Growth hormone-releasing factor is the main endogenous stimulator of somatotropin secretion. Our objective was to compare the effects of recombinant growth hormone-releasing factor and recombinant bST on somatotropin secretion, mammary function, and body composition of lactating, primiparous dairy cows. Cows (118 d of lactation) served as uninfused controls or were infused for 63 d with 12 mg/d of releasing factor or with 29 mg/d of bST. These doses elevated somatotropin in serum to concentrations of similar magnitude. The releasing factor and bST each similarly increased milk yield, yield of milk components, weight of most organs, mobilization of adipose tissue, accretion of lean tissue in the carcass, and metabolic activity (RNA) of mammary tissue. Relative to controls, neither releasing factor nor bST significantly affected cell numbers (DNA) in mammary glands or concentrations of plasmin in milk. None of the variables measured provided evidence for galactopoietic effects of releasing factor independent of somatotropin.

Effects of recombinant bovine growth hormone-releasing factor and recombinant bST on thyroxine 5'-deiodinase activities of liver and mammary gland were studied for lactating cows. Beginning on d 118 of lactation, 30 primiparous Holsteins received continuous infusions of 12 mg/d of releasing factor or 29 mg/d of bST or served as uninfused controls for 63 d. Blood samples were collected on d 1, 29, and 57, and samples of whole milk were collected at the early afternoon milking on d -5, 30, and 58. Liver and mammary tissue samples were obtained at slaughter on d 63. Infusion of releasing factor and bST decreased serum concentration of triiodothyronine by 10% and the ratio of triiodothyronine to thyroxine in serum by 20%. Concentrations of circulating triiodothyronine reflected a 30% decrease in hepatic 5'-deiodinase activity in response to infusion with releasing factor and bST. In contrast, treatment with releasing factor and bST did not affect 5'-deiodinase activity in the mammary gland and did not alter triiodothyronine concentration in milk. Data suggest that releasing factor and bST increase the hypothyroid status of the lactating cow and maintain an euthyroid condition in the mammary gland, thus enhancing the metabolic priority of the mammary gland.

Our objective was to compare the effects of recombinant bovine growth hormone-releasing factor and recombinant bST on the somatotropic cascade in lactating dairy cows. Primiparous cows were killed after 63 d of continuous daily infusion with 12 mg of releasing factor or 29 mg of bST or no infusion (controls). Both hormone infusions similarly increased mean concentration of somatotropin in serum, but pulsatility of somatotropin in serum was greater for cows given releasing factor. Both hormone infusions increased the amounts of IGF-I in serum, IGF-I mRNA in liver, and IGF-binding protein-3 in serum and decreased IGF binding protein-2 in serum, but these effects were less for cows given releasing factor than for those given bST. Both infusions decreased the number of free binding sites for IGF-I in mammary tissue. In liver, treatment did not alter the abundance of mRNA for the somatotropin receptor or the number of free binding sites for somatotropin. Results suggest that endogenous somatotropin is less effective as an IGF-I secretagogue than is exogenous bST infused continuously, yet the releasing factor and bST increased milk yield similarly. We conclude that growth hormone-releasing factor stimulates milk synthesis mostly through the same mechanisms as bST, but that serum IGF-I alone is not a good indicator of the galactopoietic potency of the two hormones.

Lactating, primiparous Holstein cows were continuously infused for 63 d with either recombinant growth hormone-releasing factor or recombinant bST or were not infused (control). The releasing factor and bST treatments reduced fat synthesis from acetate and lipoprotein lipase activity in omental adipose tissue. Also, both treatments increased hormone-sensitive lipase activity per gram of adipose tissue and reduced fatty acid esterification per milligram of protein in adipose tissue. Protein concentration in adipose tissue with both treatments was greater than that of the control, although the protein concentration was less in adipose tissue from cows treated with the releasing factor than from those treated with bST. In mammary tissue, releasing factor increased fat synthesis from acetate more than did bST treatment, but percentages of fat or short-chain fatty acids in milk were not different between treatments, nor were differences significant between treatments and control for fatty acid esterification or lipoprotein lipase activity in mammary tissue or gluconeogenesis and fatty acid esterification in liver. We conclude that protein concentration was lower in omental adipose tissue of cows treated with releasing factor than that in tissue of cows treated with bST, although both treatments similarly suppressed synthesis of fat from acetate and activity of lipoprotein lipase.