Effects of mesenteric vein n-butyrate infusion on liver metabolism by beef steers.

Effects of a 3-d mesenteric vein n-butyrate infusion (25 mmol/h) on net metabolism of nutrients by portal-drained viscera (PDV) and liver were measured in six Hereford x Angus steers. Steers were fed a pelleted 75% concentrate: 25% alfalfa diet at 135 kcal of ME/kg BW.75. Six measurements of blood flow and net metabolism of nutrients were obtained at hourly intervals immediately before beginning and ending n-butyrate infusion. Measurements were obtained during two trials, with three steers (457 kg BW, 28 mo of age in Trial 1; 478 kg BW, 19 mo of age in Trial 2) in each trial. The infusion of n-butyrate increased (P less than .01) net PDV release of n-butyrate. Infusion increased net liver removal of n-butyrate (P less than .01) and L-lactate (P less than .02) and release of beta-hydroxybutyrate (BOHB; P less than .02) and increased (P less than .03) liver extraction ratio for alanine. Net total splanchnic (PDV plus liver) release of n-butyrate (P less than .03) and BOHB (P less than .01) were increased, and net total splanchnic release of L-lactate (P less than .05) and propionate (P less than .07) were decreased by n-butyrate infusion. The infusion of n-butyrate decreased (P less than .01) net PDV release and liver removal of propionate in five of six steers. Infusion had no effect (P greater than .10) on insulin and glucagon concentration or net flux. In a companion in vitro study, L-lactate metabolism to glucose and CO2 by calf hepatocytes was decreased (P less than .08) by n-butyrate addition (2.5 mM). Effects of n-butyrate on liver L-lactate and alanine metabolism suggest that pyruvate carboxylase activity was increased, but our study failed to show a consistent effect of n-butyrate infusion on liver glucose production.     

The effects of abomasal casein infusions in growing beef steers on portal and hepatic flux of pancreatic hormones and arterial concentrations of somatomedin-C

The net release of insulin, glucagon and somatostatin by the portal-drained viscera (PDV) and their net uptake by the liver in response to 3-d abomasal infusions of casein were measured in seven multicatheterized beef steers. The steers were fed 4.3 kg DM/d of a high-concentrate diet in 12 equal meals (13.1 Mcal ME/d and 95 g N/d). In two separate experiments, the abomasal infusion of 300 g casein/d (300C) or 150 g casein/d (150C) was compared to a water infusion. Plasma flow was measured by indicator dilution and net flux by venoarterial concentration difference x plasma flow. Arterial plasma concentrations of insulin were increased (P less than .02) by either 300C or 150C. The 300C increased (P less than .03) PDV insulin release but did not affect hepatic uptake, resulting in an increased (P less than .03) total splanchnic (TSP) insulin flux. The 300C increased (P less than .05) plasma concentrations of glucagon as the result of decreased (P less than .06) hepatic extraction ratio and not as the result of increased portal release. The portal and hepatic flux of somatostatin measured as somatostatin-like immunoreactivity (SLI) were highly variable and not affected by casein infusions. Arterial plasma concentrations of somatomedin-C were not responsive to abomasal casein infusions. The abomasal infusion of 300C resulted in increased plasma concentrations of insulin via increased PDV release and increased plasma glucagon via decreased hepatic extraction ratio.     

Portal-drained visceral flux of nutrients in lambs fed alfalfa or maintained by total intragastric infusion

An experiment was performed using lambs fitted with chronic indwelling catheters in appropriate blood vessels for portal-drained visceral (PDV) flux measurements. The objective of the experiment was to evaluate PDV nutrient flux in alfalfa-fed and intragastrically infused lambs and to evaluate the effects of amount of energy and N infused on PDV nutrient metabolism. Lambs were fed alfalfa or infused with 1.64 and 10.9; 1.82 and 12.3; or 2.37 and 15.0 Mcal GE and g N/d, respectively. Arterial concentrations and PDV fluxes of glucose, L-lactate, acetate and portal blood flow were not different (P greater than .10) between alfalfa-fed and infused lambs. Net flux of alpha-amino N, ammonia N and branched-chain VFA were lower (P less than .05) and net flux of propionate, butyrate and total VFA were higher for intragastric infusion vs alfalfa. No consistent differences in PDV fluxes were noted among the three levels of energy and N infused, although the energy and N levels tested were near maintenance requirements. Nitrogen retention increased as level of energy and N infusion increased. Approximately 47, 70 and 22% of ruminally infused acetate, propionate and butyrate, respectively, were found on a net basis in portal blood as VFA. Measurements of net nutrient utilization by the PDV that eliminate the influence of ruminal fermentation are possible. How the changes in PDV tissues due to intragastric infusion influence these estimates is unknown.     

