Growing cattle in the United States consume up to 6 kg of starch daily, mainly from corn or sorghum grain. Total tract apparent digestibility of starch usually ranges from 90 to 100% of starch intake. Ruminal starch digestion ranges from 75 to 80% of starch intake and is not greatly affected by intake over a range of 1 to 5 kg of starch/d. Starch apparently digested in the small intestine decreases from 80 to 34% as starch entering the small intestine increases from 0.2 to 2 kg/d. Starch apparently digested in the large intestine ranges from 44 to 46% of starch entering the large intestine. Approximately 70% of starch digested in the small intestine appears as glucose in the bloodstream. Within the range of starch intakes that do not cause rumen upsets, increasing starch (and energy) intake increases the amount of starch digested in the rumen, increases the supply of starch to the small intestine, increases starch digested in small intestine (albeit at reduced efficiency), and increases starch digested in the large intestine, such that total tract digestibility remains relatively constant. With increased starch intake, most of the starch is still digested in the rumen, but increasing amounts of starch escape ruminal and intestinal digestion, and disappear distal to the ileocecal junction. Again, within the range of starch intakes that do not cause rumen upsets, as starch intake increases, hepatic gluconeogenesis increases, glucose entry increases, and glucose irreversible loss increases, with a significant portion lost as CO2. The ability to increase use of dietary starch to support greater weight gains or improved marbling could come from increasing starch digestion in a healthy rumen or in the small intestine, but we conclude that the main limit to use of dietary starch to support live weight gain is digestion and absorption from the small intestine. Increased oxidation of glucose at greater starch intakes may alter energetic efficiency by sparing other oxidizable substrates, like amino acids.

Three experiments were conducted to determine whether emulsifiers improve utilization of fat from diets for early-weaned pigs. In Exp. 1, 96 weanling pigs (17 d old) were used in metabolism cages, with main effects of fat source (soybean oil, tallow, lard, and coconut oil) and emulsifier treatment (no emulsifier, lecithin, and lysolecithin as 10% of the added fat). Soybean oil and coconut oil were more digestible than tallow and lard (P < .001). Tallow was more digestible when lecithin and lysolecithin were added (P < .007), and pigs fed lecithin had lower serum triglycerides and cholesterol than pigs fed lysolecithin (P < .03). In Exp. 2, 270 weanling pigs (21 d old) were used in a growth assay. Treatments were 1) control diet; 2) Diet 1 with soybean oil; 3) Diet 1 with tallow; 4, 5, and 6) Diet 3 with lecithin replacing 5, 10, and 30% of the tallow, respectively; and 7, 8, and 9) Diet 3 with lysolecithin replacing 5, 10, and 30% of the tallow, respectively. At d 14 of the experiment, digestibility of tallow was improved more by lecithin than lysolecithin (P < .008). For the total experiment (d 0 to 35), the control pigs had poorer gain:feed ratio than did the pigs fed the fat sources (P < .002). In Exp. 3, 420 weanling pigs (21 d old) were used. Treatments were 1) control diet with soybean oil; 2) Diet 1 with tallow; and 3, 4, and 5) Diet 2 with 10% of the added fat as soybean oil, lecithin, or monoglyceride, respectively. Adding soybean oil, lecithin, and monoglyceride to tallow increased digestibility of total fat (P < .07). From d 0 to 14, pigs fed soybean oil gained weight faster than pigs fed the other treatments (P < .06), and pigs fed tallow without emulsifiers had the lowest ADG. Considering all experiments, addition of emulsifiers increased digestibility of nutrients but had minimal effect on growth performance.

The effects of an Aspergillus oryzae extract containing alpha-amylase activity (Amaize TM , Alltech Inc., Nicholasville, KY) were examined in vivo and in vitro. A lactating cow study employed 20 intact and four ruminally fistulated Holstein cows in a replicated 4 × 4 Latin-square design to examine the effects of four concentrations of dietary Amaize TM extract on milk production and composition, ruminal fermentation and serum metabolite concentrations. The treatment diets contained 0, 240, 480 or 720 alpha-amylase dextrinizing units (DU) per kg of total mixed ration ( TMR) (dry-matter basis). The supplemental alpha-amylase increased the yields of milk ( P = 0·02), fat ( P = 0·02) and protein ( P = 0·06) quadratically. The maximum milk yield was obtained when 240 DU per kg of TMR were offered. Ruminal in situ starch disappearance was not affected by alpha-amylase supplementation in lactating cows or ruminally cannulated steers. Supplemental alpha-amylase extract reduced the molar proportion of propionate in the rumen of steers ( P = 0·08) and lactating cows ( P = 0·04), and in rumen-simulating cultures ( P = 0·04). The supplement also increased the molar proportions of acetate ( P = 0·06) and butyrate ( P = 0·05), and the serum beta-hydroxybutyrate ( P = 0·01) and non-esterified fatty acid ( P = 0·03) concentrations in lactating cows. The improvements in milk production appear to be a consequence of the effects of alphaamylase on ruminal fermentation and the potential changes in nutrient metabolism that result from them. We conclude that supplemental alpha-amylase may be given to modify ruminal fermentation and improve milk and component yield in lactating Holstein cattle.

