BOVINE SOMATOTROPIN AND STRESS IN DAIRY CATTLE

Dr. Robert Collier, University of Arizona

A common misconception regarding use of recombinant bovine somatotropin (rbST) in dairy cows is that animals are “stressed” by the higher levels of milk yield they achieve when being supplemented. This is an erroneous assumption, which can be easily demonstrated. Stress is normally measured by the degree of “strain” it exerts on a system. In biological systems, the degree of strain is typically measured through its impact on metabolic rate, level of production, function of the hypothalamic-pituitary-adrenal axis, and immune system. This paper will discuss the effect of rbST on these commonly used indicators of stress.

An environmental stress is typically associated with a change in metabolic rate. For example, the degree of heat or cold stress can be characterized by the change in basal metabolic rate induced by the stress. In the case of somatotropin, careful bio-energetic studies have demonstrated that basal metabolic rate of somatotropin-supplemented cows is unaltered and that nutritional requirements of bST-supplemented cows are the same as those for non-supplemented cows and are a function of the animal’s maintenance requirement, body condition and requirements for milk synthesis (12,16). This is in clear contrast to the impact of thyroid compounds (e.g. thyroprotein) which do change metabolic rate. Milk yield increases from thyroid compounds are associated with losses in body condition and eventually milk yield (3).

Another way that stress is measured in domestic animals is to evaluate production. Typically, animals that are sick or suffering discomfort demonstrate clear decreases in production and or production efficiency. This is clearly not the case with somatotropin supplementation which results in increases in milk production and feed intake of animals. Speculation that use of somatotropin would cause cows to “burn out” were based on erroneous assumptions regarding the mechanism of action. As pointed out by Bauman and McGuire (3), “Metabolic disorders would most likely occur the first few days of bST supplementation when milk yield has increased but intake has not. Suffice it to say, there is not a single mention of clinical ketosis or milk fever occurring during the first weeks of bST supplementation in any of the hundreds of published studies”. Even when cows are not adequately fed, we do not see development of a disease state with onset of somatotropin supplementation. Underfed cows which do not have available body stores to increase production when supplemented with bST demonstrate a negligible milk yield response (4,5,9). Thus, cows are not “forced” to produce milk if they are not nutritionally capable of responding to somatotropin supplementation.

An additional method of assessing impact of potential stressors on domestic animals is to examine the function of the hypothalamic-pituitary axis. This is based on evidence that under both acute and chronic stress the central nervous system of mammals evokes physiological responses that culminate in changes in secretion rate of hormones of the sympatho-adrenal axis (11). Typically, one can measure increases in secretion of Adrenal Corticotrophic Hormone (ACTH) and glucocorticoids of the adrenal. The general endocrine status of somatotropin-supplemented animals was evaluated in the acute and chronic toxicology studies as well as an endocrine challenge study during a fourth consecutive lactation of bST supplementation (1,2). In all of these studies, there was no evidence of increased secretion of glucocorticoids in animals supplemented with somatotropin. In fact, the only consistent evidence was a slight decrease in glucocorticoid concentration in somatotropin-supplemented animals that was attributed to metabolic adaptation to increased gluconeogenesis in supplemented animals. In addition to the hypothalamic adrenal axis the pituitary challenge study indicated that 4 consecutive lactations of somatotropin supplementation did not alter the ability of the pituitary to respond to endocrine challenge.

Finally, chronic stress is recognized to be immune suppressive (11). Animals that are immune suppressed are more susceptible to disease. The exact cause of the immune suppression still remains undefined but is believed to be related in part to increased secretion of adrenal glucocorticoids which suppress many immune functions. Since glucocorticoids are not increased in somatotropin-supplemented animals, one prerequisite for immune suppression would appear to be missing.

Immune function of somatotropin-supplemented animals has been measured using a variety of approaches. The immune system is sensitive to somatotropin stimulation with a number of studies demonstrating improved immune function in somatotropin-supplemented animals. The effects of somatotropin include improved thymus weight and thymosin concentration in plasma (8), improved primary lymphoid tissue in bone marrow, stimulated activation of peripheral lymphocytes and macrophages (6), improved cytokine responses to challenge (7), improved antibody synthesis (14), improved IgG level (10), augmented production of superoxide anion by macrophages and neutrophils (13). Burvenich and co-workers (15, 17) demonstrated improved production recovery from E. coli and Strep uberis mastitis in lactating dairy cows when cattle were supplemented with bovine somatotropin. In spite of these results, their laboratory reported no positive effect on neutrophil function (18) and Elvinger et al. (19) detected no effects of somatotropin on migration or chemotaxis of polymorphonuclear leukocytes. Thus, all of the evidence gathered to date does not support a negative effect of somatotropin on immune function. Quite to the contrary, the accumulated evidence supports a stimulatory role of somatotropin in regulation of the immune system. Evaluation of the mastitis incidence and duration of somatotropin treated cows indicates that duration of mastitis was not altered in cows supplemented with rbST. Thus, there is also no evidence that acute or chronic supplementation of lactating dairy cows results in suppression of the immune system.