Subclinical ammonia toxicity in steers: effects on hepatic and portal-drained visceral flux of metabolites and regulatory hormones

Four calves (avg wt 161 kg) were surgically fitted with indwelling catheters in the femoral artery and femoral, portal, hepatic and mesenteric veins to study the effects of subclinical ammonia toxicity on portal-drained viscera (PDV) and hepatic (HEP) net flux of key metabolites and pancreatic hormones. Hyperammonemia was induced via administration of ammonium chloride (NH4Cl; 12 mumol.kg BW-1.min-1) via the femoral vein catheter for 240 min; infusions were preceded (PRE) and followed (POST) by 60- and 180-min control periods, respectively. Blood samples were obtained from the arterial catheters, and portal and hepatic vein catheters. Net flux rates were calculated by multiplying venoarterial differences by blood flow. Arterial plasma ammonia N peaked (P less than .01) at 327 micrograms/dl; hepatic ammonia extraction increased (P less than .01) from 10 to 23% during NH4Cl infusion. Arterial plasma glucose concentrations increased (P less than .05) during NH4Cl infusion (90.5 vs 82.6 mg/dl) concomitant with trends toward a reduction in net HEP glucose output. Portal-drained visceral release of insulin did not increase (P greater than .10) during NH4Cl infusion despite the steady rise in circulating glucose concentration; however, cessation of NH4Cl infusion resulted in a 109% increase (P less than .05) in PDV insulin release at +60 min POST. Plasma L-lactate, nonesterified fatty acids, urea N and glucagon concentrations and net fluxes were variable throughout the experiment. Results tend to indicate that hyperammonemia reduced hepatic glucose output and glucose-mediated pancreatic insulin release.     

Effect of increasing ruminal butyrate on portal and hepatic nutrient flux in steers.

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.     

Effects of growth hormone-releasing factor and feed intake on energy metabolism in growing beef steers: net hormone metabolism by portal-drained viscera and liver.

Effects of growth hormone-releasing factor (GRF) and intake on arterial concentrations and net visceral metabolism of hormones were measured in six growing Hereford x Angus steers using a split-plot design with 4-wk injection periods within 8-wk intake periods. Steers were fed a 75% concentrate diet at two intakes and were injected s.c. twice daily with saline or GRF (10 micrograms/kg of BW). Arterial concentrations of growth hormone (GH) were measured on d 1 and d 8 to 10 of injections. Eleven measurements, obtained at 30-min intervals, of arterial concentration and net flux of hormones across portal-drained viscera (PDV) and liver were obtained on d 8 to 10 of injections (six hourly measurements were used for insulin-like growth factor-I [IGF-I] and somatostatin). The area under the GH curve and average and peak GH concentrations were increased (P less than .01) by GRF and were greater (P less than .10) at low than at high intake. Liver removal of GH was not affected by GRF or intake. Arterial IGF-I concentration was increased (P less than .05) by GRF and not affected by intake. Treatments did not affect IGF-I flux across the liver. Arterial insulin concentration was greater (P less than .05) at high than at low intake, in part because of greater (P less than .01) PDV release. Increased (P less than .10) arterial insulin concentration in GRF-treated steers was not attributable to significant changes in PDV or liver net flux. Arterial glucagon concentration was greater (P less than .01) at high than at low intake, in part because of greater (P less than .05) PDV glucagon release and decreased (P less than .10) liver extraction ratio. Effects of intake on arterial concentration of insulin and glucagon were in part due to changes in visceral metabolism, but GRF did not affect PDV or liver hormone metabolism.     

