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
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.