Cholely acid: escort for the milk cow – Dairy Forum – China Animal Husbandry Website – A useful animal husbandry website
Cholely acid: For the birth of the dairy, it is a key special period in the production of dairy production. The biggest feature of this period is energy negative and balance, which is also a high-incidence period of dairy energy metabolic disorder. When the dairy metabolism is disordered, ketopathy and fatty liver syndrome tend to go together. After the cows, the milk produces a lot of energy, but there is not enough feedstock to meet these energy needs, which leads to energy negative balance. Almost all of all ketopathy have varying degrees of liver fat accumulation, and liver fat accumulation can cause or increase ketopathy, both closely related, mutual causality. The liver is the main supply source of blood in the blood when it is in a negative balance of energy. At the last 3 weeks of the dry milk period, the dry matter intake (DMI) of the cow decreased, the body mobilized the body fat, and the fatty acid used in the form of the body into blood in the form of an inverse fatty acid (NEFA); because the liver absorbs from NEFA and blood The concentration of NEFA is proportional, so the concentration of NEFA in the liver is increased, and the speed of NEFA is synthesized in the liver. When the TG is increased, when the synthesis speed of Tg is greater than the transfer speed in the liver, it will cause fat in the liver. Accumulation forms fatty liver and causes ketosis. Fat mobilization is an inevitable result of the perinatal dairy energy, energy negative balance is cause, fat mobilization is an effect, ketone body generates increases (ketopathy) and liver fat accumulation (fatty liver) is the result. Therefore, non-esterified fatty acids (NEFA) into the blood from the adipose tissue. The liver is an important organ for nutritional regulation and production of glucose. The liver uses NEFA in the blood. In the liver, NefA can be completely oxidized into CO2 energy supply, or partially oxidized into ketone body, the capacity of the liver is limited, and most of the transferred release enters the blood circulation by other tissue Some NEFA can also be reused in the liver into triglycerides. Postpartum energy negative balance and lack of supply of carbohydrate can cause exacerbation of ketosh. The liver of non-ruminants can convert triglycerides into ultra-low density lipoprotein (VLDL) and transport it back into blood. However, ruminants transition triglycerides into extreme low density lipoprotein (VLDL) efficiency is very low, and it is easy to cause fatty liver after cows. As a national new product, bile acid can help the liver of cows exercise their their own work after childbirth, and produce glucose support lactose synthesis in milk production, prevent fatty liver. Keep the liver in time to empty triglycerides,It is very important to start a successful lactation period of cows. Bile acid is the main active ingredient of bile, which is a series of steroids produced during the cholesterol metabolism in animals, with multiple biological activity. During the utilization of fat, bile acid plays a role in three stages of fat emulsification, digestion, and absorption. Emulsification stage: as a di-parent-like, bile acid can form emulsified fat particles with fat; digestive stage: bile acid and lipase combination, activate lipase spatial structures, activate lipase; absorption stage: bile acid and fatty acid formation fusion The group carrying fatty acids to the groove surface, then the micro group is broken, the fatty acid permeability is absorbed, and the bile acid enters the liver cycle. In the liver cycle, bile acids promote the high efficiency and absorption of fat while returning to the liver, the bile acids of the liver can stimulate the secretion of bile, smooth the biliary tract, eliminate toxins, and accelerate the fat from the liver to the liver. The role of liver and care. Bile acid prevention of fatty liver action mechanism 1 bile acid can promote the synthesis of extremely low density lipoprotein (VLDL), so that fat accelerates from the liver into the hepatotomy to prevent excessive deposition of fat. 2 bile acids as signal molecules, can increase the level of SREBP-1C, inhibiting lipid synthesis; increase pPARα levels to promote lipid decomposition. Through the survey, at least 45% of the new cattle have subclinical ketogenesis, 55% -60% of new catastropolis affected by different degrees of fatty liver. Therefore, feeding bile acids have a very important influence on early feeding and production milk in the early days of “health”.
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