The net portal and hepatic flux of metabolites and oxygen consumption in growing beef steers given postruminal casein

Changes in net portal and hepatic nutrient flux and oxygen consumption in response to 3-d abomasal casein infusions were studied in seven multicatheterized beef steers. Steers were fed 4.3 kg DM/d of a high-concentrate diet in 12 equal meals. Blood flow (para-aminohippurate dilution) and net flux (venoarterial concentration difference x blood flow) across portal-drained viscera (PDV) and hepatic tissues were measured on d 3 of the abomasal infusions. In two experiments, the response to 300 (300C) and 150 (150C) g casein/d were compared, respectively, to a control water infusion. The 300C increased (P less than .05) arterial blood concentrations of alpha-amino N (AAN), urea N and ammonia; 150C increased (P less than .05) arterial urea N. Urinary urea N excretion was increased (P less than .01) by 300C and 150C. Although 300C increased net PDV release of AAN (P less than .07) and alanine (P less than .10), there was no net change in total splanchnic (TSP) flux due to an increased net hepatic uptake of AAN (P less than .01) and alanine (P less than .05). Net PDV glucose flux was decreased (P less than .05) by 300C, but net hepatic glucose flux was not affected by either level of casein. The 150C increased TSP oxygen consumption (P less than .05) and hepatic oxygen extraction (P less than .10). Approximately 26 and 30% of the casein N infused abomasally appeared in the portal blood as AAN for 150C and 300C, respectively. The sum of net PDV ammonia and AAN fluxes accounted for 47 and 88% of the N infused for 150C and 300C, respectively. These data emphasize the importance of intestinal and liver tissues in regulating the flux of nitrogenous compounds absorbed from the diet.     

Splanchnic metabolism of nutrients and hormones in steers fed alfalfa under conditions of increased absorption of ammonia and L-arginine supply across the portal-drained viscera

Effects of increased ammonia and/or arginine absorption on net splanchnic (portal-drained viscera [PDV] plus liver) metabolism of nonnitrogenous nutrients and hormones in cattle were examined. Six Hereford x Angus steers (501 +/- 1 kg BW) prepared with vascular catheters for measurements of net flux across the splanchnic bed were fed a 75% alfalfa:25% (as-fed basis) corn and soybean meal diet (0.523 MJ of ME/[kg BW(0.75).d]) every 2 h without (27.0 g of N/kg of DM) and with 20 g of urea/kg of DM (35.7 g of N/kg of DM) in a split-plot design. Net flux measurements were made immediately before and after a 72-h mesenteric vein infusion of L-arginine (15 mmol/h). There were no treatment effects on PDV or hepatic O2 consumption. Dietary urea had no effect on splanchnic metabolism of glucose or L-lactate, but arginine infusion decreased net hepatic removal of L-lactate when urea was fed (P < 0.01). Net PDV appearance of n-butyrate was increased by arginine infusion (P < 0.07), and both dietary urea (P < 0.09) and arginine infusion (P < 0.05) increased net hepatic removal of n-butyrate. Dietary urea also increased total splanchnic acetate output (P < 0.06), tended to increase arterial glucagon concentration (P < 0.11), and decreased arterial ST concentration (P < 0.03). Arginine infusion increased arterial concentration (P < 0.07) and net PDV release (P < 0.10) and tended to increase hepatic removal (P < 0.11) of insulin, as well as arterial concentration (P < 0.01) and total splanchnic output (P < 0.01) of glucagon. Despite changes in splanchnic N metabolism, increased ammonia and arginine absorption had little measurable effect on splanchnic metabolism of glucose and other nonnitrogenous components of splanchnic energy metabolism.     

