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Hyperketonemia-Ketogenesis and Ketone Body Metabolism²

Department of Physiology, New York State Veterinary College Cornell University, Ithaca, New York 14850

ABSTRACT

In bovine ketosis, hyperketonemia is only one biochemical disturbance that occurs among a multiplicity of metabolic changes. The changes can be grouped into two major categories and these are: 1 ) a reduction in available carbohydrate and 2) an increase in the quantities of fat and ketone bodies being metabolized. The two major ketone bodies, AcAc and BHB, are interconvertible and their ratio may reflect or alter the redox state of the various tissues. The ketone bodies are readily utilized, are used for milk fat production, and can account for 20 to 30% of the animal's total respiratory CO₂. There is some evidence that several tissues, notably the brain, can gradually adapt to ketone body utilization while conserving glucose. In the normal ruminant, ketone bodies are produced by the rumen epithelium from dietary fatty acids, notably butyrate, and certain ketogenic diets possibly can predispose the animal to ketosis. During active ketosis, however, most of the excess ketone bodies are produced from FFA in the liver. The excessive ketogenesis seems dependent upon two factors, both of which must operate: 1) a primary factor or FFA mobilization from the body's fat stores and 2) an hepatic factor which involves a shift in hepatic FFA utilization away from the two pathways of esterification and oxidation to CO₂ to the third pathway of partial oxidation to ketone bodies. The availability of carbohydrate seems to play a critical role in each case. Hypoglycemia will cause increased FFA mobilization from the fat stores, and insufficient carbohydrate metabolism in the liver shifts the pathways of hepatic FFA utilization from that of esterification and oxidation to CO₂ to that of ketogenesis. An insufficient mobilization or supply of precursors for the production of oxaloacetate and eventually glucose, relative to the animal's increased needs, thus may be the critical phase of the disorder.

² Author's work mainly was supported by USPHS Grant AM-05976.

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