Fructolysis

Fructolysis refers to the metabolism of fructose from dietary sources. Though the metabolism of glucose through glycolysis uses many of the same enzymes and intermediate structures as those in fructolysis, the two sugars have very different metabolic fates in human metabolism. Unlike glucose, which is metabolized widely in the body, fructose is metabolized almost completely in the liver in humans, where it is directed toward replenishment of liver glycogen and triglyceride synthesis.[1] Under one percent of ingested fructose is directly converted to plasma triglyceride.[2] 29% – 54% of fructose is converted in liver to glucose, and about quarter of fructose is converted to lactate. 15% – 18% is converted to glycogen.[3] Glucose and lactate are then used normally as energy to fuel cells all over the body.[2]

Fructose is a dietary monosaccharide present naturally in fruits and vegetables, either as free fructose or as part of the disaccharide sucrose, and as its polymer inulin. It is also present in the form of refined sugars including granulated sugars (white crystalline table sugar, brown sugar, confectioner’s sugar, and turbinado sugar), refined crystalline fructose and as high fructose corn syrups. About 10% of the calories contained in the Western diet are supplied by fructose (approximately 55 g/day).[4]

Unlike glucose, fructose is not an insulin secretagogue, and can in fact lower circulating insulin.[5] In addition to liver, fructose is metabolized in intestine, testis, kidney, skeletal muscle, fat tissue and brain,[6][7] but it is not transported into cells via insulin-sensitive pathways (insulin regulated transporters GLUT1 and GLUT4). Instead fructose is taken in by GLUT5.

  1. ^ Jump up to: a b c McGrane, MM (2006). Carbohydrate Metabolism: is and Oxidation. Missouri: Saunders, Elsevier. pp. 258–277.
  2. ^ Jump up to: a b http://www.nutritionandmetabolism.com/content/9/1/89
  3. Jump up ^ Rippe, JM; Angelopoulos, TJ (2013). “Sucrose, high-fructose corn syrup, and fructose, their metabolism and potential health effects: what do we really know?”. Adv Nutr. 4: 236–45. doi:10.3945/an.112.002824. PMC 3649104Freely accessible. PMID 23493540.
  4. Jump up ^ https://www.inkling.com/read/illustrated-reviews-biochemistry-harvey-5th/chapter-12/fructose-metabolism
  5. Jump up ^ http://press.endocrine.org/doi/abs/10.1210/jc.2003-031855
  6. Jump up ^ Douard, V; Ferraris, R. P. (2008). “Regulation of the fructose transporter GLUT5 in health and disease”. AJP: Endocrinology and Metabolism. 295 (2): E227–37. doi:10.1152/ajpendo.90245.2008. PMC 2652499Freely accessible. PMID 18398011.
  7. Jump up ^ Hundal, H. S.; Darakhshan, F; Kristiansen, S; Blakemore, S. J.; Richter, E. A. (1998). “GLUT5 expression and fructose transport in human skeletal muscle”. Advances in Experimental Medicine and Biology. 441: 35–45. doi:10.1007/978-1-4899-1928-1_4. PMID 9781312.
  8. Jump up ^ Parniak, MA; 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. PMC 1149073Freely accessible. PMID 3415647.
  9. Jump up ^ Segebarth C, Gr

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