Subclinical ammonia toxicity in steers: effects on blood metabolite and regulatory hormone concentrations

The effects of subclinical NH3 toxicity on circulating and regulatory hormone concentrations were investigated in seven Hereford steers. Ammonium chloride (NH4Cl) was infused via a right jugular vein catheter at a rate of 12 mumol NH4Cl.kg BW-1.min-1 for 240 min. This was preceded (PRE) and followed (POST) by saline infusions of 120 and 180 min, respectively. Blood samples were taken at 20-min intervals via a left jugular vein catheter. Metabolite and hormone concentrations during NH4Cl and POST periods were compared to PRE values using the Student's t-test procedure. Plasma NH3 was elevated rapidly (P less than .001) and peaked at 503 micrograms/dl 220 min into NH4Cl infusion. Plasma urea-N and glucose increased (P less than .001) 39 and 12%, respectively, during NH4Cl infusion and remained elevated 180 min POST. Whole blood L-lactate concentrations peaked (P less than .05) at 18% above PRE between 160 and 240 min into the NH4Cl infusion and gradually returned to PRE values, whereas pyruvate levels were not altered (P greater than .10). Plasma nonesterified fatty acids peaked (P less than .001) at 94% above PRE levels 40 min into NH4Cl infusion, thereafter declining to PRE concentrations. Whole blood acetoacetate and beta-hydroxybutyrate concentrations were not altered (P greater than .10) by NH4Cl administration. Plasma insulin concentration decreased (P less than .05) 26 to 46% during NH4Cl infusion and increased (P less than .05) 89 to 122% during POST. Plasma glucagon levels were not altered by NH4Cl infusion, so molar insulin:glucagon ratio changes resembled those of insulin. Plasma epinephrine, norepinephrine and dopamine did not vary (P greater than .10) with treatment. These results support the hypothesis that the hyperglycemia observed during hyperammonemia may result from an under-utilization of glucose by insulin-sensitive tissues.     

Effects of feeding endophyte-infected fescue hay on portal and hepatic nutrient flux in steers

Six Holstein steers (313 +/- 10 kg BW) surgically fitted with hepatic portal, mesenteric venous, mesenteric arterial, and hepatic venous catheters were used in a replicated crossover design experiment to evaluate the feeding of Acremonium coenophialum-infected fescue hay on portal-drained visceral and hepatic nutrient metabolism. Only four steers had functional hepatic catheters. Infected (INF) and endophyte-free (EF) fescue hays were harvested on the same day in May, at the soft dough stage of maturity, from a similar location in southeast Kansas. The hay was chopped through a 2.5-cm screen and fed in 12 portions daily. Intake was limited to 5.2 kg of DM/d to equalize consumption. Each experimental period lasted 21 d. Dietary CP concentration was greater for INF than for EF (9.9 vs 8.6%); however, apparent digestibilities of DM (52.6%) and N (37%) were not different. Ruminal total VFA concentrations and molar proportions were not different with the exception of butyrate, which was increased (P less than .10) for steers when they were fed INF. Feeding of INF increased (P less than .05) arterial beta-hydroxybutyrate concentration and decreased (P less than .10) arterial butyrate concentration. Steers fed EF showed a greater (P less than .05) portal-arterial concentration difference for acetate and an increased (P less than .05) net portal flux of acetate (500 vs 620 mmol/h). No differences in net flux were noted for any of the other VFA, glucose, lactate, urea N, insulin, glucagon, or prolactin.(ABSTRACT TRUNCATED AT 250 WORDS)     

静脉灌注VFA盐对水牛采食量及血浆某些代谢物和激素水平影响的研究

3头健康雄性去势水牛 ,在正常饲养 (NF)和禁食 2 4h后 (FA) 2种状态下 ,经颈静脉分别灌注 50 0mL的 2mol/L丙酸钠、 1mol/L乙酸钠和 2mol/L乙酸钠。3头正常饲养牛灌注等量生理盐水作为对照。分时段经颈静脉血管瘘管采集血样 ,测定血浆葡萄糖、胰岛素和IGF Ⅰ及各时段采食量。NF动物灌注丙酸钠后 6h内的采食量显著低于对照组 (P <0 0 5) ;灌注乙酸钠 ,低浓度在 3h和 2 4h有显著影响 (P <0 0 1 ) ,高浓度对全天的采食量均有显著影响(P <0 0 1 ,P <0 0 0 1 )。灌注后 ,胰岛素水平均显著地高于对照组。灌注丙酸钠后 ,血液葡萄糖水平低于灌注前和同期对照组的水平 ,乙酸钠对血糖无影响。灌注丙酸钠或乙酸钠后 ,血浆IGF Ⅰ水平下降 ,但差异不显著。FA动物灌注丙酸钠 ,采食量均显著低于对照组。乙酸钠对采食没有显著影响。血浆胰岛素水平在灌注后均显著升高。灌注丙酸钠后 ,血糖水平在 6h内显著高于其他组。乙酸钠无明显影响。丙酸钠灌注后血浆IGF Ⅰ水平比灌注前上升差异显著 ,乙酸钠灌注组显著下降 (P <0 0 5)。     

