Pregastric fermentation along with production practices that are dependent on high-energy diets means ruminants rely heavily on starch and protein assimilation for a substantial portion of their nutrient needs. While the majority of dietary starch may be fermented in the rumen, significant portions can flow to the small intestine. The initial phase of small intestinal digestion requires pancreatic α-amylase. Numerous nutritional factors have been shown to influence pancreatic α-amylase secretion with starch producing negative effects and casein, certain amino acids and dietary energy having positive effects. To date, manipulation of α-amylase secretion has not resulted in substantial changes in digestibility. The second phase of digestion involves the actions of the brush border enzymes sucrase-isomaltase and maltase-glucoamylase. Genetically, ruminants appear to possess these enzymes; however, the absence of measurable sucrase activity and limited adaptation with changes in diet suggests a reduced capacity for this phase of digestion. The final phase of carbohydrate assimilation is glucose transport. Ruminants possess Na+-dependent glucose transport that has been shown to be inducible. Because of the nature of pregastric fermentation, ruminants see a near constant flow of microbial protein to the small intestine. This results in a nutrient supply, which places a high priority on protein digestion and utilization. Comparatively, little research has been conducted describing protein assimilation. Enzymes and processes appear consistent with non-ruminants and are likely not limiting for efficient digestion of most feedstuffs. The mechanisms regulating the nutritional modulation of digestive function in the small intestine are complex and coordinated via the substrate, neural and hormonal effects in the small intestine, pancreas, peripheral tissues and the pituitary—hypothalamic axis. More research is needed in ruminants to help unravel the complexities by which small intestinal digestion is regulated with the aim of developing approaches to enhance and improve the efficiency of small intestinal digestion.
Glucagon-like peptide-2 (GLP-2) increases small intestinal mass and blood flow in nonruminants but its effect in ruminants is unknown. Eight Holstein calves with an ultrasonic flow probe around the superior mesenteric artery and catheters in the carotid artery and mesenteric vein were paired by age and randomly assigned to treatment of a control (0.5% of BSA in saline; n=4) or GLP-2 (50 μg/kg of body weight of bovine GLP-2 in BSA; n=4) given subcutaneously every 12h for 10 d. Blood flow was measured on d 0 (acute) and d 10 (chronic) and included 3 periods: baseline (saline infusion), treatment (infusion of BSA or 1,000 pmol of GLP-2/kg of body weight per h), and recovery (saline infusion). On d 11, calves were killed 2h after injection of 5-bromo-2'-deoxyuridine (BrdU). Gastrointestinal tissues were weighed and epithelial samples were obtained to determine villus height, crypt depth, and BrdU staining. Infusion of GLP-2 increased superior mesenteric artery blood flow to 175% of baseline on d 0 but to only 137% of baseline after chronic treatment. Compared with that of the control, GLP-2 increased small intestinal mass by 24% by increasing epithelial mass in the jejunum and ileum. Additionally, GLP-2 increased villus height, crypt depth, and BrdU-labeling in small intestinal segments. These results demonstrate that GLP-2 induces similar increases in small intestinal blood flow and growth in ruminants to those observed in nonruminants. Furthermore, GLP-2 increases small intestinal blood flow in ruminants but this response is attenuated after 10 d of GLP-2 administration. In cattle, GLP-2 may be an important hormone in the regulation of intestinal blood flow and epithelial growth.
22 September 2020 in Frontiers in Veterinary Science
Interest is increasing regarding use of Cannabidiol (CBD) in companion animals due to anecdotal evidence of beneficial behavioral and health effects. The purpose of this investigation was to evaluate the influence of CBD on behavioral responses to fear-inducing stimuli in dogs. Sixteen dogs (18.1 ± 0.2 kg) were utilized in a replicated 4 × 4 Latin square design experiment with treatments arranged in a 2 × 2 factorial, consisting of control, 25 mg CBD, trazodone (100 mg for 10–20 kg BW, 200 mg for 20.1–40 kg BW), and the combination of CBD and trazodone. A fireworks model of noise-induced fear was used to assess CBD effectiveness after 7 d of supplementation. Each test lasted a total of 6 min and consisted of a 3 min environmental habituation phase with no noise and a 3 min noise phase with a fireworks track. Plasma was collected 1 h before, immediately after, and 1 h following testing for cortisol analysis. Behaviors in each 3 min block were video recorded, and heart rate (HR) sensors were fitted for collection of HR and HR variability parameters. Research personnel administering treats and analyzing behavioral data were blinded as to the treatments administered. Data were tested for normality using the UNIVARIATE procedure in SAS, then differences examined using the MIXED procedure with fixed effects of treatment, period, time, and treatment x time interaction. Inactivity duration and HR increased during the first minute of the fireworks track compared with 1 min prior (P < 0.001 and P = 0.011, respectively), indicating the fireworks model successfully generated a fear response. Trazodone lowered plasma cortisol (P < 0.001), which was unaffected by CBD (P = 0.104) or the combination with CBD (P = 0.238). Neither CBD nor trazodone affected the duration of inactivity (P = 0.918 and 0.329, respectively). Trazodone increased time spent with tail relaxed (P = 0.001). CBD tended to increase HR (P = 0.093) and decreased the peak of low- and high-frequency bands (LF and HF, P = 0.011 and 0.022, respectively). These results do not support an anxiolytic effect of CBD in dogs given 1.4 mg CBD/kg BW/d.
25 June 2009 in Asian-Australasian Journal of Animal Sciences
Ruminants possess the capacity to digest very large amounts of starch. However, in many cases diets approach 60% starch and even small inefficiencies present opportunities for energetic losses. Ruminal starch digestion is typically 75-80% of starch intake. On average, 35-60% of starch entering the small intestine is degraded. Of the fraction that escapes small-intestinal digestion, 35-50% is degraded in the large intestine. The low digestibility in the large intestine and the inability to reclaim microbial cells imposes a large toll on post-ruminal digestive efficiency. Therefore, digestibility in the small intestine must be optimized. The process of starch assimilation in the ruminant is complex and remains an avenue by which increases in production efficiency can be gained. A more thorough description of these processes is needed before we can accurately predict digestion occurring in the small intestine and formulate diets to optimize site of starch digestion.