Roles for insulin and glucagon in the development of ruminant ketosis -- a review.
Ketonemia can be a physiological response to a reduction in dietary intake. It also may occur when energy demands exceed the energy intake. Normally, alimentary ketogenesis is the major source of ketone bodies in ruminants. During ketonemia there is increased hepatic ketone body production. During physiological ketosis, the mobilization of free fatty acids is inadequate to support a high rate of hepatic ketogenesis. However, during clinical ketosis, the hormonal status (low insulin, high glucagon/insulin ratio) in combination with hypoglycemia promotes excessive lipid mobilization and a greater hepatic removal of fatty acids and switches the liver to a higher rate of ketogenesis. The low insulin, furthermore, can impair maximal ketone body utilization, thus exacerbating the hyperketonemia.
D000138:Acidosis / Q000662:veterinary*; D000818:Animals; D002417:Cattle; D002418:Cattle Diseases / Q000209:etiology* / Q000378:metabolism; D005260:Female; D005934:Glucagon / Q000502:physiology*; D007328:Insulin / Q000502:physiology*; D007657:Ketone Bodies / Q000378:metabolism; D007662:Ketosis / Q000209:etiology / Q000378:metabolism / Q000662:veterinary*; D009747:Nutritional Physiological Phenomena; D011247:Pregnancy; D012756:Sheep; D012757:Sheep Diseases / Q000209:etiology* / Q000378:metabolism
D007328:Insulin; D007657:Ketone Bodies; D005934:Glucagon