Developmental alterations in the regulation of glucagon and insulin secretion in Holstein calves

Twenty-one Holstein bull calves were randomly assigned at birth to 3 groups. Two groups (each of 7 calves) were raised as follows: fed a milk diet alone or fed milk with grain supplementation after 2 weeks of age; studies were done when calves reached 4 weeks of age. The 3rd group was fed on milk with grain supplementation until weaning after which the calves were maintained on grain and pasture. These calves (older calves) were studied at 12 weeks of age. Either propionate (0.28 mmol/kg) or glucose (0.56 mmol/kg) was injected IV in a random order. Samples of blood were obtained from the calves before and immediately after injections were done and at 2, 5, 10, 15, 30, 45, and 60 minutes after secretagogue injection. Plasma was examined for glucose by a glucose oxidase procedure and for immunoreactive insulin (IRI) and glucagon (IRG) by radioimmunoassay. The IRI response to the injection of glucose was greater in older calves (P less than 0.02). Patterns of IRI secretion, as determined by heterogeneity of regression, showed age differences for both secretagogues (P less than 0.05). Base-line IRG was greater in milk/grain-fed calves than in milk-fed calves (P less than 0.05). Mean IRG response to propionate injection was higher (P less than 0.05) in milk/grain-fed calves than in milk-fed calves. Plasma glucose concentration increased in older calves, but decreased in milk-fed calves after propionate injection. The data indicate that maturation in the ruminant is accompanied by altered regulation of insulin and glucagon secretion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Propionate is not an important regulator of plasma leptin concentration in dairy cattle

Propionate was recently shown to increase leptin synthesis in rodents. To determine if a similar effect occurs in ruminants, propionate was administered to lactating dairy cows. In experiment 1, 31 cows were given an intrajugular Na propionate bolus (1,040 micromol/kg body weight), increasing plasma propionate from 160 to 5,680 microM and plasma insulin from 6.8 to 77.8 microIU/mL. Plasma leptin concentration decreased from 2.11 ng/mL before bolus to 1.99 ng/mL after dosing (P<0.05) with no differences in leptin concentrations at 20, 50, and 100 min post-bolus (P>0.10). In experiment 2, 12 cows were used in a duplicated 6 x 6 Latin square experiment to assess the dose-response effect of ruminal propionate infusion on plasma leptin concentration. Sodium propionate was infused at rates of 0, 260, 520, 780, 1040, or 1,300 mmol/h, while total short-chain fatty acid infusion rate was held constant at 1,300 mmol/h by addition of Na acetate to the infusate. Coccygeal blood was sampled following 18 h of infusion. Increasing the rate of propionate infusion linearly increased plasma propionate concentration from 180 to 330 microM (P<0.001) and plasma insulin concentration from 6.7 to 9.1 microIU/mL (P<0.05). There was a quadratic response in plasma leptin concentration (P=0.04) with a maximum at 780 mmol/h propionate, but leptin concentrations increased by no more than 8% relative to the 0 mmol/h propionate infusion. Leptin concentrations were correlated with insulin concentrations but not with propionate concentrations in plasma. Propionate is not a physiological regulator of leptin secretion in lactating dairy cows.     

