Difference between fructose and glucose

Difference between glucose and fructose

Pawel Malczewski
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Similarities of glucose and fructose

Before going through the differences, it is important to note that there are some common characteristics of glucose and fructose, exerting varied effects on the body, and undergoing different metabolic processes.

Both fructose and glucose are monosaccharides, have the same caloric values (roughly 4Cal/g), and the same molecular formula of CC6H1206.

Differences between glucose and fructose

Absorption (1)Vos MB, Lavine JE. Dietary fructose in nonalcoholic fatty liver disease. AASLD. Hepatology. Volume 57, Issue 6 June 2013 Pages 2525–2531. Available here. (2)Rao SS, Attaluri A, Anderson L, Stumbo P. The Ability of the Normal Human Small Intestine to Absorb Fructose: Evaluation by Breath Testing. Clin Gastroenterol Hepatol. 2007 Aug; 5(8): 959–963. Available here. (3)Suri SZ, Empie MW. Fructose metabolism in humans – what isotopic tracer studies tell us. Nutr Metab (Lond). 2012; 9: 89. Available here.

Fructose: is poorly absorbed and can cause fructose intolerance. It is moved to the colon, where it undergoes fermentation by bacteria producing gas, bloating and diarrhea.

Glucose: is well absorbed.

Brain interaction (4)Laterra J, Keep R, Betz LA, Goldstein GW. Basic Neurochemistry: Molecular, Cellular and Medical Aspects. Philadelphia: Lippincott-Raven; 1999. 6th edition. Available here.

Fructose: is slowly up taken through the brain barrier, causing the reduction of neural activity.

Glucose: is up taken quickly to the brain barrier where it is metabolised using most of the oxygen available in the brain. Glucose raises the level of neural activity for about 20 minutes after its consumption.

Cell entrance (5)Douard V, Ferraris RP. Regulation of the fructose transporter GLUT5 in health and disease. Am J Physiol Endocrinol Metab. 2008 Aug; 295(2): E227–E237. Available here. (6)Rajan AS. Regulation of Glucose Uptake. Medscape. Available here.

Fructose: is mainly (but not exclusively) metabolised by the liver. Other cells that accept fructose (although to a much lesser extent) are testicles, kidneys, skeletal muscles, fat tissue and brain. Fructose is up taken to the cells via a transporter called GLUT5 and also via GLUT2, to a smaller extent, which accepts fructose to the liver cells.

Glucose: is up taken to most of the cells in the body for metabolism. It uses the following transporters to distribute glucose to corresponding cells: GLUT1 (to all cells), GLUT2 (to gut, liver and pancreas), GLUT3 (to central nervous system and brain), GLUT4 (to cells that need insulin to be up-taken such as skeletal muscles, fatty tissue and heart).

Diabetics risk (7)Bantle JP. Dietary Fructose and Metabolic Syndrome and Diabetes. J Nutr. 2009 Jun; 139(6): 1263S–1268S. Available here.

Fructose: presents a long term risk for diabetics. Fructose only slightly increases blood glucose levels and insulin production after a meal. It does not cause sudden spikes in insulin levels and doesn’t present an immediate danger if over-consumed. A chronic excess of fructose, however, leads to increased lipid production, obesity, insulin resistance and metabolic syndrome, all of which are associated with increased long-term risk of diabetes.

Glucose: a high intake presents an immediate danger for diabetics, since it has a high glycemic index and load. This means that an overdose of glucose causes sudden spikes of insulin which can be dangerous and even fatal for diabetics.

Energy source (8)Lustig RH. Fructose: It’s “Alcohol Without the Buzz. Adv Nutr March 2013 Adv Nutr vol. 4: 226-235, 2013. Available here.

Fructose: is a non-essential energy source that has a similar action in the body to ethanol (with the exception of the effects on the brain).

Glucose: is a primary and preferred energy source and required by the brain cells. Note: ketones can serve as a substitute but a high ketogenic diet may not be sustainable in the long term.

Energy storage as glycogen (9)Rizkalla SW. Health implications of fructose consumption: A review of recent data. Nutrition & Metabolism20107:82. Available here.

Fructose: needs to be converted into glucose first in order to be stored in glycogen stores.

Glucose: gets stored as glycogen in the liver and muscle cells.

Food sources (10)Agricultural Research Service. United States Department of Agriculture National Nutrient Database for Standard Reference Release 27. Available here.

Fructose: not present in starch.

Glucose: present in starch.

