Review/Oorsig Volume 22, Issue 03 - Page 29

Volume 22 • Issue 03 • 2018 GLUCOSE BST PROLACTIN PLACENTAL LACTOGEN POSITIVE ENERGY BALANCE Chromium _ HIGH INSULIN INSULIN _ RESISTANCE Hormone sensitive lipase GLYCER OL L IV E R C E L L NEFA NEFA Malonyl CoA GLYCEROL _ GLUCOSE FAT STO RES + + CPT-1 ACETYL CoA MACRO- VESICLE MACRO- VESICLE KETONE PRODUCTION MITOCHONDRIUM Diagram illustrating how constant high energy levels before calving leads to the formation of large fat droplets in the liver cells lactogen, prolactin and other hormones that are secreted at the time surrounding calving. This is called adipose sensitivity, and together with the fact that these obese cows have large fat stores, leads to the sudden very fast break-down of fat stores and transportation of non-esterified fatty acids (NEFA) to the liver. In the liver an enzyme called carnitine palmitoyltransferase-1 (CPT1) is responsible for the transport of NEFA into the mitochondrium, where it can be metabolised into Acetyl-CoA for gluconeogenesis or ketogenesis. CPT1 is inhibited by high levels of Malonyl CoA, a glucose substrate in the hepatocyte cytoplasm, leading to the formation of fat droplets containing esterified fats (macro-vesicles) in the hepatocyte cytoplasm. The formation of macro-vesicles is a normal physiological mechanism of the cow to store excess energy, and only becomes a problem when these vesicles become large enough to impair normal liver function. This happens when about 60% of the liver cell is occupied by fat. The liver would normally utilise the stored fat by excreting it in the form of very low density lipoproteins (VLDL), once again a fuel source for tissues elsewhere in the body. VLDL’s are formed by combining triglycerides (fat in macro-vesicles) with phospholipids, proteins and cholesterol, after which it forms micro-vesicles in the liver cytoplasm which excrete the VLDL’s directly into the blood. This can only happen in the presence of adequate phospholipid, cholesterol and protein. This pathway is not well developed in ruminants. A shortage of especially phospholipid compounds seems to be responsible for the accumulation of triglycerides in liver cells. Therefore total serum cholesterol indirectly measures the presence of VLDL in blood and consequently measures the liver’s ability to produce VLDL. If VLDL production is compromised, fatty infiltration will ensue Cholesterol levels are decreased in ketosis, while dietary choline is required for the formation of phospholipid. It has further been shown that the secretion of micro- vesicles into the blood is inhibited by a decreased ratio of Poly-unsaturated fatty acids to saturated fatty acids (PUFA:SFA). This holds promise as a possible way through which the liver’s ability to excrete fat can be improved by manipulating the dietary PUFA:SFA ratio. Normal liver function plays a role in many crucial physiological processes like: • detoxification of toxic and potentially toxic substances - i.e. the breakdown of certain hormones, 29