retention and whole-body protein synthesis without affecting protein degradation. Subsequently, Eisemann et al. (1989b) reexamined this in rapidly growing steers and found that bST treatment increased L-[¹⁴C]-leucine use for protein synthesis and that whole-body rates of leucine oxidation decreased. Furthermore, they noted that the additional nitrogen retained was deposited with an incremental efficiency of approximately 50 percent. Other studies with growing lambs and cattle have demonstrated that the fractional rate of protein synthesis is increased in skeletal muscle with bST treatment (Pell and Bates, 1987; Eisemann et al., 1989a). A recent study with growing pigs indicates that pST treatment increased rates of whole-body protein turnover; however, the absolute increment in protein synthesis rate was greater than that for breakdown, leading to the increased net nitrogen retention (Tomas et al., 1992).

One of the critical events that occurs during postnatal muscle growth is an increase in muscle DNA content. This event is important because postnatal accretion of DNA is a key factor in regulating muscle growth (Allen, 1988). This increase is caused by proliferation of satellite cells that reside between the sarcolemma and basement membrane of myofibers. These cells have the ability to fuse with the myofiber and thereby contribute their nucleus to the cell. Thus, during postnatal muscle growth the increase in muscle DNA is coordinated with the increase in muscle protein. As discussed above, ST increases the rate of protein accretion markedly. The effects of ST appear to be not only caused by changes in protein metabolism but also by changes in the rate of satellite cell proliferation. One of the growth factors that has been shown to stimulate proliferation of satellite cells is IGF-I (Allen, 1988). This observation is significant because the mitogenic effects of ST are mediated indirectly by IGF-I (Florini, 1987).

Administration of bST to lactating dairy cows results in major adaptations in mammary tissue metabolism. The change that occurs in the shape of the lactation curve with long-term bST administration indicates that the number of secretory cells in the glands and/or the synthetic capacity of each mammary epithelial cell must increase (Bauman et al., 1985). Recent studies with lactating goats have demonstrated that bST treatment prevented the normal decline in mammary cell number and increased the activity of key enzymes involved in milk synthesis (22 weeks; 27 percent increase in milk yield) (Knight et al., 1990). Baldwin (1990) demonstrated that bST-treated cows had increased RNA per mammary gland, indicating an increase in protein synthetic capacity. In addition, scientists have reported significant increases or trends for increases in activities of several enzymes from bST-treated cows and goats (Baldwin, 1990; Knight et al., 1990, 1992).

A major paradox is that bST does not appear to directly mediate its effects on the mammary gland. bST does not have any direct effect on milk synthesis in bovine mammary tissue in vitro (Gertler et al., 1983) and bovine mammary cells appear to lack bST receptors (Akers, 1985; Collier et al., 1989). However, this is not completely resolved; some recent studies have reported mRNA for somatotropin receptors in mammary tissue from several species including cows (Glimm et al., 1990; Jammes et al., 1991). There has been some suggestion that IGF-I may mediate the galactopoietic effects of bST because bovine mammary epithelial cells do have receptors for IGF-I (Collier et al., 1989). Prosser et al. (1989) reported that infusion of IGF-I (1.1 nMol/min) for 6 hours into the pudic artery of lactating goats increased milk secretion by 30 percent. Recently, Davis et al. (1989) conducted a study in which IGF-I was infused (43 nMol/hour via jugular catheter) into lactating goats on days 4 to 6 of a 10-day experimental period. Although bST administration increased milk production, there was no increase in milk yield of the group infused with IGF-I, even though blood concentrations of IGF-I were comparable between the two groups. An additional complication is that IGFs in physiological fluids are bound to soluble, high-affinity IGF-binding proteins (IGFBP). Although we do not have a clear understanding of how the IGF complex is able to mediate mammary function, it is apparent that changes in circulating concentrations of IGF-I and some of the IGFBP are closely tracking the biological events and magnitude of milk responses that occur with bST treatment (see review by Bauman and Vernon, 1993).

Consistent with the increases in milk yield, bST treatment has been shown to increase cardiac output and mammary blood flow (Mepham et al., 1984; Davis et al., 1988; Fullerton et al., 1989). Based on current concepts of mammary biology, it is probable that the alteration in blood flow is a consequence of changes in mammary tissue metabolism rather than the cause of these changes.

Somatotropins alter an array of physiological processes in domestic animals treated chronically with the hormone. These effects are precisely coordinated to alter the flow of nutrients among the tissues of the body. ST alters many metabolic pathways in numerous tissues and changes tissue responses to other endocrine signals. Overall, these alterations in metabolism and cell proliferation lead to the production responses observed in meat and dairy animals. It is likely that as we increase our understanding of how ST functions, we will be able to develop ways to further potentiate the stimulatory effects of ST or identify alternative strategies that increase not only growth performance and milk yield but, more important, the efficiency of production.

Front Matter (R1-R12)

Executive Summary (1-2)

1. Introduction (3-4)

2. Mechanisms of Action of Metabolic Modifiers (5-22)

3. Effect of Somatotropin on Nutrient Requirements of Dairy Cattle (23-29)

4. Effect of Metabolic Modifiers on Nutrient Requirements of Growing Ruminants (30-37)

5. Effect of Metabolic Modifiers on Nutrient Requirements of Growing Swine (38-51)

6. Effect of Metabolic Modifiers on Nutrient Requirements of Poultry (52-58)

References (59-73)

Authors (74-74)

Index (75-82)