To examine the effects of nutrient restriction during midgestation to late gestation on maternal and fetal digestive enzyme activities, 41 singleton ewes (48.3 ± 0.6 kg of BW) were randomly assigned to dietary treatments: 100% (control; CON; n = 20) or 60% of nutrient requirements (restricted; RES; n = 21) from day 50 until day 90 (midgestation). At day 90, 14 ewes (CON, n = 7; RES, n = 7) were euthanized. The remaining ewes were subjected to treatments of nutrient restriction or remained on a control diet from day 90 until day 130 (late gestation): CON-CON (n = 6), CON-RES (n = 7), RES-CON (n = 7), and RES-RES (n = 7) and were euthanized on day 130. The fetal and maternal pancreas and small intestines were weighed, subsampled, and assayed for digestive enzyme activity. One unit (U) of enzyme activity is equal to 1 µmol of product produced per minute for amylase, glucoamylase, lactase, and trypsin and 0.5 µmol of product produced per minute for maltase and isomaltase. Nutrient restriction during midgestation and late gestation decreased (P < 0.05) maternal pancreatic and small intestinal mass but did not affect fetal pancreatic or small intestinal mass. Maternal nutrient restriction during late gestation decreased (P = 0.03) fetal pancreatic trypsin content (U/pancreas) and tended to decrease (P < 0.08) fetal pancreatic trypsin concentration (U/g), specific activity (U/g protein), and content relative to BW (U/kg of BW). Nutrient restriction of gestating ewes decreased the total content of α-amylase (P = 0.04) and tended to decrease total content of trypsin (P = 0.06) and protein (P = 0.06) in the maternal pancreas on day 90. Nutrient restriction during midgestation on day 90 and during late gestation on day 130 decreased (P = 0.04) maternal pancreatic α-amylase-specific activity. Sucrase activity was undetected in the fetal and maternal small intestine. Nutrient restriction during late gestation increased (P = 0.01) maternal small intestinal maltase and lactase concentration and tended to increase (P = 0.06) isomaltase concentration. Realimentation during late gestation after nutrient restriction during midgestation increased lactase concentration (P = 0.04) and specific activity (P = 0.05) in the fetal small intestine. Fetal small intestinal maltase, isomaltase, and glucoamylase did not respond to maternal nutrient restriction. These data indicate that some maternal and fetal digestive enzyme activities may change in response to maternal nutrient restriction.

The hypothesis of this experiment was that dietary fructose would influence visceral organ mass, carbohydrase activity, and mRNA expression of carbohydrases and nutrient transporters in the small intestine in neonatal calves. Therefore, our objective was to use the neonatal calf as a model to evaluate the effects of postruminal fructose supply on small intestinal carbohydrate assimilation. Ten calves (<7 d of age; 41.2 ± 1.46 kg of body weight) were fed milk replacer at 2.0% of body weight daily (816 ± 90.5 g/d; 272 ± 30.1 g/L; dry-matter basis) in 2 equal portions and assigned to the following dietary treatment groups: (1) milk replacer (control; n = 6) or (2) milk replacer + 2.2 g of fructose/ kg of body weight (fructose; n = 4). Calves were fed dietary treatments for 28 d, with jugular blood sampled every 7 d before and after the morning feeding. Calves were slaughtered, and visceral weights were recorded. Postruminal carbohydrase activities were assayed. Quantitative real-time PCR was conducted for small intestinal mRNA expression of nutrient transporters [solute carrier family 2 member 5 (GLUT5), solute carrier family 2 member 2 (GLUT2), and solute carrier family 5 member 1 (SGLT1)], carbohydrases (lactase, maltase-glucoamylase, and sucrase-isomaltase), and ketohexokinase (KHK). Data were analyzed using MIXED procedures in SAS version 9.4 (SAS Institute Inc, Cary, NC). Dietary fructose supplementation decreased serum glucose concentration. Small intestinal mass was greater in calves supplemented with fructose. Dietary fructose supplementation did not influence pancreatic α-amylase, small intestinal isomaltase, or maltase activities. Sucrase activity was undetected in the small intestine. Dietary fructose supplementation increased small intestinal glucoamylase activity per gram of tissue by 30% and increased maltase-glucoamylase mRNA expression by 6.8-fold. Dietary fructose supplementation did not influence mRNA expression of GLUT5, SGLT1, GLUT2, or KHK. Dietary fructose supplementation increased small intestinal lactase mRNA expression by 3.1-fold. Sucrase-isomaltase mRNA expression in the small intestine decreased 5.1-fold with dietary fructose supplementation. Dietary fructose supplementation does not induce sucrase activity in neonatal calves; however, sucrase-isomaltase may be transcriptionally regulated by dietary fructose in neonatal calves. More research is needed to compare glucose and fructose at isocaloric intakes to examine effects of dietary fructose at equal metabolizable energy intake.

