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Fructokinase, Fructans, Intestinal Permeability, and Metabolic Syndrome: An Equine Connection?
Abstract: Fructose is a simple sugar present in honey and fruit, but can also exist as a polymer (fructans) in pasture grasses. Mammals are unable to metabolize fructans, but certain gram positive bacteria contain fructanases and can convert fructans to fructose in the gut. Recent studies suggest that fructose generated from bacteria, or directly obtained from the diet, can induce both increased intestinal permeability and features of metabolic syndrome, especially the development of insulin resistance. The development of insulin resistance is driven in part by the metabolism of fructose by fructokinase C in the liver, which results in oxidative stress in the hepatocyte. Similarly, the metabolism of fructose in the small bowel by intestinal fructokinase may lead to increased intestinal permeability and endotoxemia. While speculative, these observations raise the possibility that the mechanism by which fructans induce laminitis could involve intestinal and hepatic fructokinase. Further studies are indicated to determine the role of fructanases, fructose and fructokinase in equine metabolic syndrome and laminitis.
Publication Date: 2013-02-27 PubMed ID: 23439477PubMed Central: PMC3576823DOI: 10.1016/j.jevs.2012.05.004Google Scholar: Lookup The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
- Journal Article
Summary
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This paper investigates the possible link between fructose (a sugar found in honey and fruit), its derivatives, and the development of increased intestinal permeability and features of metabolic syndrome in horses, which could contribute to conditions like insulin resistance and laminitis.
Understanding the Components
- Fructokinase C and intestinal fructokinase are enzymes that metabolize fructose. These enzymes exist in the liver and the small intestine respectively. Their activity reportedly triggers oxidative stress in liver cells and increases intestinal permeability, leading to a state of endotoxemia (toxins in the blood).
- Fructans are polymer forms of fructose that mammals, including horses, cannot metabolize. However, certain bacteria present in the gastrointestinal tract of these animals, are capable of breaking down fructans into fructose.
Proposing the Link
- The researchers report that recent studies demonstrate a connection between the fructose metabolized from the diet, or generated by bacteria, and the development of an increased intestinal permeability and symptoms of metabolic syndrome, particularly insulin resistance.
- Insulin resistance is a condition in which cells are unable to efficiently use the insulin produced, leading to the need for increased insulin production, and potentially, the development of type 2 diabetes.
Fructose, Fructokinase and Laminitis
- The symptoms observed led the researchers to hypothesize that these mechanisms might also be involved in the development of equine metabolic syndrome and laminitis in horses.
- Laminitis is a painful condition affecting horse’s hooves and can lead to lameness. The condition has long been associated with the consumption of grass rich in fructans, but the mechanism through which this occurs has yet to be fully elucidated.
Future Research Directions
- The paper concludes by emphasizing the need for further research to understand the roles of fructanases (enzymes that metabolize fructans), fructose, and fructokinase in relation to equine metabolic syndrome and laminitis.
- Understanding these mechanisms could enable the development of preventive measures or treatments for these conditions in horses, potentially having a significant impact in the field of equine health.
Cite This Article
APA
Johnson RJ, Rivard C, Lanaspa MA, Otabachian-Smith S, Ishimoto T, Cicerchi C, Cheeke PR, Macintosh B, Hess T.
(2013).
Fructokinase, Fructans, Intestinal Permeability, and Metabolic Syndrome: An Equine Connection?
J Equine Vet Sci, 33(2), 120-126.
https://doi.org/10.1016/j.jevs.2012.05.004 Publication
Researcher Affiliations
- Division of Renal Diseases and Hypertension, University of Colorado, Aurora, Colorado, USA.
Grant Funding
- R01 HL068607 / NHLBI NIH HHS
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Citations
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