Myrthe Gilbert and co-workers published a paper entitled “Fermentation in the Small Intestine Contributes Substantially to Intestinal Starch Disappearance in Calves”, which resulted in a cover image of a calf on the June issue of The Journal of Nutrition. In this paper, the rate-limiting enzyme in starch hydrolysis is assessed and starch fermentation in the small intestine is quantified, using milk-fed calves as a model for ruminants.
In ruminants and milk-fed calves, the proportion of ingested starch that disappears in the small intestine is lower than in monogastric animals. This indicates that starch digestion is limited in ruminants, but the rate-limiting enzyme is unknown. Furthermore, there are indications that fermentation, rather than enzymatic hydrolysis to glucose, is in part responsible for the disappearance of starch from the small intestine of ruminants. To investigate this, milk-fed calves were used as a model to study the rate-limiting enzyme in starch hydrolysis and to quantify starch fermentation in the small intestine of ruminants.
Forty male Holstein-Friesian calves of 13 weeks of age were fed milk replacers in which part of the lactose was replaced by one of four starch products varying in molecular size and branching. These starch products required different (ratios of) starch-degrading enzymes to achieve complete hydrolysis to glucose, i.e. gelatinized starch requires a-amylase and (iso)maltase, maltodextrin requires (iso)maltase and a-amylase, maltodextrin with a high degree of a-1,6-branching requires isomaltase, maltase, and a-amylase, and maltose requires maltase.
After an adaptation period of 14 weeks, starch product fermentation in the entire digestive tract was estimated using an indirect 13C method. Total tract fermentation of starch products equalled 89% of intake, irrespective of the starch product used. Disappearance of starch product before the terminal ileum averaged 62% and disappearance of starch product at the total tract level averaged 99% of the starch product intake. By difference, this shows that 37% of the starch product intake was fermented in the large intestine. After correcting for milk replacer fermented in the rumen, the starch product fermentation in the small intestine was estimated at 41% of the starch product intake, or 66% of small intestinal disappearance. This shows that small intestinal starch disappearance in calves, and possibly ruminants, is largely due to fermentation. This was corroborated by analysis of brush border enzyme activities and by the lack of appearance of 13C glucose originating from the starch products in the systemic circulation. Furthermore, the lack of differences between starch products suggests that maltase is the rate-limiting enzyme.
You can find the complete paper via the following link.