Summary of the Effects of rbST on the Measures of Stress

References

  1. 1. Adriaens, F.A., D.L. Hard, M.A. Miller, R.H. Phipps, R.H. Sorbet, R.L. Hintz and R. J. Collier. 1994. Pituitary response to thyrotropin, corticotropin and gonadotropin releasing hormones in lactating cows treated with sometribove for a fourth consecutive lactation. Submitted: Domestic Animal Endo.
  2. 2. Adriaens, F.A., M.A. Miller, D.L. Hard, R.F. Weller, M.D. Hale and R.J. Collier. 1992. Long-Term effects of sometribove in lactating cows during a fourth consecutive lactation of treatment: Insulin and somatotropin responses to glucose infusion. J. Dairy Sci. 75:472-480.
  3. 3. Bauman, D.E., and M.A. McGuire, 1994. Paradox of BST: Why Cows Don’t Burnout. In Proceedings Minnesota Dairy Health Conference. pp 27-40.
  4. 4. Bauman, D.E. and R.G. Vernon. 1993. Effects of exogenous somatotropin on lactation. Ann. Rev. Nutr. 13:437-461.
  5. 5. Chalupa, W. and D.T. Galligan. 1989. Nutritional implications of somatotropin for lactating cows. J. Dairy Sci. 72:2510-2524.
  6. 6. Elsasser, T.H., and N.C. Steele., 1992. Growth hormone directed nutrient partitioning: Immune system-pituitary gland communication. In: Pennington Cent. Nutr. Ser., 2, Science of Food Regulation. pp. 164-186.
  7. 7. Exon, J.H., J.L. Bussiere, and J.R. Williams. 1990. Hypophysectomy and growth hormone replacement effects on multiple immune responses of rats. Brain Behav. Immun. 4:118-128.
  8. 8. Gelato, Marie C., 1993. Growth hormone, insulin like growth factor I and immune function. Trends endocrinol. Metab., 4:106-110.
  9. 9. Hoogendoon, C.J., S.N. McCutcheon, G.A. Lynch, B.W. Wickham and A.K.H. MacGibbon. 1990. Production responses of New Zealand Friesian cows at pasture to exogenous recombinantly derived bovine somatotropin. Anim. Prod. 51:431-439.
  10. 10. Marsh, J.A., W.C. Gause, S. Sandhy and C.G. Scanes. 1984. enhanced growth and immune development in dwarf chickens treated with mammalian growth hormone and thyroxine. Proc. Soc. Exp. Biol. Med., 175:351-360.
  11. 11. Minton, J.E., 1994. Function of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system in models of acute stress in domestic farm animals. J. Anim. Sci. 72:1891-1898.
  12. 12. National Research Council. 1994. Metabolic Modifiers: Effects on the Nutrient Requirements of Food Producing Animals. National Academy Press, Washington, D.C. pp 23-29.
  13. 13. Snow, C.E., 1985. Insulin and growth hormone function as minor growth factors that potentiate lymphocyte activation. J. Immunol., (Suppl. 2): 776S-778S.
  14. 14. Takada, Y., H. Bando, Y. Miyamoto, M Kosaka and T. Sano. 1991. Effect of growth hormone on immune function in normal and hypophysectomised rats. Nippon Naibunpi Gakkai Zasshi. 67:1162-1177.
  15. 15. Vandeputte-Van Messom, G. and C. Burvenich. 1993. Effect of somatotropin on changes in milk production and composition during coliform mastitis in periparturient cows. J. Dairy Sci. 76:3727-3741.
  16. 16. Vernon, R. G. 1989. Influence of somatotropin on metabolism. In: K. Sejrsen, M. Vestergaard, and A. Neimann-Sorensen, eds. Use of Somatotropin in Livestock Production. Elsevier applied Science, NY, pp 31-50.
  17. 17. Hoeben, D., C. Burvenich, P.J. Eppard and D.L. Hard. 1999. Effect of recombinant bovine somatotropin on milk production and composition of cows with Streptococcus uberis mastitis. J. Dairy Sci. 82:1671-1683.
  18. 18. Hoeben, D., C. Burvenich, E. Smits, P.J. Eppard and D.L. Hard. 1999. Effect of bovine somatotropin on neutrophil function and clinical signs during Streptococcus uberis mastitis. J. Dairy Sci. 82: 1465-1481.
  19. 19. Elvinger, F., P.J. Hansen, H.H. Head and R.P. Natzke. 1991. Actions of bovine somatotropin on polymorphonuclear leukocytes and lymphocytes in cattle. J. Dairy Sci. 74:2145-2152.

POSILAC is a registered trademark of Monsanto Technology LLC.

Source: University of Arizona
Author: Robert Collier, DVM

Comments are closed.