Gout (11)Narins RG, Weisberg JS, Myers AR. Effects of carbohydrates on uric acid metabolism. ScienceDirect. Metabolism. Volume 23, Issue 5, May 1974, Pages 455–465. Available here. (12)Singh JA, Reddy SG, Kundukulam J. Risk Factors for Gout and Prevention: A Systematic Review of the Literature. Curr Opin Rheumatol. 2011 Mar; 23(2): 192–202. Available here.

Fructose: a high intake produces uric acid, which increases the risk of gout.

Glucose: hasn’t been associated with an increased risk of gout.

Insulin response and glycemic index (13)The University of Sydney. Search for the Glycemic Index Available here.

Fructose stimulates insulin in a much lesser degree than glucose. The glycemic index and load are much higher for glucose than fructose.

CarbsGlycemic IndexServe (g)Glycemic Load
Glucose (14)The University of Sydney. Glycemic Index of Glucose. Available here.1001010
Fructose (15)The University of Sydney. Glycemic Index of Fructose. Available here.23102

Leptin resistance (16)Bantle JP. Dietary Fructose and Metabolic Syndrome and Diabetes. J Nutr. 2009 Jun; 139(6): 1263S–1268S. Available here. (17)Pan H, Guo J, Su Z. Advances in understanding the interrelations between leptin resistance and obesity. Physiology and Behaviour. Volume 130, 10 May 2014, Pages 157–169. Available here.

Fructose: has a minor impact on insulin release after a meal. Insulin increases the release of leptin, a hormone that inhibits appetite. If there is less insulin in circulation, leptin levels are not as high and appetite is not suppressed as effectively as after glucose intake. As a result, a high fructose diet leads to overeating.

Glucose: has a more significant effect on leptin. Glucose increases insulin production which increases the release of leptin, sending us a signal that we should stop eating, therefore, suppressing our appetite.

Metabolism (18)Suri SZ, Empie MW. Fructose metabolism in humans – what isotopic tracer studies tell us. Nutr Metab (Lond). 2012; 9: 89. Available here.

Assuming the same amount of fructose and glucose is ingested, the summary of the products of metabolism is:

Fructose: almost 100% of the ingested fructose goes to the liver cells for metabolism. Because of a much higher amount of fructose entering the liver cells, more VLDL particles are generated, causing dyslipidaemia. The excessive fat production will also generate free fatty acids that enter the muscle cells, causing insulin resistance. Lipid droplets that will remain in the liver, can lead to fatty liver disease. A by-product of fructose metabolism, JNK1, will cause inflammation and decrease liver insulin sensitivity. (read more..)

Glucose: 20% of the glucose ingested gets to the liver. Some is stored as glycogen and some enters mitochondria, where is utilised for cellular energy. A small amount of VLDL particles is produced from unused mitochondria energy. High amounts of VLDLs are associated with increased risk of heart disease. (read more..) The rest is absorbed and metabolised by most (but not all e.g. sperm) cells in the body. Glucose is especially important in the brain, where is metabolised as a primary fuel source.

Molecular shape (19)Berg JM, Tymoczko JL. Stryer L. Biochemistry. Section 11.1Monosaccharides Are Aldehydes or Ketones with Multiple Hydroxyl Groups W. H. Freeman and Company.5th edition. Available here.

Both fructose and glucose are monosaccharides, called hexose, containing six carbon atoms and have a formula C6H12O6. However, they differ in their ring structures. The differences in shape mean that some enzymes, with specific shapes of active sites (a place where substance fits into the enzyme), will accept one but not the other.

Fructose: five member ring structure.
Fructose structure
Glucose: six member ring structure.
Glucose structure
Sperm (20)Schirren C. Relation between fructose content of semen and fertility in man. J Reprod Fertil June 1, 1963 5 347-358 Available here. (21)Frenette G, Thabet M, Sullivan R. Polyol Pathway in Human Epididymis and Semen. Journal of Andrology. Volume 27, Issue 2, pages 233–239, March-April 2006. Available here.

Fructose: sperm cells use fructose as their energy source.

Glucose: needs to be converted to fructose in order to be used by the sperm as an energy source.

Sweetness ranking (22)White JS. Sucrose, HFCS, and Fructose: History, Manufacture, Composition, Applications, and Production. Available here.

Fructose: Fructose tastes 1.17 times sweeter than sucrose (table sugar). Fructose is 1.74 sweeter than glucose.

Glucose: Sucrose (table sugar) tastes 1.49 times sweeter than glucose.

Triglycerides (23)Bantle JP. Dietary Fructose and Metabolic Syndrome and Diabetes. J Nutr. 2009 Jun; 139(6): 1263S–1268S. Available here. (24)Hudgins LC, Parker TS, Levine DM, Hellerstein MK. A Dual Sugar Challenge Test for Lipogenic Sensitivity to Dietary Fructose. The journal of Clinical Endocrinology & Metabolism.Volume 96, Issue 3. Available here.

