kretchmer, N; Hollenbeck CB (1991). Sugars and Sweeteners. CRC Press, Inc.. 
  35. ↑ 35.0 35.1 Use link to FoodData Central (USDA) and then search for the particular food, and click on "SR Legacy Foods".
  36. ↑ 36.0 36.1 36.2 "High Fructose Corn Syrup: Questions and Answers". US Food and Drug Administration. 5 November 2014. https://www.fda.gov/Food/IngredientsPackagingLabeling/FoodAdditivesIngredients/ucm324856.htm. 
  37. ↑ White, J. S (2008). "Straight talk about high-fructose corn syrup: What it is and what it ain't". American Journal of Clinical Nutrition 88 (6): 1716S–1721S. doi:10.3945/ajcn.2008.25825B. PMID 19064536. 
  38. ↑ Guthrie, FJ; Morton FJ (2000). "Food sources of added sweeteners in the diets of Americans". Journal of the American Dietetic Association 100 (1): 43–51. doi:10.1016/S0002-8223(00)00018-3. PMID 10646004. 
  39. ↑ "Calories and nutrient composition for fructose, dry powder per 100 g". USDA National Nutrient Database, version SR-28. May 2016. https://ndb.nal.usda.gov/ndb/foods/show/8681. 
  40. ↑ "Calories and nutrient composition for sucrose granules per 100 g". USDA National Nutrient Database, version SR-28. May 2016. https://ndb.nal.usda.gov/ndb/foods/show/6319. 
  41. ↑ Stipanuk, Marsha H (2006). Biochemical, Physiological, and Molecular Aspects of Human Nutrition, 2nd Edition. W.B. Saunders, Philadelphia, PA. 
  42. ↑ 42.0 42.1 Shi, Ya-Nan; Liu, Ya-Jin; Xie, Zhifang; Zhang, Weiping J. (5 June 2021). "Fructose and metabolic diseases: too much to be good". Chinese Medical Journal 134 (11): 1276–1285. doi:10.1097/CM9.0000000000001545. PMID 34010200. PMC 8183764. https://journals.lww.com/cmj/Fulltext/2021/06050/Fructose_and_metabolic_diseases__too_much_to_be.4.aspx. Retrieved 15 February 2022. 
  43. ↑ 43.0 43.1 Fujisawa, T; Riby J; Kretchmer N (1991). "Intestinal absorption of fructose in the rat". Gastroenterology 101 (2): 360–367. doi:10.1016/0016-5085(91)90012-a. PMID 2065911. 
  44. ↑ Ushijima, K; Fujisawa T; Riby J; Kretchmer N (1991). "Absorption of fructose by isolated small intestine of rats is via a specific saturable carrier in the absence of glucose and by the disaccharidase-related transport system in the presence of glucose". Journal of Nutrition 125 (8): 2156–2164. doi:10.1093/jn/125.8.2156. PMID 7643250. 
  45. ↑ Ferraris, R (2001). "Dietary and developmental regulation of intestinal sugar transport". Biochemical Journal 360 (Pt 2): 265–276. doi:10.1042/0264-6021:3600265. PMID 11716754. 
  46. ↑ 46.0 46.1 Beyer, PL; Caviar EM; McCallum RW (2005). "Fructose intake at current levels in the United States may cause gastrointestinal distress in normal adults". J. Am. Diet. Assoc. 105 (10): 1559–1566. doi:10.1016/j.jada.2005.07.002. PMID 16183355. 
  47. ↑ Ravich, WJ; Bayless TM; Thomas, M (1983). "Fructose: incomplete intestinal absorption in humans". Gastroenterology 84 (1): 26–29. doi:10.1016/S0016-5085(83)80162-0. PMID 6847852. 
  48. ↑ Riby, JE; Fujisawa T; Kretchmer, N (1993). "Fructose absorption". American Journal of Clinical Nutrition 58 (5 Suppl): 748S–753S. doi:10.1093/ajcn/58.5.748S. PMID 8213606. 
