There are several situations in livestock feeding in which feed intake is below the optimum level. This could be due to scarcity (e.g. drought, overcrowding, etc.) or as a result of an adaptive response (e.g. heat stress, immuno-activation).
The decrease in energy and nutrient intake limits the production performance of the animal below its genetic potential and jeopardizes the profitability of the farm. Feed restriction and malnutrition cause an intestinal barrier dysfunction; reduce the number of epithelial cells, cell proliferation and migration rates, and the height of the villi and, on the other hand, increase the rate of intestinal cell loss and apoptosis.
In addition, feed restriction reduces the functionality of the Paneth cells which secrete antimicrobials, compromising the immune defense capacity of the gut and altering the microbiome.
Because of this effect on the intestinal barrier function, feed restriction increases the risk of passage of endotoxins from the intestinal lumen to the portal, lymphatic and circulatory systems. This activates the immune system and causes a well-characterized inflammatory response. Immuno-activation reorganizes the distribution of nutrients away from economically important functions, contributing to a reduction in profitability and compromising animal well-being.
In the scientific literature, the severity and duration of feed restriction varies considerably and its effects on intestinal health have not been extensively studied in ruminants, so it is unclear the magnitude of restriction necessary to compromise the function of the intestinal barrier.
It was for this reason, that the main objective of a study conducted by researchers at Iowa State University (Kvidera et al., 2017) was to identify how progressive feed restriction affected the circulating biomarkers that were a reflection of the increase in intestinal permeability.
A total of 28 Holstein cows (157 days in milk) received one of the following dietary treatments for five days:
- 100% of ad libitum intake (AL100)
- 80% of AL intake (AL80)
- 60% of AL intake (AL60)
- 40% of AL intake (AL40)
- 20% of AL intake (AL20)
Feed restriction caused metabolic changes in cows
As expected, as the magnitude of feed restriction increased, body weight, energy balance and milk production decreased linearly.Metabolic changes were observed that includedreducinginsulin and urea nitrogen in blood and increasing circulating non-esterified fatty acids linearly as restriction increased; no effect on glucose was observed.
In addition, the hepatic fat content increased in cows on treatments AL40 or AL20. Similarly, heart and respiratory frequencies decreased linearly with feed restriction.
No obvious health disorders were observed, so the increase in circulating inflammatory biomarkers was apparently caused by the passage of intestinal luminal content into the circulation due to the reduced integrity of the intestinal barrier. Circulating endotoxins increased as food restriction intensified.
Lipopolysaccharides binding protein, serum amyloid protein A and circulating haptoglobin increased by increasing feed restriction, indicating that the inflammatory response was also increased. Circulating lymphocytes were also increased by increasing feed restriction, but no treatment effects were observed on any other parameters of immune cells, including total white blood cells, neutrophils, monocytes, eosinophils and basophils.
Feed restriction caused changes in intestinal morphology
Cows from the AL100 and AL40 treatments were slaughtered to evaluate intestinal histology. The width of the jejunum villi, the depth of the crypts and the area of the caliciform cells, as well as the height of the ileum villi, the depth of the crypt and the area of the caliciform cells, were reduced (36, 14, 52, 22, 28 and 25%, respectively) in AL40 cows compared to AL100 controls. Cell proliferation in the ileum tended to decrease (14%) in AL40 vs AL100 cows.
In short, progressive feed restriction increased circulatory markers of inflammation, probably due to increased intestinal permeability as evidenced by changes in intestinal epithelial barrier.
S. K. Kvidera, E. A. Horst, M. V. Sanz Fernandez, M. Abuajamieh, S. Ganesan, P. J. Gorden, H. B. Green, K. M. Schoenberg, W. E. Trout, A. F. Keating, and L. H. Baumgard. Characterizing effects of feed restriction and glucagon-like peptide 2 administration on biomarkers of inflammation and intestinal morphology. 2017. J. Dairy Sci. 100:9402–9417.
© 2020 Dairy Knowledge Center. All Rights Reserved.