Ketosis

Ketosis is defined as a metabolic disorder in which the level of ketone bodies in body fluids is greatly elevated. Ketosis can occur in any animal under conditions of starvation; however, it is most common in ruminants due to their dependence on gluconeogenesis to meet glucose needs. In ruminants, ketone bodies (p hydroxybutyrate and acetoacetate) are a product of normal metabolism by the liver and ruminal epithelium when animals are in positive energy balance. Acetoacetate is the parent ketone, however, normally most is reduced to p hydroxybutyrate. Acetone is produced from acetoacetate as a result of spontaneous decarboxylation.1-1-1 Peripheral tissues use p hydroxybutyrate and acetoacetate to provide an immediate source of energy or to synthesize long-chain fatty acids for storage. Under conditions of negative energy balance, fat mobilization from adipose tissue increases, leading to an increase in circulating concentration of nonesterified fatty acids (NEFA), an increase in ketone body production by liver, and an increase in ke-tone bodies in the blood (Fig. 1). In liver, entry of NEFA into the mitochondria is regulated by carnitine palmitoyl transferase I (CPTI). Hypoglycemia results in an increase in the activity of CPTI and increased flux of NEFA into the mitochondria.1-2-1 Increased partition of

NEFA to ketone body formation rather than oxidation could be due to a relative deficiency of oxaloacetate. In ketosis, the amount of acetoacetate and acetone increase relative to p hydroxybutyrate. Both of these compounds are toxic to the central nervous system.[1-

Ketosis is associated with both negative energy balance and hypoglycemia. In dairy cows, ketosis occurs most commonly in the first 3 8 weeks of lactation. At this stage of lactation, the cow is in negative energy balance, insulin concentration is decreased, glucagon concentration is increased, hormone-sensitive lipase activity is increased, and there is increased mobilization of NEFA. At the same time, the cow may be hypoglycemic due to an insufficient rate of gluconeogenesis relative to the amount of glucose needed by the mammary gland, for synthesis of lactose and the glycerol portion of milk fat, as well as glucose needs of other body tissues. In ewes and does, the condition is most commonly associated with the last month of gestation in females carrying twins. Intake declines and the rate of gluconeogenesis is not adequate to meet the demands of fetal tissues as well as glucose needs of other body tissues.[3] Cows with clinical ketosis will decrease feed intake and milk production, but may spontaneously recover from the disease. In ewes and does, the condition is often fatal. They may recover if birth occurs or if lambs or kids are removed by cesarean section.[1-

Presence of ketone bodies in urine or milk are signs of ketosis. Diagnosis is difficult prior to observation of clinical signs. Serum concentrations of p hydroxybutyrate from 1.2 1.4 mM have been suggested to indicate subclinical ketosis. Milk tests can also be used to measure acetone and acetoacetate or p hydroxybutyrate.[4- Treatments include intravenous administration of glucose, feeding glucose precursors such as propylene glycol, administration of glucocorticoid hormones, and use of methanogenic inhibitors. Propylene glycol, which is not fermented and is converted to pyruvate after absorption, may be administered as a drench or included in the grain mix. Administration of glucocorticoid hormones such as dexamethasone will promote increased gluconeogenesis from amino acids. Methanogenic inhibitors such as chloral hydrate can also be used to increase propionate production in the rumen and consequently increase gluconeogenic

precursors.[1,4-

Ketone Bodyformation From Nefa

Fig. 1 Potential pathways of nonesterified fatty acid (NEFA) metabolism in liver. In conditions of undernutrition, fat is mobilized from adipose tissue, resulting in increased NEFA concentration in plasma and increased NEFA uptake by liver. In ketosis, there is an increase in the proportion of acetyl CoA converted to ketone bodies. Fatty liver arises as the formation of triacylglycerols from NEFA increases without a corresponding increase in secretion of very low density lipoproteins (VLDL).

Fig. 1 Potential pathways of nonesterified fatty acid (NEFA) metabolism in liver. In conditions of undernutrition, fat is mobilized from adipose tissue, resulting in increased NEFA concentration in plasma and increased NEFA uptake by liver. In ketosis, there is an increase in the proportion of acetyl CoA converted to ketone bodies. Fatty liver arises as the formation of triacylglycerols from NEFA increases without a corresponding increase in secretion of very low density lipoproteins (VLDL).

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