Growth hormone or bovine somatotropin treatment in dairy cattle

Studies aimed at increasing milk production have been under way for 15 years to assess the use of bovine somatotropin (BST). Cows only have to be treated every 2, 3 or 4 weeks with recombinant BST, at the equivalent of a 14-35 mg daily dose. Milk production increases markedly by the second day post-treatment, with a mean 17% increase after 4-10 weeks (Figures. 1a and 3). The increased feed intake, due to the increased milk production, only occurs after 3-8 weeks (Figure 1b), which means that the energy balance remains negative for 10-12 weeks (Figure 1c). Several factors influence the effects of BST. Recombinant BST is more efficient than natural growth hormone, and better results are obtained with daily injections as compared to weekly administration. Moreover, cows that have had several prior lactations respond better to BST. Injections administered after the WOth day of lactation in European cattle breeds are the most efficient, whereas zebus show almost no response at this time (Figures 1 and 2). The energy balance has to be positive for milk production to increase, without any milk modifications, in response to BST. It is possible to administer BST repeatedly through two successive lactations, but the increased milk production will be slightly lower during the second lactation. BST indirectly affects mammary cells through the insulin-like growth factor 1 (IGF1), a mediator produced in the liver. IGF1 increases blood flow through mammary cells and their metabolism. Blood triodothyronine levels are also increased. BST likely affects the carbohydrate metabolism by lowering extramammary oxidation of glucose and hepatic gluconeogenesis, thus increasing the quantity of glucides available for lactose synthesis. BST also induces a rise in blood levels of glycerol and nonesterified fatty acids. However, it takes a few weeks before fatty acid synthesis increases in the udders, i.e. milk produced at the beginning of treatment has high levels of long fatty acids, derived directly from the blood, whereas there are low levels of short fatty acids, which are synthesized in udders. Throughout each lactation, BST treatments can induce a 15-57% increase in fatty acid production as a result of the higher quantity of highbutterfat milk produced. Udder protein metabolism is not substantially modified by BST. BST does not seem to increase the incidence or prevalence of clinical mastitis. Any increases in this disorder will be due to the higher milk production, not to BST itself (Figure 4). BST increases cellular milk levels by about 60% (Figure 5) - therefore cows that had high initial levels could surpass the acceptable limit (400,000/ml). BST tends to decrease the incidence of metabolic diseases, as long as the feeding regime is adapted to the high milk production. BST has negative effects on breeding, in terms of intervals between calving and the first heat or successful mating, and on the number of inseminations required to achieve gestation. As is the case with mastitis, high milk production is a critical factor here (Figure 6). BST can be administered without any major drawbacks after a cow has conceived. Cheese processing is not altered by BST treatment, with a few exceptions where yields decrease or the manufacturing technique has to be modified. The best effects of BST are obtained when it is administered over a period of several months. BST treatments can be conducted in regions with very low milk production, but on several conditions: sufficient fodder reserves to meet the increased feed requirements; after calving, cows should not be treated for 3 months, when their energy balance is back to normal and they have been inseminated; any cattle presenting with subclinical mastitis should not be treated. After BST treatments, more milk can be produced with fewer cows. It should be kept in mind that generalizing the use of BST would have a considerable impact on dairy production structures.