Intestinal physiology and peptidase activity in male pigs are modulated by consumption of corn culture extracts containing fumonisins

M Lessard, G Boudry, B Seve, IP Oswald, and JP Lalles, 2009. Journal of Nutrition, 139: 1303–1307.

10-Aug-2010 (15 years 9 months 27 days ago)
Mycotoxins are secondary metabolites of fungi contaminating food and feed ingredients. Their consumption represents a potential health hazard for humans and animals. Fumonisins are a group of structurally related mycotoxins produced by Fusarium verticillioides that are commonly found on corn. Prolonged exposure to Fumonisin B1 (FB1) disturbed transepithelial electrical resistance (TER) in intestinal epithelial cells (IEC) lines, suggesting alterations in intestinal barrier function. Surprisingly, there is no in vivo information to date for supporting these in vitro observations. The major reason may be due to the cost of feeding large farm animals for many days with pure FB1. The present work was aimed at testing the hypothesis that repeated consumption of an extract rich in fumonisins alters absorption, secretion, and barrier function of porcine small intestine.

Intra-litter pairs of pigs (n = 36) weaned at 28 d, were fed the vehicle (control) or the extract (providing 1.5 mg FB1/kg body weight) daily for 9 d starting 7 d post-weaning. After slaughter, the jejunal mucosa of pigs was mounted in Ussing chambers (UC).

Extract consumption for 9 d decreased the gain:feed ratio (P = 0.04) and increased liver weight (P = 0.01). Basal net ion secretion (P = 0.02), sodium-dependent glucose absorption (P = 0.02), and theophylline-induced secretion (P<0.01) of the jejunal mucosa determined in UC were higher in pigs fed the extract than in controls. By contrast, jejunal permeability to the horseradish peroxidase model protein in UC was not influenced by extract consumption. Ileal villi tended to be longer (P = 0.07) and jejunal aminopeptidase N activity was lower (P<0.01) in pigs fed the extract.

In conclusion, consumption of an extract rich in fumonisins for 9 d has the potential to alter intestinal physiology, villous architecture, and enzyme activities.