Best calf starter formula for rapid rumen growth
The calf is functionally a monogastric. At birth all four compartment of ruminant stomach except abomasum are nonfunctional, undeveloped, and small in size and disproportionate to the adult digestive system . The rumen of the neonatal calf occupies about 25% volume of the whole stomach . The rumen only starts to grow at two to three weeks of age and growth will continue until about 6 months of age. In these first weeks of life, the milk bypasses the rumen, reticulum and omasum. During this period non-functional and undeveloped rumen, reticulum and omasum do not play any role in digestion.
Gastrointestinal tract development
Ruminant gastric anatomy and physiology undergo significant changes during early development. Calves are born with their abomasum as the only functional part of the four-stomach system, with the reticulorumen very undeveloped. The rumen needs to change both structurally and functionally as the calf grows. In addition, early weaning is desired in dairy calves because pre-weaning calf growth is expensive in both feed and management. For successful economic weaning, early rumen development is necessary and has been studied extensively.
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| How to speed up rumen development in newborn calf |
The gastrointestinal (GI) tract of calves is not fully developed at birth. This predominantly refers to the rumen. Rumen volume is very small at birth and rumen papillae are nearly absent.It stays this way for the first two to three weeks, until regular solid feed intake starts. The abomasum and small intestine, on the other hand, begin to undergo rapid development right away. This is because these regions of the GI tract are the main sites of liquid feed (milk or milk replacer) digestion. Since liquid feed is the main source of nutrients for calves prior to solid feed intake, which usually takes place in the second or third week of life, the development of the abomasum and small intestine has a huge impact on the growth and health of calves at a very early stage of life. Rumen development, on the other hand, occurs gradually and is driven predominantly by solid feed intake and short chain fatty acids produced by microbes in the rumen.
Why butyrate?
Rumen VFA provide 70% of the total energy needs of a ruminant. The three most abundant VFA produced in the rumen are acetate, propionate, and butyrate. Acetate is primarily needed for peripheral energy, and in the adult cow part of it is incorporated into milk fat. Propionate is used to produce glucose for energy in the liver. However, the role of butyrate for the ruminant is quite different. More than 80% of butyrate produced in the rumen is metabolized to ketone bodies (BHB and acetoacetate) before being transported to the rest of the body for energy needs. It also has an alternative pathway to convert it directly to available energy for the rumen, and therefore it is of primary importance for the development of the rumen. Butyrate is a natural end product of microbial fermentation of carbohydrates in the GI tract. Its production is especially high in the rumen, particularly when animals are fed diets high in starch and simple sugars. When solid feed high in these carbohydrates is offered, it results in high butyrate production in the rumen and a substantial acceleration of rumen epithelium and rumen papillae development.
This, in turn, results in high solid feed intake and efficient solid feed digestion at a very early age. Butyrate is also present in whole milk. Prior to the development of the rumen, this source of butyrate has a substantial impact on calf GI tract development, particularly the development of the abomasum, small intestine and pancreas.
For the first two to three weeks of life, butyrate production in the calf’s rumen is minimal, due to low solid feed intake and not yet fully developed rumen microflora.At this stage, dietary butyrate supplementation may allow for substantial acceleration of GI tract development. Furthermore, newborn calves are often fed milk replacers, instead of whole milk, which, in most cases, lack butyrate, due to the use of alternative fat sources, instead of milk fat.
Dietary supplementation
Butyrate can be supplemented in liquid feed (milk or milk replacer), solid feed (starter mixture) or both. Since liquid feeds bypass the rumen via the esophageal groove and enter the abomasum, but solid feeds enter the rumen, the method of butyrate supplementation determines the region of the GI tract directly exposed to its action. When it is supplemented in liquid feed, butyrate predominately affects the abomasum and small intestine. If it’s added to solid feed, it primarily affects the rumen.
Nevertheless, the addition of butyrate into liquid feed may affect rumen development, and butyrate supplementation in solid feed may affect abomasum and small intestine development, especially when the protected form of butyrate is used in solid feed. For example, the stimulatory effect of butyrate added into milk replacer on abomasum and small intestine development may result in higher solid feed intake. This, in turn, speeds up rumen development.
Besides different methods of butyrate supplementation, various sources of butyrate can be used in feeds. Butyrate can be supplemented as a salt (sodium, calcium) or as ester of butyrate and glycerol (e.g., mono-, di- or tributyrin or mixture of those).These butyrate sources differ substantially in terms of their physicochemical properties and impact on the calf’s GI tract. From the above mentioned, sodium butyrate is the most often used source of butyrate in feeds for calves. Sodium butyrate easily dissolves in water and rapidly dissociates in water solutions.
When this source of butyrate is used in feed, butyrate action is located predominantly in the stomach (forestomach, abomasum). Calcium butyrate, on the other hand, is much less soluble in water solutions than sodium butyrate. Therefore, at least part of the butyrate delivered in this form is expected to bypass the stomach and enter the small intestine. When delivered as mono-, di- or tributyrin, butyrate must be released from glycerol by lipase before it elicits its effect on the GI tract .Further modulation of butyrate impact on the GI tract can be obtained by its protection from degradation in the stomach. This can be done by butyrate embedding in the fat (lipid) matrix , commonly referred to as microencapsulation or fat coating.Micro-encapsulated butyrate is only partially released in the stomach and most of the active substance is gradually released along the entire small intestine. The remaining portion of encapsulated butyrate, not released into the stomach and small intestine, can be released into the large intestine, as a result of microbial lipase action.