NEW ASPECTS OF KETONE-BODIES IN ENERGY-METABOLISM OF DAIRY-COWS - A REVIEW

Citation
P. Holtenius et K. Holtenius, NEW ASPECTS OF KETONE-BODIES IN ENERGY-METABOLISM OF DAIRY-COWS - A REVIEW, Journal of veterinary medicine. Series A, 43(10), 1996, pp. 579-587
Citations number
43
Categorie Soggetti
Veterinary Sciences
ISSN journal
0931184X
Volume
43
Issue
10
Year of publication
1996
Pages
579 - 587
Database
ISI
SICI code
0931-184X(1996)43:10<579:NAOKIE>2.0.ZU;2-W
Abstract
Increased lipolysis, low insulin/glucagon ratios and malonyl-CoA conce ntrations are prerequisites for ketogenesis. From an aetiological view point, there are two quite different types of metabolic disorders in w hich ketosis can occur, the hypoglycaemic-hypoinsulinaemic and the hyp erglycaemic-hyperinsulinaemic type. The former, Type I, generally occu rs 3-6 weeks after calving in cows whose milk secretion is so extensiv e that the demand for glucose exceeds the capacity for glucose product ion. To protect the body from hazardous protein degradation by a high rate of gluconeogenesis, this process is inhibited and the increased e nergy requirements are met by the elevated utilization of ketone bodie s. In this strong catabolic metabolic state the plasma levels of gluco se and insulin are very low, the levels of ketone bodies are high and there are small risks for fat accumulation in the liver cells. The hyp erglycaemic, hyperinsulinaemic form, Type II, generally occurs earlier in lactation. An important aetiologic factor is overfeeding in the dr y period, which can lead to disturbances in the hormonal adaptation of metabolism at calving with increased plasma levels of insulin and glu cose and often but not always also with hyperketonaemia. If combined w ith stress, there may be increased lipolysis in adipose tissues, lipid synthesis and accumulation in the liver, i.e. the development of fatt y liver. This hyperglycaemic form of disturbance has many similarities with the initial stage of non-insulin-dependent (Type II) diabetes in humans. It has been shown that ketone bodies inhibit protein degradat ion and thereby gluconeogenesis and also are able to spare glucose by inhibiting glucose utilization. They also can inhibit lipolysis and fu nction as a regulatory safety system, replacing insulin, in situations when the activity of this hormone is low, as in Type I ketosis. Keton e bodies thus have important functions as substrates replacing glucose in many tissues and also as signal substances in the regulation of en ergy metabolism.