Review/Oorsig Volume 22, Issue 03 - Page 28

Oorsig/Review Hormone sensitive lipase is the enzyme that causes break-down of fat, and is stimulated by low insulin, somatotropin, prolactin and other hormones. In type I ketosis, large amounts of fat is broken down and transported to the liver as Non-esterified fatty acids (NEFA), where it is metabolised into Acetyl-CoA. During a glucose shortage, insulin levels are low, indirectly leading to high levels of Acetyl-CoA in the liver where it forms ketone bodies. All lactating dairy cows have a certain level of ketone bodies in circulation as fuel for milk production, but when oxaloacetate becomes depleted glucose can not be formed from ketones anymore and the organ mostly affected by this is the brain. This leads to anorexia and other clinical signs. Ketones are actively excreted in the urine (beta- hydroxy butyrate) and milk, or excreted through the lungs (acetone), while high levels are toxic to the brain. Predisposing factors of type I ketosis Insufficient Dry Matter Intake (DMI) is key: • • • • • • high milk production High producing dairy cows are genetically programmed to produce milk even to the detriment of other bodily needs. high producing dairy cows just cannot physically eat enough food for their energy needs in early lactation and depend on the mobilization of their fat reserves to prevent an energy deficiency. Rumen size and activity are also diminished in the peripartum period. change of diet: a sudden change over from dry cow diet to a lactation diet may disturb rumen function, as well as reduce DMI type of diet: ratio between volatile fatty acids produced: Increased intake of fodder types that will generate proportionally more acetic and butyric acid and less propionic acid, e.g. grass, maize silage, high protein diets will predispose to ketosis. The body uses energy to excrete excessive nitrogen and the production of butyrate (ketogenic) will increase with a high percentage protein in the diet, butyrate is formed in certain types of silage (especially silage made from plants with a high moisture content). This butyrate from external sources is ketogenic, lack of exercise has been incriminated as a predisposing factor, 28 • • • in some herds a deficiency of cobalt and phosphorus seems to play a role - cobalt is needed for the formation of Vit B12 which is needed as a co factor where propionate enters the CAC - also review the effect of cobalt deficiency on rumen microbe activity, stress plays a role in limiting dietary intake and increasing energy needs, certain breeds and certain families within breeds are susceptible, indicating a possible genetic link - the prevalence of ketosis has decreased since the Holstein has become the dominant dairy breed in the world. Recently it has been suggested that the heritability of ketosis is not necessarily linked to milk production level, but that variation in ketone levels exist within groups of animals under the same management with similar milk production levels. Note: Maize kernels contain a glucose polymer that can bypass the rumen microorganisms and be directly absorbed from the intestines and will thus have an antiketogenic effect. Pathophysiology of type II ketosis or fat cow (fatty liver) syndrome Type II ketosis is a peripartum (compare with type I ketosis) syndrome in high producing dairy cows where fat droplets will accumulate in liver cells to the extent that normal liver function is disturbed. This will lead to an exaggerated response of the animal to common postpartum illnesses. The onset of type II ketosis is earlier during the production cycle of the cow, and in actual fact the factors leading to the condition occur some time before the syndrome is seen. Over-feeding of cows in the time before calving leads to high levels of glucose, continually stimulating the secretion of insulin, the hormone responsible to maintain glucose levels. Insulin normally inhibits hormone sensitive lipase, but due to the constant high levels, hormone sensitive lipase becomes refractory to the inhibitory stimulus of insulin. This is called insulin resistance, and reminds of the pathogenesis of type II diabetes mellitus in humans, from there the term type II ketosis. Recent rese ɍѕ́ѡЁ ɽմͥ)́хЁɽѕѥٔɽЁձ)ɕͥхՔѼձɕͥхɵ)͕ͥѥ͔ٕٔ́ȵ͕ͥѥٔѼѡ)ɵѥձՍ́ͽѽɽх