The present review summarises the potential nutritional and physiological functions of betaine as a feed additive in relation to performance criteria in livestock production. Betaine, the trimethyl derivative of the amino acid glycine, is a metabolite of plant and animal tissues. In plants, betaine is particularly synthesised and accumulated as an osmoprotectant against salt and temperature stress. In animals, betaine is the product of choline oxidation or it originates from nutritional sources. Over the past decades, numerous studies have been carried out to investigate the potential effects of betaine supplementation on animal performance. Due to its chemical structure, betaine shows the characteristics of a dipolar zwitterion resulting in osmoprotective properties. Promoting effects on the intestinal tract against osmotic stress occurring during diarrhoea or coccidiosis have been reported following betaine supplementation in pigs and poultry. There is also some evidence that dietary betaine may improve the digestibility of specific nutrients. As a product of choline oxidation, betaine is involved in transmethylation reactions of the organism. Betaine as a methyl donor provides its labile methyl groups for the synthesis of several metabolically active substances such as creatine and carnitine. Supplementation with betaine may decrease the requirement for other methyl donors such as methionine and choline. There is also some evidence for enhanced methionine availability after dietary supplementation of betaine resulting in improved animal performance. Alterations in the distribution pattern of protein and fat in the body have been reported following betaine supplementation. A more efficient use of dietary protein may result from a methionine-sparing effect of betaine, but also direct interactions of betaine with metabolism-regulating factors have to be considered. Though the mode of action of betaine as a carcass modifier remains open, there is, however, growing evidence that betaine could have a positive impact both on animal performance and carcass quality.

The human intestinal microbial ecosystem plays an important role in maintaining health. A multitude of diseases including diarrhoea, gastrointestinal inflammatory disorders, such as necrotising enterocolitis (NEC) of neonates, and obesity are linked to microbial composition and metabolic activity. Therefore, research on possible dietary strategies influencing microbial composition and activity, both preventive and curative, is being accomplished. Interest has focused on pre-and probiotics that stimulate the intestinal production of beneficial bacterial metabolites such as butyrate, and beneficially affect microbial composition. The suitability of an animal model to study dietary linked diseases is of much concern. The physiological similarity between humans and pigs in terms of digestive and associated metabolic processes places the pig in a superior position over other non-primate models. Furthermore, the pig is a human-sized omnivorous animal with comparable nutritional requirements, and shows similarities to the human intestinal microbial ecosystem. Also, the pig has been used as a model to assess microbiota -health interactions, since pigs exhibit similar syndromes to humans, such as NEC and partly weanling diarrhoea. In contrast, when using rodent models to study diet -microbiota -health interactions, differences between rodents and humans have to be considered. For example, studies with mice and human subjects assessing possible relationships between the composition and metabolic activity of the gut microbiota and the development of obesity have shown inconsistencies in results between studies. The present review displays the similarities and differences in intestinal microbial ecology between humans and pigs, scrutinising the pig as a potential animal model, with regard to possible health effects.

The processing of dietary lipids can be distinguished in several sequential steps, including their emulsification, hydrolysis and micellization, before they are absorbed by the enterocytes. Emulsification of lipids starts in the stomach and is mediated by physical forces and favoured by the partial lipolysis of the dietary lipids due to the activity of gastric lipase. The process of lipid digestion continues in the duodenum where pancreatic triacylglycerol lipase (PTL) releases 50 to 70% of dietary fatty acids. Bile salts at low concentrations stimulate PTL activity, but higher concentrations inhibit PTL activity. Pancreatic triacylglycerol lipase activity is regulated by colipase, that interacts with bile salts and PTL and can release bile salt mediated PTL inhibition. Without colipase, PTL is unable to hydrolyse fatty acids from dietary triacylglycerols, resulting in fat malabsorption with severe consequences on bioavailability of dietary lipids and fat-soluble vitamins. Furthermore, carboxyl ester lipase, a pancreatic enzyme that is bile salt-stimulated and displays wide substrate reactivities, is involved in lipid digestion. The products of lipolysis are removed from the water-oil interface by incorporation into mixed micelles that are formed spontaneously by the interaction of bile salts. Monoacylglycerols and phospholipids enhance the ability of bile salts to form mixed micelles. Formation of mixed micelles is necessary to move the non-polar lipids across the unstirred water layer adjacent to the mucosal cells, thereby facilitating absorption.

In pigs, the microbial ecosystem of the gastrointestinal tract (GIT) is influenced by various factors; however, variations in diet composition have been identified as one of the most important determinants. Marked changes in fermentation activities and microbial ecology may occur when altering the diet, for example, from milk to solid feed during weaning. In that way, access of pathogens to the disturbed ecosystem is alleviated, leading to infectious diseases and diarrhea. Thus, there is increasing interest in improving intestinal health by use of dietary ingredients suitable to beneficially affect the microbial composition and activity. For example, fermentable carbohydrates have been shown to promote growth of beneficial Lactobacillus species and bifidobacteria, thereby enhancing colonization resistance against potential pathogens or production of short-chain fatty acids, which can be used as energy source for epithelial cells. On the other hand, fermentation of protein results in the production of various potentially toxic products, such as amines and NH3, and is often associated with growth of potential pathogens. In that way, excessive protein intake has been shown to stimulate the growth of potentially pathogenic species such as Clostridium perfringens, and to reduce fecal counts of beneficial bifidobacteria. Therefore, it seems to be a promising approach to support growth and metabolic activity of the beneficial microbiota by developing suitable feeding strategies. For example, a reduction of dietary CP content and, at the same time, dietary supplementation with fermentable carbohydrates have proven to successfully suppress protein fermentation. In addition, the intestinal microbiota seems to be sensible to variations in dietary protein source, such as the use of highly digestible protein sources may reduce growth of protein-fermenting and potentially pathogenic species. The objective of the present review is to assess the impact of dietary protein on microbiota composition and activity in the GIT of piglets. Attention will be given to studies designed to determine the effect of variations in total protein supply, protein source and supplementation of fermentable carbohydrates to the diet on composition and metabolic activity of the intestinal microbiota.

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