Nutritional Strategies to Prevent Fatty Liver in Dairy Cattle
Fatty liver is defined as an accumulation of fat, mainly Triacylglycerol (TAG) in liver. Fatty liver is one of the important metabolic diseases of post parturient dairy cows occurring due to negative energy balance. It usually develops before and during parturition. Fatty liver at calving is commonly associated with ketosis. Negative energy balance, hormonal changes (that accompany parturition) and lactogenesis contribute to development of fatty liver. It is an important economic disease because cows that develop fatty liver are affected by multiple metabolic and infectious diseases. It usually develops after calving with peak incidence at about 10 days in milk.
Fatty liver in dairy cows is a disease that affects the cows after pregnancy (or postpartum). It has been known to cause the culling of over 25% of cows globally. It is a typical variant of non-alcoholic fatty liver in dairy cows disease (NAFLD), that has caused severe effects on the dairy industry production throughout the world post-calving. To get to the solution, prevention, and enhance our study about this topic, we must understand it from the core. Relevant information is fairly crucial to tackle the disease and decrease its impact. And, overall make the dairy industry function smoothly and sustainably.
Fatty liver in dairy cows syndrome, a common kind of metabolic illness induced by food imbalance after birthing, is common in herds of dairy cattle on industrial farms around the globe. In the initial nursing phase, high-yielding dairy cows that produce a generous amount of milk, particularly those with an everyday milk supply of 30 kg or over, are much more likely to develop fatty liver in dairy cows disease.
Energy balance and fatty liver In states of negative energy balance mobilization of body fat reserves is triggered, results in the release of nonesterified fatty acids (NEFAs) from adipose tissue. The liver retains approximately 15%–20% of the NEFAs circulating in blood and thus accumulates increased amounts during periods when blood NEFA concentrations are increased. At calving, plasma concentrations of NEFAs are often increased (>1,000 μEq/L). Blood flow to liver and concentration of NEFAs in blood is related to hepatic uptake of NEFAs. In liver NEFAs completely oxidized to CO2. Excess NEFAs in liver may partial oxidized to form ketones or esterified to form triglycerides (TGs).When blood glucose concentrations are low, NEFAs are generally oxidized to form Ketone. Ketones upto some level can serve as an energy source for many tissues but excessive production adversely affect animal behavior and performance. Esterification to form TGs is acceptable if they are exported as very low-density lipoproteins (VLDLs). Excessive intracellular triglyceride accumulation in liver cells results in disturbed liver function and cell damage. Fatty liver can develop within 24 hr of an animal going off feed. Although lipid accumulation in the liver is a reversible process, the slow rate of triglyceride export as lipoprotein causes the disorder to persist for an extended period. Depletion of the liver lipid content usually begins when the cow reaches positive energy balance and may take several weeks to fully subside.
Categories of fatty liver:
Fatty liver in dairy cows is categorized into following types
- Mild type: When liver triacylglycerol (TAG) 1-5% wet weight and total lipid 5- 20% of volume ·
- Moderate type: When liver TAG 5-10% wet weight and total lipid 20-40 % of volume.
· Severe type: When liver TAG > 10% wet weight and total lipid >40% of volume. Even mild fatty liver is associated with decreased health status and reproductive performance of dairy cows.
Clinical finding of fatty liver:
Fatty liver is likely to develop concurrently with another disease. There are no pathognomonic clinical signs of fatty liver disease in cattle. The typically disorders that are seen at or shortly after calving are- typically disorders that are seen at or shortly after calving are-
· Metritis
· Mastitis
· Abomasal displacement
· Hypocalcemia
· Impaired reproductive ability
· Lameness
The condition is often associated with feed intake depression, decreased milk production, and ketosis.
Fatty Liver in Dairy Cows: Non-esterified Fatty Acids (NEFAs)
Fatty Liver in Dairy Cows is common nowadays. In circumstances of bad energy balance, hormone signals induce the mobilization of body fat stores, which leads to the discharge of nonesterified fatty acids (NEFAs) from fatty tissue. Because the liver maintains 15%–20% of the NEFAs flowing in the system, it collects more in time while blood NEFA levels are higher. The biggest growth comes during lactation when plasma levels are frequently >1,000 Eq/L. If the cow is not fed, ratios can reach more elevated heights. The liver could either oxidize or esterify the NEFAs it absorbs. Triglyceride is the major esterification result that can be discharged as a component of quite a low-density lipoprotein (VLDL) or retained in liver cells. Because of reduced VLDL synthesis, ruminants go through at a far slower rate than most animals. As a result, triglycerides build in the presence of enhanced hepatic NEFA absorption and esterification. NEFA oxidation results in the synthesis of ATP via the tricarboxylic acid cycle or the creation of ketones by peroxisomal or oxidation. If blood glucose levels are insufficient, ketone production is promoted. Since insulin inhibits fat transfer from fat cells, situations that generate lower blood glucose & insulin levels result in fatty liver in dairy cows.
