Abstract
Abstract The small intestine plays an important role in post-ruminal carbohydrate digestion and there is limited information on its function in response to nutritional adaptation. To examine the effects of nutrient restriction and realimentation on fetal small intestinal carbohydrase activities during mid- to late-gestation, 41 singleton ewes (48.3±0.6 kg BW) were randomly assigned to dietary treatments: 100% (control; CON; n = 20) or 60% of nutrient requirements (restricted; RES; n = 21) from day 50–90 (mid-gestation) of gestation. At day 90, 14 ewes (CON, n = 7; RES, n = 7) were slaughtered. The remaining ewes were subjected to treatments of nutrient restriction or remained under a control diet from day 90–130 (late-gestation): CON-CON (n = 6), CON-RES (n = 7), RES-CON (n = 7), and RES-RES (n = 7) and were slaughtered at day 130. The fetal small intestine was weighed, subsampled, and assayed for carbohydrase (maltase, isomaltase, glucoamylase, lactase, and sucrase) activity. Enzyme activity was expressed as U/g and U/g protein. Protein concentration was expressed as mg/g intestine. Differences between means were determined using contrasts in the MIXED procedure of SAS. Small intestinal mass increased (P < 0.001) with day of gestation. Sucrase activity was undetected in the small intestine. Day of gestation did not affect carbohydrase development in the fetal small intestine. Nutrient restriction did not affect glucoamylase, maltase, or isomaltase activities. There was a significant mid-gestation treatment × late-gestation treatment interaction for lactase activity (P < 0.05). Realimentation during late-gestation after nutrient restriction during mid-gestation increased lactase activity in the fetal small intestine. These data demonstrate that fetal mucosal carbohydrases are imprinted early in gestation and brush border α-glycohydrolases involved in starch digestion (maltase, isomaltase, glucoamylase) do not respond to maternal nutrient restriction in sheep. Nutrient restriction of ewes during mid-gestation followed by realimentation during late-gestation may be a programming strategy to increase fetal lactase activity.
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