Energy is a basic, essential nutrient provided with the ration for all animals. However, in ruminant and monogastric animals, the processes of energy metabolism differ due to the original way in which energy is obtained and processed from dietary components. In ruminants, energy contained in feed, mainly in the form of carbohydrates, is fermented in the forestomachs (rumen) by bacteria, being converted into short-chain fatty acids (primarily acetic, propionic and butyric). These fatty acids, once absorbed into the bloodstream, become the main source of energy supply for the animal's body. In ruminants, the absorption of glucose and fatty acids from the gut plays a secondary role in meeting energy needs. This mode of energy metabolism is the result of the evolutionary adaptation of these animals to plant foods as their main diet.
One of the negative effects of this adaptation is the risk of ketosis, caused by an excessive increase in the concentration of ketone bodies in the animal's blood. These bodies, such as betahydroxyacetic acid, acetoacetic acid and acetone, accumulate as a result of insufficient glucose available to the liver. The reasons for this phenomenon are too little glucose supplied from the gastrointestinal (intestinal) tract, insufficient glucose production from gluconeogenesis and marginal glycogen stores. At the same time, the temporary excess of fatty acids in the hepatocytes causes them not to be fully burned in the Krebs cycle, leading to the formation of ketone bodies.
There are two types of ketosis in high-yielding dairy cows:
Type II, characteristic of the perinatal period, is primarily associated with excessive mobilization of adipose tissue. The cow's liver is then "flooded" with fatty acids, which often leads to ketosis and hepatic steatosis. This is a result of the stress associated with parturition, which depresses feed intake and thus results in a high negative energy balance.
Type I, called spontaneous, occurs in the later stages of lactation and the main cause is glucose deficiency. This is due to insufficient starch in the feed ration and insufficient dry matter intake.
Appropriate measures can be taken to prevent ketosis in dairy cows:
Avoid fattening cows during the suckling period by assessing a BCS (Body Condition Score) of 3.5. An obese cow has worse postpartum ration eating, leading to greater fat mobilization and an increased risk of type II ketosis.
Ensure a balanced and high-calorie ration for lactating cows, especially in the period immediately after calving (called "fresh cows"). A high dry matter intake will help provide more glucose and other compounds that support gluconeogenesis in the liver.
Use special "anti-ketosis" additives that contain glucoplastic compounds, improve the palatability of the ration and protect the liver from excessive mobilization of fat from spare tissue.
In this context, it is worth noting products such as Ketocure or Energymax Vit, based on pharmaceutical glycerin. They contain glycerin, which acts as a compound that improves the taste and texture of the TMR, as well as a source of energy for the rumen and aids in the process of gluconeogenesis. In addition, they include propylene glycol, a substance with recognized glucoplastic properties, niacin to protect liver cells, and vitamins A, D3 and E to promote regeneration of cows after calving and prevent oxidative stress.
Boluses are also gaining popularity, including Ketostop. It is a complex solution for the prevention of ketosis in dairy cows. It consists of two boluses - an herbal bolus and an energy and vitamin bolus. They support energy metabolism, improve appetite and stimulate liver function. A serving of Ketostop contains as much as 10,000 mg of niacin, which has a direct effect on energy metabolism and supports the liver. In addition, vitamins A, D3 and E support recovery of cows after calving, while sodium propionate provides a source of energy, and a blend of
