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Metabolic Changes in Liver Associated with Spontaneous Ketosis and Starvation in Cows^{1, 2,}

Fels Research Institute and Department of Biochemistry, Temple University Medical School, Philadelphia, Pennsylvania and Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Kennett Square, Pennsylvania

Although some information is available concerning the physiological alterations in vivo associated with spontaneous bovine ketosis, a broad study of pathways and possible changes of enzyme activities has not been carried out. To this aim, liver samples were taken from spontaneously ketotic cows, from the same cows when normal, and when starved for 96 hours. Measurements were made to ascertain the degree of ketosis and to compare changes in lipid synthesis, substrate oxidation, enzyme activities and the level of several metabolic intermediates. This research was particularly directed to a comparison of differences and similarities between the normal and spontaneously ketotic animal and between spontaneous ketosis and starvation ketosis. The liver of the spontaneously ketotic cow had a lower activity of mitochondrial NAD-malate dehydrogenase than the normal, higher levels of lactate, pyruvate, acetoacetate and ß-hydroxybutyrate, and a substantially lower concentration of citrate. Livers from the spontaneously ketotic cows, when compared to with those of the starved animal, had a lower activity of mitochondrial pyruvate carboxylase, lower levels of NADH and higher levels of citrate, ß-hydroxybutyrate and acetoacetate. Many other parameters of carbohydrate and lipid metabolism were measured and found to be unchanged from the normal in the two ketotic conditions. Notable among these was the lack of any alterations in the activity of phosphoenolpyruvate carboxykinase or levels of oxaloacetate. These findings conflict with the oxaloacetate shortage theory of bovine ketosis as generally stated.

² These studies were supported (in part) by Public Health Service Research Grants no. AM-04927, AM-11279 and AM-05487 from the National Institute of Arthritis and Metabolic Diseases; by Grant HD-02758 from the National Institute of Child Health and Human Development and by Grant CA-07174 from the National Cancer Institute.

Manuscript received 2 January 1968.