Six Holstein steers (mean +/- SE BW = 344 +/- 10 kg) fitted with hepatic, portal, and mesenteric vein and mesenteric artery catheters and a ruminal cannula were used in a 6 x 6 Latin square design to evaluate the effects of increasing ruminal butyrate on net portal-drained visceral and hepatic nutrient flux. Steers were fed a 40% brome hay, 60% concentrate diet in 12 portions daily at 1.25 x NEm. Water (control) or butyrate at 50, 100, 150, 200, or 250 mmol/h was supplied continuously via the ruminal cannula. Simultaneous arterial, portal, and hepatic blood samples were taken at hourly intervals from 15 to 20 h of ruminal infusion. Portal and hepatic blood flow was determined by continuous infusion of P-aminohippurate, and net nutrient flux was calculated as the difference between venous and arterial concentrations times blood flow. Ruminal and arterial concentrations and total splanchnic flux of butyrate increased (P less than .01) with increased butyrate infusion. Arterial concentrations of acetate (P less than .10), alpha-amino-N (P less than .05), and glucose (P less than .01) decreased with increased butyrate, whereas arterial beta-hydroxybutyrate (P less than .01) and acetoacetate (P less than .05) increased. Increased butyrate produced an increased portal-drained visceral flux of acetoacetate and an increased net hepatic flux of beta-hydroxybutyrate. Urea N and glucose net portal and hepatic fluxes were not affected by ruminal butyrate. Alpha-amino-N uptake by the liver decreased with increased butyrate (P less than .10). Simple linear regression (r2 = .985) indicated that 25.8% of ruminally infused butyrate appeared in portal blood as butyrate. Only 14% could be accounted for as net portal-drained visceral flux of acetoacetate plus beta-hydroxybutyrate.

Twenty (12 Holstein, 8 Longhorn cross) calves (198 kg and 7 mo old) were used in a randomized complete block design to evaluate the effects of dietary forage concentration and feed intake on carbohydrase activities and small intestinal (SI) morphology. Calves were individually fed 90% forage (alfalfa) or a 90% concentrate (50% sorghum: 50% wheat) diet at either one or two times NEm for 140 d and slaughtered; tissues and small intestinal digesta were collected. Increased feed intake increased (P less than .05) pancreatic weight, alpha-amylase and glucoamylase activities in the pancreas, SI length and SI digesta weight. Forage-fed calves gained faster (P less than .01) and had greater (P less than .05) pancreatic protein concentrations, alpha-amylase and glucoamylase activities in the pancreas and greater SI digesta alpha-amylase activities than grain-fed calves did. Increased feed intake increased (P less than .01) mucosal weight/cm small intestine only in forage-fed calves and increased (P less than .05) SI surface/volume only in grain-fed calves. Mucosal weight was greatest (P less than .05) at the terminal ileum, surface/volume was greatest (P less than .05) in the duodenum, and mucosal protein concentration was highest (P less than .05) in the SI mid-section. Mucosal lactase was higher (P less than .05) in proximal segments, whereas mucosal isomaltase was higher in middle and distal segments of the small intestine. For mucosal maltase activity, there was a feed intake x SI sampling site interaction (P less than .05) and for trehalase, a diet x feed intake x SI sampling site interaction (P less than .05). The SI distribution patterns of maltase and isomaltase were similar, as were those of trehalase and lactase. The alpha-amylase activity in the pancreas and SI morphology were influenced greatly by diet composition and feed intake by calves.

