Post by deb on Apr 28, 2012 11:02:32 GMT -5
Hi all, I know there has been some discussion on this board before regarding gout and fructose, but I just wanted to share some research that I found - we have a family history of gout (my dad has it and I started getting attacks in my 20's) - and thought this was interesting - the first article is from 1990 and discusses a previous article that, like the 1990 one, demonstrated that not only may people with familial gout be heterozygous carriers for HFI, but they exhibit metabolic changes similar to HFI folks upon fructose ingestion, only with much larger doses of fructose than what an HFI person needs to cause symptoms:
www.ncbi.nlm.nih.gov/pmc/articles/PMC54948/
The other article of interest is this one from 2009, which shows that the intestinal glucose and fructose transporter, GLUT9, also appears to play a role in the development of gout. This, like other articles on the GLUT transporters, also suggests that they are much more highly expressed in the presence of fructose (especially GLUT5, a major transporter of fructose).
This could explain the increased sensitivity to fructose after removing it from the diet. In other words, if these transporters are not activated by continuous fructose intake, then when fructose is ingested, it has a really hard time being absorbed by the small intestine, and instead continues on down to the large intestine, where it is not supposed to be. This results in bloating, malabsorption of nutrients, abdominal pain, etc. - so could be a relevant mechanism in both DFI and HFI:
ajpendo.physiology.org/content/297/4/E831.full
Best,
Deb
www.ncbi.nlm.nih.gov/pmc/articles/PMC54948/
The other article of interest is this one from 2009, which shows that the intestinal glucose and fructose transporter, GLUT9, also appears to play a role in the development of gout. This, like other articles on the GLUT transporters, also suggests that they are much more highly expressed in the presence of fructose (especially GLUT5, a major transporter of fructose).
This could explain the increased sensitivity to fructose after removing it from the diet. In other words, if these transporters are not activated by continuous fructose intake, then when fructose is ingested, it has a really hard time being absorbed by the small intestine, and instead continues on down to the large intestine, where it is not supposed to be. This results in bloating, malabsorption of nutrients, abdominal pain, etc. - so could be a relevant mechanism in both DFI and HFI:
ajpendo.physiology.org/content/297/4/E831.full
Best,
Deb