1. Circulating concentrations of glucose, propionate, lactate and pyruvate, and net exchange of these compounds across the liver and gut, were measured in lactating and non-lactating dairy cows (a) in the normal fed state, (b) before, during and after intravenous infusion of an aqueous solution of glucose, propionate or lactate (lactating cows only) in fed animals, and (c) before and during 6 days of food deprivation. 2. In the normal fed state, gut output of propionate, hepatic output of glucose and hepatic uptake of lactate were all higher in the lactating group. There was a net uptake of pyruvate across the liver in the lactating cows and a net output in the non-lactating cows. In the lactating cows there was a net uptake of lactate and pyruvate by the splanchnic bed (i.e. gut and liver combined). 3. In the lactating cows, the glucose and propionate infusions had the following effects: decrease in net hepatic uptake of lactate; a switch in pyruvate exchange across the liver from uptake to output; suppression of uptake of lactate and pyruvate by the splanchnic bed; increase in the magnitude of the liver (propionate uptake)/(glucose output) ratio. Lactate infusion did not affect hepatic propionate uptake. 4. Food deprivation increased hepatic extraction of lactate and pyruvate and decreased the liver (propionate uptake)/(glucose output) ratio in both groups. 5. It is concluded that mechanisms exist to ensure an inverse relationship between the availability to the cow of glucose or propionate and utilization by the splanchnic bed of endogenously derived lactate and pyruvate.

1. Four parameters of insulin metabolism were compared in catheterized lactating and non-lactating Friesian x Ayrshire dairy cows. 2. The four parameters, i.e. arterial and portal-venous concentrations of insulin, and pancreatic output and hepatic uptake of insulin, were approx. 2-, 3-, 3- and 5-fold higher respectively in the non-lactating cows than in the lactating cows in the normal fed state. Statistical significance was not achieved for the differences in magnitude in the case of the latter two parameters, however. 3. All four parameters increased significantly about 4-fold when non-lactating cows were infused intravenously with glucose for 48 h at a rate of 4.2 mmol/min. The parameters also increased in the lactating cows during glucose infusion, but the values reached were substantially lower than in the non-lactating cows and the increases were not statistically significant. 4. Arterial insulin concentrations doubled in the non-lactating cows during a 3 h infusion of propionate into a mesenteric vein, but remained unaltered in the lactating cows. 5. Differences in insulin concentration and output between the lactating and non-lactating cows were not consistently related to differences in either glucose concentration or glucose-entry rate. Arterial propionate concentrations were similar in both groups of cows at all times. 6. It is concluded that in the dairy cow, insulin secretion in response to an insulinotropic agent is diminished during lactation.

1. Three adult dairy cows were fitted with cannulas in a mesenteric, portal, hepatic and jugular vein and a carotid artery. They received infusions of step-wise increasing amounts of ammonia as ammonium acetate via a mesenteric vein until NH, intoxication occui.red. Sodium acetate was used in control infusions. The maximum rate of uptake of NH, by the liver and the conccntrations of glucose, urea, lactate, acetate and bilirubin in blood were measured.2. During the infusions of ammonium acetate the liver extracted almost all the NH, qresent in the portal vein until an infusion rate of approximately 15.0mmol/min was reached. The maximum capacity of the liver to remove NH, during its first pass was on average 1.84mmol/min per kg wet weight. The cows became intoxicated when arterial plasma ammonia concentrations reached 0.8 mmol/l. Concentrations of NH, in jugular venous blood were between 66 and 74'7; of those in the carotid.In ruminants much of the protein and non-protein nitrogen in the diet is normally metabolized to ammonia 1)y rumenal micro-organisms. Some of this NH, is incorporated into microbial protein but a proportion of it (depending upon rumen pH) is absorbed through the rumen wall. If this NH, reaches the systemic circulation it is very toxic. In most physiological conditions it is converted in the liver to the less toxic urea thus keeping the NH, concentration in the systemic circulation low. However, under certain circumstances, for example when cattle are fed rations containing large amounts of either readily degradable protein or nou-protein nitrogen the amount of NH, which enters the portal circulation may exceed the rate at which the liver can metabolize it. The concentration of NH, in the systemic circclation will then increase until, when arterial NH, concentrations are approximately 1 .O mmol/l, the cow shows clinical signs of NH, intoxication (Davidovitch et al. !977).One factor which will affect the susceptibility of the dairy cow to NH, intoxication is, therefore, the capacity 01' its liver to metabolize NH,. When systemic NH, concentrations increase there is also an increase in blood concentrations of glucose, lactate, pyruvate and free fatty acids (Visek, 1972;Barej et al. 1974;Garwacki et al. 1979). The capacity of the bovine liver to metabolixe NH, has not been measured in vivo.This report describes an experiment in which NH,, as ammonium acetate (NH,Ac), was infused in increasing amounts into a mesenteric vein of three adult cows until they became intoxicated. The uptake of NH, by the liver was measured by determining the NH, concentration in portal and hepatic venous blood.