High fructose amounts produce much higher levels of triglycerides (fats) during its metabolism in the liver than glucose. Studies show that there are approximately 30% more triglycerides in the blood on a high fructose diet than on high glucose diet. Please note, however, that the triglyceride production also depends on the level of physical activity and glycogen stores. For instance, triglyceride production from fructose does not have much impact in elite athletes.

References   [ + ]

1. Vos MB, Lavine JE. Dietary fructose in nonalcoholic fatty liver disease. AASLD. Hepatology. Volume 57, Issue 6 June 2013 Pages 2525–2531. Available here.
2. Rao SS, Attaluri A, Anderson L, Stumbo P. The Ability of the Normal Human Small Intestine to Absorb Fructose: Evaluation by Breath Testing. Clin Gastroenterol Hepatol. 2007 Aug; 5(8): 959–963. Available here.
3. Suri SZ, Empie MW. Fructose metabolism in humans – what isotopic tracer studies tell us. Nutr Metab (Lond). 2012; 9: 89. Available here.
4. Laterra J, Keep R, Betz LA, Goldstein GW. Basic Neurochemistry: Molecular, Cellular and Medical Aspects. Philadelphia: Lippincott-Raven; 1999. 6th edition. Available here.
5. Douard V, Ferraris RP. Regulation of the fructose transporter GLUT5 in health and disease. Am J Physiol Endocrinol Metab. 2008 Aug; 295(2): E227–E237. Available here.
6. Rajan AS. Regulation of Glucose Uptake. Medscape. Available here.
7. Bantle JP. Dietary Fructose and Metabolic Syndrome and Diabetes. J Nutr. 2009 Jun; 139(6): 1263S–1268S. Available here.
8. Lustig RH. Fructose: It’s “Alcohol Without the Buzz. Adv Nutr March 2013 Adv Nutr vol. 4: 226-235, 2013. Available here.
9. Rizkalla SW. Health implications of fructose consumption: A review of recent data. Nutrition & Metabolism20107:82. Available here.
10. Agricultural Research Service. United States Department of Agriculture National Nutrient Database for Standard Reference Release 27. Available here.
11. Narins RG, Weisberg JS, Myers AR. Effects of carbohydrates on uric acid metabolism. ScienceDirect. Metabolism. Volume 23, Issue 5, May 1974, Pages 455–465. Available here.
12. Singh JA, Reddy SG, Kundukulam J. Risk Factors for Gout and Prevention: A Systematic Review of the Literature. Curr Opin Rheumatol. 2011 Mar; 23(2): 192–202. Available here.
13. The University of Sydney. Search for the Glycemic Index Available here.
14. The University of Sydney. Glycemic Index of Glucose. Available here.
15. The University of Sydney. Glycemic Index of Fructose. Available here.
16. Bantle JP. Dietary Fructose and Metabolic Syndrome and Diabetes. J Nutr. 2009 Jun; 139(6): 1263S–1268S. Available here.
17. Pan H, Guo J, Su Z. Advances in understanding the interrelations between leptin resistance and obesity. Physiology and Behaviour. Volume 130, 10 May 2014, Pages 157–169. Available here.
18. Suri SZ, Empie MW. Fructose metabolism in humans – what isotopic tracer studies tell us. Nutr Metab (Lond). 2012; 9: 89. Available here.
19. Berg JM, Tymoczko JL. Stryer L. Biochemistry. Section 11.1Monosaccharides Are Aldehydes or Ketones with Multiple Hydroxyl Groups W. H. Freeman and Company.5th edition. Available here.
20. Schirren C. Relation between fructose content of semen and fertility in man. J Reprod Fertil June 1, 1963 5 347-358 Available here.
21. Frenette G, Thabet M, Sullivan R. Polyol Pathway in Human Epididymis and Semen. Journal of Andrology. Volume 27, Issue 2, pages 233–239, March-April 2006. Available here.
22. White JS. Sucrose, HFCS, and Fructose: History, Manufacture, Composition, Applications, and Production. Available here.
23. Bantle JP. Dietary Fructose and Metabolic Syndrome and Diabetes. J Nutr. 2009 Jun; 139(6): 1263S–1268S. Available here.
24. Hudgins LC, Parker TS, Levine DM, Hellerstein MK. A Dual Sugar Challenge Test for Lipogenic Sensitivity to Dietary Fructose. The journal of Clinical Endocrinology & Metabolism.Volume 96, Issue 3. Available here.

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