  49. ↑ Rumessen, JJ; Gudman-Hoyer E (1986). "Absorption capacity of fructose in healthy adults. Comparison with sucrose and its constituent monosaccharides". Gut 27 (10): 1161–1168. doi:10.1136/gut.27.10.1161. PMID 3781328. 
  50. ↑ Skoog, SM; Bharucha AE (2004). "Dietary fructose and gastrointestinal symptoms: a review". Am. J. Gastroenterol. 99 (10): 2046–50. doi:10.1111/j.1572-0241.2004.40266.x. PMID 15447771. 
  51. ↑ Fujisawa, T, T; Mulligan K; Wada L; Schumacher L; Riby J; Kretchmer N (1993). "The effect of exercise on fructose absorption". Am. J. Clin. Nutr. 58 (1): 75–9. doi:10.1093/ajcn/58.1.75. PMID 8317393. 
  52. ↑ Quezada-Calvillo, R; Robayo CC; Nichols BL (2006). Carbohydrate Digestion and Absorption. Missouri: Saunders, Elsevier. pp. 182–185. ISBN 978-1-4160-0209-3. 
  53. ↑ Hajduch, E; Litherland GJ; Turban S; Brot-Laroche E; Hundal HS (Aug 2003). "Insulin regulates the expression of the GLUT5 transporter in L6 skeletal muscle cells". FEBS Letters 549 (1–3): 77–82. doi:10.1016/S0014-5793(03)00773-7. PMID 12914929. 
  54. ↑ MA Parniak; Kalant N (1988). "Enhancement of glycogen concentrations in primary cultures of rat hepatocytes exposed to glucose and fructose". Biochemical Journal 251 (3): 795–802. doi:10.1042/bj2510795. PMID 3415647. 
  55. ↑ Jia, Guanghong; Aroor, Annayya R.; Whaley-Connell, Adam T.; Sowers, James R. (June 2014). "Fructose and Uric Acid: Is There a Role in Endothelial Function?" (in en). Current Hypertension Reports 16 (6): 434. doi:10.1007/s11906-014-0434-z. ISSN 1522-6417. PMID 24760443. 
  56. ↑ Medina Villaamil (2011-02-01). "Fructose transporter Glut5 expression in clear renal cell carcinoma" (in en). Oncology Reports 25 (2): 315–23. doi:10.3892/or.2010.1096. ISSN 1021-335X. PMID 21165569. 
  57. ↑ 57.0 57.1 McGrane, MM (2006). Carbohydrate metabolism: Synthesis and oxidation. Missouri: Saunders, Elsevier. pp. 258–277. ISBN 978-1-4160-0209-3. 
  58. ↑ 58.0 58.1 Sul, HS (2006). Metabolism of Fatty Acids, Acylglycerols, and Sphingolipids. Missouri: Saunders, Elsevier. pp. 450–467. ISBN 978-1-4160-0209-3. 
  59. ↑ Rizkalla, Salwa W (2010). "Health implications of fructose consumption: A review of recent data". Nutrition & Metabolism 7 (1): 82. doi:10.1186/1743-7075-7-82. ISSN 1743-7075. PMID 21050460. 
  60. ↑ Thorens, Bernard; Mueckler, Mike (2010). "Glucose transporters in the 21st Century (Review)". American Journal of Physiology. Endocrinology and Metabolism 298 (2): E141–E145. doi:10.1152/ajpendo.00712.2009. ISSN 0193-1849. PMID 20009031. 
  61. ↑ "Glycemic index". Glycemic Index Testing and Research, University of Sydney (Australia) Glycemic Index Research Service (SUGiRS). 2 May 2017. http://www.glycemicindex.com/foodSearch.php. 
  62. ↑ Patricia M. Heacock; Steven R. Hertzler; Bryan W. Wolf (2002). "Fructose Prefeeding Reduces the Glycemic Response to a High-Glycemic Index, Starchy Food in Humans". Journal of Nutrition 132 (9): 2601–2604. doi:10.1093/jn/132.9.2601. PMID 12221216. 

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