Portal-drained visceral metabolism of 3-hydroxybutyrate in sheep

The present experiment was conducted to study the impact of portal-drained visceral (PDV) metabolism of arterial 3-OH-butyrate on estimates of the portal recovery of intraruminally infused butyrate. Three multicatheterized and rumen-fistulated Leicester ewes were subjected to three intraruminal infusion protocols in a Latin square design: control (C; water), butyrate (B; 20 mmol x h(-1)), and butyrate (20 mmol x h(-1)) + propionate (40 mmol x h(-1)) (BP). During the experiments, the sheep were infused with 1,2,3,4-13C4-D-3-OH-butyrate in a mesenteric vein. Portal recoveries of intraruminally infused butyrate and propionate were obtained by comparing Treatments B and BP, respectively, with Treatment C. The portal net appearance of butyrate and the portal net appearance of butyrate + 3-OH-butyrate accounted for 20 +/- 2% and 48 +/- 14% of intraruminally infused butyrate, respectively. Metabolism by the PDV tissues accounted for 32 to 44% of the whole-body irreversible loss rate of 3-OH-butyrate (12.0 to 24.7 +/- 0.5 mmol x h(-1)). The portal net appearance of butyrate plus the unidirectional PDV output of 3-OH-butyrate accounted for 62 +/- 5% of the intraruminally infused butyrate, and this estimate was comparable to the portal recovery of intraruminally infused propionate (62 +/- 7%). The results from the present study show that the extent of epithelial butyrate oxidation is overestimated and the portal recovery of butyrate carbon underestimated if only portal net appearance rates of butyrate and 3-OH-butyrate are considered.     

Effect of exogenous glucagon and free fatty acids on gluconeogenesis in fasting neonatal pigs

Thirty-two pigs (1 d old) were used to determine if exogenous glucagon and(or) free fatty acids (FFA oleic acid) would enhance gluconeogenesis and glucose homeostasis during fasting. Pigs were acquired at birth, fitted with an indwelling arterial cannula (via umbilicus) and fasted 24 h to deplete liver glycogen. A jugular cannula was inserted nonsurgically 8 to 10 h before initiation of a primed-continuous infusion consisting of control (excipient), glucagon (Glu), oleic acid (FFA), or both glucagon and oleic acid (Glu-FFA). Plasma Glu averaged 395 pg/ml preinfusion and was similar across treatments. The concentration increased fivefold (P less than .05) by 80 min for Glu and Glu-FFA pigs and remained constant thereafter (160 min: 2,379, 2,258 pg/ml; 240 min: 2,355, 2,274 pg/ml, respectively). Glucagon infusion did not alter plasma glucose after 240 min of infusion (control, 50 vs Glu, 51 mg/dl); however, Glu-FFA effected an increase (60 mg/dl, P less than .10). In contrast, pigs infused with FFA alone had a lower glucose concentration (40 mg/dl, P less than .10). Rate of glucose synthesis was determined using liver slices, acquired immediately postinfusion, with alanine and lactate as substrate (7.5 mM). The rate of synthesis was not altered by Glu or Glu-FFA infusion (2.91, 2.43 mumol glucose X g-1 X h-1 vs 2.91 for control). In contrast, exogenous FFA reduced synthesis to 1.85 mumol glucose X g-1 X h-1 (P less than .05) with lactate as substrate. It appears that Glu is not the primary factor limiting gluconeogenesis in fasting newborn pigs.(ABSTRACT TRUNCATED AT 250 WORDS)     

Splanchnic metabolism of volatile fatty acids absorbed from the washed reticulorumen of steers

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.     

Effects of short- or long-term infusions of acetate or propionate on luteinizing hormone, insulin, and metabolite concentrations in beef heifers

