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 23 May 2018

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News

Fried potatoes may aggravate inflammatory bowel disease

Potato glycoalkaloids adversely affect intestinal permeability and aggravate inflammatory bowel disease, claims a team from Alberta, Canada.

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The researchers investigated the role of potato glycoalkaloids on intestinal barrier integrity, and published the findings in the latest issue of Inflammatory Bowel Diseases.

Disruption of epithelial barrier integrity is important in the initiation and cause of inflammatory bowel disease (IBD).

The glycoalkaloids, solanine (S) and chaconine (C), are naturally present in potatoes. They can permeabilize cholesterol-containing membranes, and lead to disruption of epithelial barrier integrity.

Frying potatoes concentrates glycoalkaloids.

Interestingly, the prevalence of IBD is highest in countries where fried potatoes consumption is highest.

The effect of varying concentrations of solanine and chaconine on intestinal permeability and function were examined.

Solanine (0-50 µM), chaconine (0-20 µM), or a 1:1 mixture (0-20 µM) were exposed to T84 cultured epithelial monolayers for varying periods of time. This determined concentration response effect on epithelial permeability.

Glycoalkaloids disrupted intestinal barrier integrity in animals predisposed to IBD.
Inflammatory Bowel Diseases
Next, a 1:1 mixture (5 µM) of solanine-to-chaconine (C:S) was exposed to sheets of normal murine small intestine.

The sheets came from both control and interleukin-10 gene-deficient mice. This was to determine whether glycoalkaloids affected intestine from mice with a genetic predisposition for IBD greater than controls.

Finally, the effects of glycoalkaloids on colonic histologic injury were examined in mice orally fed amounts of glycoalkaloids that would normally be consumed in a human diet.

Glycoalkaloids embedded and permeabilized the T84 monolayer epithelial membrane bilayer in a concentration-dependent fashion, with the 1:1 mixture greater than chaconine, and chaconine greater than solanine.

In vitro experiments also illustrated a concentration-dependent disruption of intestinal barrier integrity in animals with a genetic predisposition to develop IBD, but not in control animals.

Similarly, the group found that in vivo oral feeding experiments demonstrated that C:S ingestion, at physiologic concentrations, aggravated histologic colonic injury in mice genetically predisposed to developing IBD.

Bijal Patel, of the University of Alberta, Edmonton, concluded on behalf of fellow authors, "Concentrations of glycoalkaloids normally available while eating potatoes can adversely affect the mammalian intestine and can aggravate IBD."

Inflamm Bowel Dis 2002; 8 (5): 340-6
11 September 2002

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