Liver Problems and Dysfunction
High intracellular triglyceride build-up in liver tissues causes liver problems and dysfunction. In 24 hours of an animal being off fed, fatty liver in dairy cows can occur. Despite the fact that fat excess in the liver is recoverable, the slow pace of triglyceride export as lipoprotein allows the condition to last for a long time. When the cow establishes a favourable energy balance, the liver lipid level starts to deplete and can take many weeks to totally cease. Overeating or neutral energy stability does not cause fatty liver in dairy cows. Excessive energy intake for upkeep and production functions will not culminate in triglyceride build-up in hepatic tissue. Unless the animal becomes overwhelmed and therefore limits the content of the diet, will triglycerides be deposited.
Researches Pertaining to Fatty Liver in Dairy Cows
Randomly choosing dairy cows from commercial farms over the past years revealed that 48.85 percent of dairy cows (n = 346) were detected with moderate or acute fatty liver in dairy cows syndrome within two weeks of postpartum. Within two weeks of lactation, 40 percent to 60 percent of high-yielding dairy cows (day milking production > 35 kg) develop mild to serious fatty liver disease. Furthermore, on a cattle ranch, the two weeks following parturition might make up a significant portion to 50% of illness, which is consistent with the findings. The high rate of slaughtering of dairy cows during their initial postpartum phase and it’s creating a serious worry in the current dairy sector.
Fatty Liver in Dairy Cows: Prevention and Cure
Maintaining your cattle’s health is certainly one of the most significant parts to keep your farm up to date and your clients happy. Therefore, you must comprehend what to do in case your farm identifies a fatty liver in dairy cows problem. First up, you must be able to recognize it to help the cows further.
Approaches to prevent or treat fatty liver:
Approaches to prevent or treat fatty liver can be subdivided into three main categories:
a) Reduce blood NEFAs by decreasing TG lipolysis in adipose tissue
b) Increase complete hepatic oxidation of NEFAs
c) Increase the rate of VLDL export from the liver. The drawback of the first strategy is that it impedes a process that is intended to support lactation. The second strategy has limitations as well. Complete oxidation of NEFAs yields ATP, the energy currency of cells, of which there is a finite requirement. If complete oxidation is to continue beyond that necessary to provide energy for maintenance of the liver, it must be uncoupled from ATP production, whichresults in energy being lost as heat. The third strategy of increasing VLDL export is the most logical but little is known about what limits VLDL export in ruminants.
Nutritional strategies to prevent or treat fatty liver
Different nutritional practices to prevent or treat fatty liver canbe divided into two main categories:
(1) Diet formulation to increase energy density
(2) Inclusion of feed additives to modify metabolism in a way to reduce the likelihood of liver TG accumulation. Diet formulation to increase energy density is typically done to minimize the magnitude of negative energy balance and reduce fatty acidmobilization from adipose tissue.
Increasing nutrient density of transition diets: Grain feeding during the dry period is a means to enhance papillae growth in the rumen. Increased papillae growth in rumen provides more surface area for absorption of volatile fatty acids and minimize the risk of ruminal acidosis post-partum when grain feeding increases dramatically. Besides this grain feeding during dry period has been promoted as a means to reduce lipid-related metabolic disorders such as fatty liver. This could occur by a couple mechanisms. Firstly, feeding additional grain leads to greater propionate production in the rumen. Propionate is an insulin secretagogue; insulin is antilipolytic and has the potential to decrease adipose tissue lipolysis. Increasing grain in the diet could increase its digestibility and, therefore, increase DM and energy intake. During 3–4 week prefresh transition period, grain feeding should be increased to prevent fatty liver in dairy cattle.
Supplementation of dietary fat to increase dietary energy density:
Energy density of transition diets can be increased by fat supplementation. Mobilization of fatty acids reduced after supplementation of fatty acids in diets of transition cows. These dietary fatty acids are incorporated into intestinally synthesized lipoproteins that are metabolized predominantly by tissues other than the liver. Dietary supplemental fat helps in increasing adipose tissue lipolysis rather than decreases it Liver uses fatty acids which gets mobilized from adipose tissues. Dry matter intake (DMI) depression is common problem in postpartum period. Feeding fat in transition period acclimatize the dairy animals to fat, reduced the chances of DMI depression.