Background Small intestinal starch digestion in ruminants is potentially limited by inadequate production of carbohydrases. Previous research has demonstrated that small intestinal starch digestion can be improved by postruminal supply of casein or glutamic acid. However, the mechanisms by which casein and glutamic acid increase starch digestion are not well understood. Objectives The objective of this experiment was to evaluate the effects of duodenal infusions of starch with casein or glutamic acid on postruminal carbohydrase activities in cattle. Methods Twenty-two steers [mean body weight (BW) = 179 ± 4.23 kg] were surgically fitted with duodenal and ileal cannulas and limit-fed a soybean hull–based diet containing small amounts of starch. Raw cornstarch (1.61 ± 0.0869 kg/d) was infused into the duodenum alone (control), or with 118 ± 7.21 g glutamic acid/d, or 428 ± 19.4 g casein/d. Treatments were infused continuously for 58 d and then steers were killed for tissue collection. Activities of pancreatic (α-amylase) and intestinal (maltase, isomaltase, glucoamylase, sucrase) carbohydrases were determined. Data were analyzed as a randomized complete block (replicate group) design using the GLM procedure of SAS to determine effects of infusion treatment. Results Duodenal casein infusion increased (P &lt; 0.05) pancreatic α-amylase activity by 290%. Duodenal glutamic acid infusion increased (P &lt; 0.03) duodenal maltase activity by 233%. Duodenal casein infusion increased jejunal maltase (P = 0.02) and glucoamylase (P = 0.03) activity per gram protein by 62.9% and 97.4%, respectively. Duodenal casein infusion tended to increase (P = 0.10) isomaltase activity per gram jejunum by 38.5% in the jejunum. Sucrase activity was not detected in any segment of the small intestine. Conclusions These results suggest that small intestinal starch digestion can be improved in cattle with increased small intestinal flow of casein through increases in postruminal carbohydrase activities.

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Ergot alkaloids from endophyte-infected (Epichloë coenophiala) tall fescue (Lolium arundinaceum) induce vasoconstriction. Previous work has shown that serotonin receptor subtype, 5HT 2A , is present in bovine ruminal (R) and mesenteric (M) vasculature, plays a role in vasoconstriction, and could be influenced by ergot alkaloids. To determine the influence of ergot alkaloids on 5HT 2A , the vasoactivity of an agonist selective for 5HT 2A , (4-bromo-3,6-dimethoxybenzocyclobuten-1-yl) methylamine HCl (TCB-2), was evaluated using bovine ruminal and mesenteric arteries and veins (RA, RV, MA, MV) that were exposed to ergovaline (ERV) prior to or during the TCB-2 additions. Ruminal and mesenteric blood vessel segments were collected, cleaned, and cut into 2-to 3-mm cross-sections. Vessel segments were incubated in Krebs-Henseleit buffer containing 0, 0.01 or 1 µM ERV for 2 h prior to TCB-2 dose response or exposed to ERV concentrations simultaneously during TCB-2 dose response. For the dose response portion of the study, vessels were suspended in a multimyograph containing 5 mL of continuously oxygenated Krebs-Henseleit buffer and equilibrated to 1 g tension for 90 min.