Rumen-fistulated lactating cows were individually fed on hay or silage and intakes were monitored during 3 h treatment periods and for 2 h after. Each experiment used five, six or seven animals and the treatments were applied in a Latin Square design. Sodium acetate infusions of 14-11.0 mol in 4.5 litres water caused a dose-related depression in hay intake, the extent being 82 g dry matter (DM)/mol infused (P < 0.01). Sodium acetate infusions of 6.0-15.0 mol in 4.5 litres water caused a dose-related depression in silage intake of 118 g DM/mol infused. Rumen fluid pH for both diets was unaffected by treatment. Acetate and Na concentrations were increased and significantly negatively correlated with intake of both diets. Infusions of 2-8 mol sodium propionate caused a dose-related depression of hay intake which was significant when cow and day effects were accounted for. Sodium propionate infusions of 4-8 mol significantly depressed silage intake by 140 g DM/mol infused (P < 0.001). Rumen fluid pH was unaffected by treatment while propionate and Na concentrations were elevated and significantly negatively correlated with intake for both diets. Inflation of a rubber balloon in the rumen with 125-20 litres warm water resulted in a dose-dependent depression in hay intake of 6 6 g DM/I distension (P < 0.05). There was significant overeating during the 2 h following the 20 titre treatment. With silage, 1 5 2 5 litres of balloon distension for 3 h resulted in a dose-dependent depression in intake of 28 g DM/I distension (P < 0.001). There was no significant overeating during the 2 h following distension. When given in physiological amounts, at the lower end of the range used in these experiments, acetate, propionate and distension of the rumen did not significantly affect hay intakes. However, in each case the linear relationship between intake depression and level of treatment suggested that these factors could contribute to the control of feed intake.

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SUMMARYMetabolite production rates were determined in the portal vein and hepatic veins of catheterized adult dairy cows maintained under normal conditions of husbandry. The production rates were calculated from the metabolite concentrations in arterial, portal and hepatic-venous blood, and from the rates of blood flow in the portal vein and the hepatic veins. In general, qualitatively similar metabolite production was observed in three non-lactating and two lactating cows, but production rates tended to be higher in the lactating cows due to higher blood flow rates.About half the lactate utilized by the liver was absorbed from the gut, while the other half was derived from endogenous sources. Lactate absorbed from the gut was quantitatively of less significance than propionate as a substrate for hepatic metabolism. Even in cows that were well fed, there was a net production of ketone bodies from the liver that was almost as great as the net production from the gut. However, while the liver produced D-3-hydroxybutyrate it took up acetoacetate. In the lactating cows, acetate, propionate and butyrate were absorbed from the gut in the proportions of 9·5:2·5:1, respectively. About 90% and 80% of the absorbed propionate and butyrate, respectively, were taken up by the liver.On the routine hay/concentrate diet there was little net uptake or output of glucose by the gut. However, there was consistent production of glucose by the liver, amounting to a maximum, in this study, of about 11 mol/24 h, assuming constant glucose production throughout the 24 h day. The rate of carbon dioxide appearance in the portal vein was about twice that of oxygen uptake by the gut. The liver used oxygen, and produced carbon dioxide, at nearly equal rates. The uptake of glucogenic substrates by the liver accounted adequately for the observed rates of hepatic gluconeogenesis.In one of the lactating cows it was observed that there was a net production of acetate by the liver that amounted to half the net absorption of acetate from the gut (ethyl alcohol was not the precursor of this acetate) and that (glutamine + asparagine) and serine had the highest rates of appearance in the portal vein and the highest rates of uptake by the liver.