Dairy cows fed silage are subjected to various alcohols and low molecular weight esters. Four lactating Holstein cows fitted with ruminal cannulas and permanent indwelling catheters in the hepatic portal vein, hepatic vein, mesenteric vein, and mesenteric artery were used to study the absorption of alcohols into portal blood and the metabolism of feed alcohols in the rumen and splanchnic tissues. The cows were allocated to 4 experimental treatments in a Latin square design. All treatments were formulated as total mixed rations with the same overall nutrient composition, differing by the source of corn silage. Treatments were a control silage and 3 qualities of problematic corn silage (silage with Fusarium toxin, Penicillium-infected silage, and silage with a high propanol content). Feeding was followed by a decreasing ruminal pH, as well as decreasing molar proportions of ruminal acetate and isobutyrate. The ruminal concentrations of total VFA, ethanol, propanol, 2-butanol, ethyl acetate, propyl acetate, glucose, and L-lactate, and molar proportions of propionate, butyrate, isovalerate, valerate, and caproate increased after feeding. Treatments affected ruminal concentrations of propanol, propyl acetate, and butyrate and a strong correlation was observed between ruminal propyl acetate and the molar proportion of butyrate (r = -0.79). Arterial concentrations of ethanol, propanol, propanal, acetone (sum of acetone and acetoacetate), 3-hydroxybutyrate, L-lactate, glutamate, and glutamine increased, and the arterial concentration of glucose decreased after feeding, but no effects of treatment were observed for arterial variables. The postprandial increase in arterial ethanol was maintained for 5 h. The net portal release of ethanol tended to decrease with the treatment with the lowest ethanol content, and the net splanchnic release of ethanol increased after feeding, but overall, the net splanchnic flux of ethanol was not different from zero, in agreement with the liver being the major organ for alcohol metabolism. The net portal flux and net hepatic flux of propanol were affected by treatment. All dietary ethanol and propanol were accounted for by absorption of the respective alcohol into the portal blood. The hepatic extraction ratios of ethanol and propanol were, on average, 63 to 66%, and no indications of saturation of hepatic alcohol metabolism were observed at any time. We concluded that typical amounts of alcohols in corn silage do not interfere with splanchnic metabolism of any of the measured variables and do not saturate hepatic pathways for alcohol metabolism. However, even low concentrations of alcohols in feed might affect ruminal metabolism and are followed by hours of elevated peripheral blood concentrations of alcohols.

No abstract

Six steers fitted with a ruminal cannula and chronic indwelling catheters in the mesenteric artery, mesenteric vein, hepatic portal vein, hepatic vein, as well as in the right ruminal vein were used to study metabolism of VFA absorbed from buffers in the emptied and washed reticulorumen. [2-(13)C]Acetate was infused into a jugular vein to study portal-drained visceral (PDV) uptake of arterial acetate, hepatic unidirectional uptake of acetate, and whole-body irreversible loss rate (ILR). Isobutyrate was infused into the right ruminal vein to calibrate VFA fluxes measured in the portal vein. On sampling days, the rumen was emptied and incubated in sequence with a 0-buffer (bicarbonate buffer without VFA), a VFA-buffer plus continuous intraruminal infusion of VFA, and finally another 0-buffer. Ruminal VFA absorption was determined as VFA uptake from the VFA-buffer and metabolic effects determined as the difference between metabolite fluxes with VFA-buffer and 0-buffers. Steady absorption rates of VFA were maintained during VFA-buffer incubations (4 h; 592+/-16, 257+/-5, 127+/-2, 17+/-<1, 20+/-<1 mmol/h, respectively, of acetate, propionate, butyrate, isovalerate, and valerate). The portal flux of acetate corrected for PDV uptake of arterial acetate accounted for 105+/-3% of the acetate absorption from the rumen, and the net portal flux of propionate accounted for 91+/-2% of propionate absorption. Considerably less butyrate (27+/-3%) and valerate (30+/-3%) could be accounted for in the portal vein. The sum of portal VFA and 3-hydroxybutyrate as well as lactate represented 99+/-3% of total VFA acetyl units and 103+/-2% of VFA propionyl units. Estimates are maximum because no accounting was made for lactate derived from glycolysis in the PDV. The net splanchnic flux of VFA, lactate, 3-hydroxybutyrate, and glucose accounted for 64+/-2% of VFA acetyl units and 34+/-5% of VFA propionyl units. Results indicate that there is a low "first-pass" uptake of acetate and propionate in the ruminal epithelium of cattle, whereas butyrate and valerate are extensively metabolized, though seemingly not oxidized to carbon dioxide in the epithelium but repackaged into acetate, 3-hydroxybutyrate, and perhaps other metabolites. When PDV "second-pass" uptake of arterial nutrients is accounted for, PDV fluxes of VFA, lactate, and 3-hydroxybutyrate represent VFA production in the gastrointestinal tract and thereby VFA availability to the ruminant animal.