Role of feed additives for prevention or treatment of fatty liver:
Role of feed additives for prevention or treatment of fatty liver:
Depending on the basis of intended mode of action feed additives can be classified into different categories:
reduce adipose lipolysis, enhance hepatic VLDL secretion, or increase hepatic fatty acid oxidation.
i. Reduction of adipose lipolysis: Compounds that decrease adipose tissue lipolysis include propylene glycol (PG), monensin, chromium (Cr), niacin, and conjugated linoleic acid (CLA).
ii. Propylene glycol: Oral drenches of propylene glycol @ 1 L/d in last 10 d prepartum period have been demonstrated to prevent fatty liver and ketosis by increasing plasma glucose and insulin concentrations and decreasing plasma BHBA and NEFA concentrations. The effectiveness of propylene glycol to increase plasma glucose concentrations depends on the dosage and the mode of administration, since drenching of PG is difficult, it should be added in diet of animals. But addition of PG in total mixed ration is not effective.
iii. Niacin: In most of the recent studies oral administration of niacin or nicotinic acid failed to prevent fatty liver. The proposed mode of action was that supraphysiological concentrations of niacin decrease NEFA mobilization from adipose tissue; however, achieving supraphysiological plasma concentrations by oral administration is difficult, because niacin is degraded in the rumen. The supply of niacin to the ruminant comes from three main sources: dietary niacin, conversion of tryptophan to niacin and ruminal synthesis of niacin. Niacin is widely distributed in feedstuffs of plant as well as of animal origin. The by-products of animal and fish origin, distiller’s grains, yeast, various distillation and fermentation solubles and certain oilseed meals are good sources.
iv. Propionate salts: Administration of ammonium and calcium propionate orally and administration of 1 kg/d of glycerol to the diet in the periparturient period decrease the plasma BHBA and NEFA concentrations, respectively.
v. Monensin : Feeding monensin during the last month before parturition has prevented fatty liver. The primary mode of action of monensin is that it improves the glucose supply to cows by changing ruminal fermentation and VFA production in favor of propionate
vi. Chromium: Chromium is an essential nutrient for animals. It acts to potentiate the action of insulin as part of the glucose tolerance factor. Since insulin is antilipolytic and its action during the periparturient period may be diminished due to insulin resistance, Cr may have potential to moderate plasma NEFA concentrations and reduce hepatic TG accumulation. In dairy animals inorganic Cr sources are poorly absorbed; organic forms are more available.
vii. Suppression of milk fat synthesis: Suppression of milk fat synthesishas been suggested as a mechanism to improve energy balance of fresh cows and, therefore, indirectly reduce adipose tissue lipolysis. Specifically, fatty acids with a trans-10 double bond, particularly trans-10, cis-12 CLA are known to inhibit mammary lipid synthesis.
viii. Enhancing hepatic VLDL secretion: Choline and methionine are feed additives that have the potential to enhance VLDL export from the liver. Phosphatidylcholine is a constituent of VLDL and for its synthesis Choline serves as a substrate. Methionineacts as a methyl donor for Phosphatidylcholine synthesis and also it is required for synthesis of protein (a constituent of VLDL). During the periparturient period, if the choline supply is limited when feed intake is low, synthesis of VLDL could be limited and fatty liver could result. Supply of choline to ruminants should be in protected form because the microbial population in the rumen quickly degradesdietary choline.
ix. Altering hepatic fatty acid metabolism: Recent research has shown that dietary fats high in stearic acid2 (C18:0) and low in palmitic (C16:0), oleic (C18:1) and linoleic (C18:2) acids may reduce liver triglyceride accumulation in early lactation cows. Stearic acid appears to be preferentially used by either the liver for oxidation (energy) and/or by the mammary gland for milk fat secretion. Minimizing stress is also important for prevention of fatty liver. Sudden changes in environment should be avoided. For example, changes in ration, housing, temperature, herdmates etc. may cause a reduction in feed intake and trigger catecholaminemediated increases in fat mobilization.
Signs
Have a look at the signs related to this disease-
Fatty Liver in Dairy Cows: Prevent the Occurrence
The digestion of fat and fatty liver may be avoided if cows calved at the appropriate body state. A calf’s overall health score of 2.5 to 3 would be optimal. Cows must be kept clean and dry at this point and kept at the same weight during the long drought. It is best to avoid switching diets throughout this time. Overweight cows can be given glucose injections as a precautionary approach. Stress reduction is critical for fatty liver avoidance. It is best to prevent abrupt changes in the surroundings. Modifications in diet, shelter, heat, herd mates, and other factors, for instance, might reduce feed consumption and activate catecholamine-mediated fat transformation.
Medication
Without medical intervention, fatality rates can rise significantly to 25%. There is no available cure for fatty liver other than a lengthy IV glucagon infusion. Cows with fatty liver are susceptible to a variety of metabolic and viral disorders, and their milk output suffers as a result. As a consequence, they are commonly euthanized.
CONCLUSIONS
Fatty liver disease is an important metabolic disease of transition period due to negative energy balance which directly affects health and productivity of animal without showing any particular clinical symptom. Increased NEFA concentration in blood change metabolic activities and immunophysiological conditions in animal which can be prevent through dietary manipulation of energy intake, slowing lipolysis and enhancing hepatic VLDL secretion by using additives like propylene glycol, monensin, chromium, niacin, conjugated linoleic acid, choline, methionine and dietary fats.
Compiled & Shared by- This paper is a compilation of groupwork provided by the Team, LITD (Livestock Institute of Training & Development)
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Reference-On Request
