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Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Kennett Square
ABSTRACT
Some of the known metabolic changes in spontaneously ketotic cows could be explained by either a glucose shortage in the mammary gland or by a shortage of nicotinamide adenine nucleotide coenzymes. These changes include decreases in glucose oxidation in the pentose cycle and the citric acid cycle (9), the decrease in fatty acid synthesis from acetate (4), and perhaps the increase in mammary ketogenesis from acetate (3). A primary decrease in glucose availability in mammary cells could lead to shortages of 2-glycerophosphate, NADPH, and oxalacetate, and therefore to decreased disposal of acetyl-CoA in the citric acid cycle and in lipogenesis (1). This would leave more acetyl-CoA available for ketogenesis.
The mammary arterio-venous difference of glucose is about 10 mg/100 ml, both in normal and spontaneously ketotic cows (8). Provided there is no decrease in blood flow rate during spontaneous ketosis, the next possible step which could be impaired, and so lead in effect to an intracellular glucose shortage, is the glucokinase reaction, i.e., the phosphorylation of glucose by the enzyme hexokinase (Figure 1).
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