Two trials were conducted to evaluate the effects of short- (Trial 1) or long-term (Trial 2) intraruminal isocaloric infusions of acetate or propionate on secretion of LH, insulin, and selected metabolites in short- or long-term energy-restricted beef heifers. In Trial 1, 16 Angus heifers were assigned on d 6 to 12 of a synchronized estrous cycle (estrus = d 0) to a body weight-maintenance (BWM; n = 4) or an energy-restricted, body weight-loss (BWL; n = 12) treatment. On d 12 of a synchronized estrous cycle, heifers received PGF2alpha to synchronize estrus, and 12 h later BWL heifers received intraruminal, isocaloric infusions of acetate, propionate, or vehicle for 6 h and BWM heifers received vehicle concurrently. Mean plasma LH and LH pulse frequencies and amplitudes were not affected by treatment (P > .05). In contrast, infusion of propionate increased plasma insulin (P < .05) and reduced plasma concentration of NEFA (P < .05). In Trial 2, six ovariectomized Angus heifers were energy-restricted for 30 d. On d 14 and 26 of restriction, heifers began receiving intraruminal isocaloric infusions of acetate or propionate for 96 h in a switchback approach. Intraruminal infusions of vehicle for 6 h preceded infusions of acetate or propionate. Jugular blood was collected at 12-min intervals during infusions of vehicle and during the last 6 h of infusion of acetate or propionate. Mean concentration of LH and amplitude of pulses of LH were lower during acetate vs propionate or vehicle infusion (P < .05). Infusion of propionate increased insulin relative to acetate or vehicle infusion (P < .05). Plasma NEFA were reduced by infusion of propionate (P < .05) and increased by infusion of acetate (P < .05).     

Serum triiodothyronine and thyroxine concentrations in weanling horses fed carbohydrate by direct gastric infusion

Plasma glucose and serum insulin, thyroxine, and triiodothyronine concentrations were monitored in 6 weanling Thoroughbreds after direct gastric infusion of solutions containing sucrose or casein. Neither plasma glucose nor serum hormone concentrations were affected by infusions of water or by infusions of 326 or 424 g of casein/250 kg of body weight. However, glucose and hormone concentrations increased significantly (P less than 0.001) after infusions of 649 or 844 g of sucrose/250 kg. Initial rates of increase were more rapid and increases were subsequently reversed more rapidly when 844 g of sucrose/250 kg was infused than when 649 g of sucrose/250 kg was infused. Soluble carbohydrate in the digestive tract triggered specific responses in the serum thyroid hormone concentrations of weanling horses. Magnitudes and durations of these responses appeared to depend on the amount of carbohydrate present.     

Hepatic morphology and effects of intravenous injection of sodium propionate on plasma propionate and glucose in fed and fasted dairy cattle

Sodium propionate (3 mmol/kg) was injected IV into 8 nonlactating dairy cows before and after 6 days (144 hours) of fasting. During fasting, long-chain fatty acids in plasma increased from 0.30 +/- 0.05 (SE) mM to 1.09 +/- 0.15 mM (P less than 0.05). Liver fat increased from 0.5 +/- 0.3% to 9.3 +/- 1.7% (P less than 0.05). Half-life of injected sodium propionate increased significantly (P less than 0.05) from 7.6 +/- 0.5 minutes to 10.1 +/- 1.0 minutes during fasting. Sulfobromophthalein half-life did not change significantly (3.8 +/- 0.79 minutes to 5.3 +/- 1.3 minutes). Increases in plasma glucose concentrations after propionate loading were significantly less during fasting than during feeding. Thus, the change in glucose concentration served as an indicator of hepatic conversion of propionate to glucose. Increases in glucose concentration of less than 2 mM at 30 minutes after propionate loading indicated that liver function was altered in nonlactating dairy cows.     

Effects of glucagon and insulin on lipolysis and ketogenesis in sheep.

The hepatic and portal productions of acetoacetate and beta-hydroxybutyrate and lipolysis were studied in normal and insulin-controlled alloxan-diabetic sheep. Since hyperinsulinemia is associated with glucagon administration, the latter group of sheep were used to maintain constant plasma insulin levels. After control values were obtained glucagon was infused intraportally at 90 mug/hr for two hours. The ketone body production by portal drained viscera was not significantly affected by glucagon. In alloxanized sheep, glucagon significantly (P less than 0.01) increased net hepatic production of acetoacetate (from -0.54 +/- 0.08 to 0.46 +/- 0.07 g/hr). Lipolysis also increased. However, in the normal sheep, hyperinsulinemia prevented any stimulatory effect of glucagon on hepatic ketogenesis and lipolysis. Therefore, while glucagon appears capable of stimulating ketogenesis andlipolysis, these effects are readily suppressed by insulin.