In vivo kinetic techniques were used to quantify changes in metabolism of propionate, glucose, and blood CO2 when glucose was infused intravenously at 0, 342, or 737 g/d into four lactating cows. Neither production of milk or milk fat nor composition of milk was changed. Production of milk protein increased for the high glucose treatment. Isotope dilution data were used to calculate irreversible losses of rumen propionate, plasma glucose, and blood CO2 and to determine a unique solution for flux of C in this three-pool system. Irreversible losses of propionate and CO2 were not changed. Infusions of glucose increased irreversible loss of glucose in proportion to amounts infused, thus indicating there was no change in endogenous production of glucose. For the control, 52% of the C flux of blood glucose was derived directly from rumen propionate and another 26% came from other gluconeogenic substrates. Flux of C into glucose from exogenous sources increased in proportion to amounts of glucose infused. Flux of C from rumen propionate remained constant. The rate of C leaving the glucose pool, other than as CO2, tended to increase with infusion of glucose, and oxidation of glucose tended to increase for the high glucose treatment. High producing cows adjusted to increased exogenous glucose by increasing glucose utilization and without decreasing endogenous glucose production.

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Acute effects of dietary 1,3-butanediol and tributyrin on concentrations of glucose, beta-hydroxybutyrate, and insulin in plasma were compared in lactating goats. In Experiment 1, glucose was decreased by intraruminal administration of 75 or 150 g of 1,3-butanediol or by 84 or 168 g of tributyrin. Tributyrin caused transient hyperglycemia immediately after administration. beta-Hydroxybutyrate was increased in a dose-dependent manner by tributyrin and increased independently of dose by 1,3-butanediol. Tributyrin, but not 1,3-butanediol. Tributyrin, but not 1,3-butanediol, caused large increases of insulin in plasma. In Experiment 2, 75 g of 1,3-butanediol or 84 g of tributyrin administered intraruminally decreased glucose, whereas 73 g of butyric acid (pH 5.6) increased glucose compared with water or 25.6 g of glycerol. All treatments produced transient hyperglycemia immediately after administration. Tributyrin, butyric acid, or 1,3-butanediol greatly increased beta-hydroxybutyrate compared with administration of water or glycerol. Concentrations of beta-hydroxybutyrate in both experiments increased more slowly for 1,3-butanediol than for tributyrin. Both 1,3-butanediol and tributyrin decreased glucose and increased beta-hydroxybutyrate. Because 1,3-butanediol does not stimulate increases of insulin in plasma, it may be more desirable than tributyrin for inducing metabolic changes characteristic of lactation ketosis.

glucose pool, other than as CO2, increased with infusion of glucose, and the oxidation of glucose tended to increase for the highest glucose treatment.

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