Prior to puberty, elevated nutrient intake has been shown to negatively affect prepubertal mammary development in the heifer. The objective of this study was to evaluate the effects of increased nutrient intake on mammary development in Holstein heifers at multiple body weights from birth through puberty. Specifically, this study evaluated the effects of nutrient intake and body weight at harvest on 1) total weight and DNA content of the parenchyma (PAR) and mammary fat pad (MFP) and 2) PAR and MFP composition. Starting at 45 kg of body weight, heifers (n = 78) were assigned to either a restricted (R) or elevated (E) level of nutrient intake supporting 650 (R) or 950 (E) g/d of body weight gain. Heifers were harvested at 50-kg increments from 100 to 350 kg of body weight. Mammary fat pad weight and DNA content were greater in E- than in R-heifers. Additionally, E-heifers had a greater fraction of lipids and a smaller fraction of protein in their MFP than did R-heifers. Parenchyma weight and DNA were lower in E- than in R-heifers; however, when analyzed with age as a covariate term, treatment was no longer a significant term in the model. Level of nutrient intake had no effect on the lipid, protein, or hydroxyproline composition of the PAR. Collectively, these data demonstrate that PAR is refractory to the level of nutrient intake whereas MFP is not. Furthermore, the covariate analysis demonstrated that age at harvest, not the level of nutrient intake, was the single greatest determinant of total PAR DNA content.
It is well documented that elevated nutrient intake prior to puberty reduces prepubertal mammary development in the bovine. The companion paper demonstrated that age at harvest is a primary determinant of parenchymal (PAR) mass and that any effects of elevated energy intake on mechanisms regulating mammary development are dwarfed by this effect of time. Therefore, it is hypothesized that while causing a decrease in prepubertal PAR mass, elevated nutrient intake will have no effect on growth characteristics of the mammary gland. The objectives of this experiment were to evaluate the effects of increased nutrient intake from early in life on 1) mammary epithelial cell proliferation, 2) mammary PAR DNA accretion rates, and 3) the dynamics of prepubertal allometric PAR growth. Holstein heifers (n = 78) were fed from 45 kg of body weight either elevated (E) or restricted (R) levels of nutrients to support 950 (E) or 650 (R) g/d of body weight gain. Six heifers per treatment were harvested at 50-kg increments from 100 to 350 kg of body weight. Heifers on the E plane of nutrition had higher plasma leptin and less PAR DNA than their body weight-matched R-intake cohorts. Despite this reduction in PAR DNA, treatment did not negatively influence mammary epithelial cell proliferation or the PAR DNA accretion rate. Dynamics of allometric and isometric mammary growth were also unaffected by the level of nutrient intake, as was exit from allometric growth. This work represents the first demonstrating that the level of nutrient intake and the concomitant increase in plasma leptin have no measurable influence on 1) the rate of PAR DNA accretion, 2) mammary epithelial cell proliferation, or 3) total PAR mass and, by default, the local or systemic controls that coordinate these processes.
This study was conducted to determine the effects of exogenous porcine somatotropin (pST) on the dietary lysine requirement and efficiency of absorbed lysine utilization for pigs during the 20- to 60-kg phase of growth. Seventy-two crossbred pigs (20 +/- 0.7 kg body wt) received daily intramuscular injections of either excipient (0 dose) or pST (150 micrograms/kg body wt) and were fed diets in which protein and lysine concentrations ranged from 6.4 to 23.5 g/100 g diet and from 0.40 to 1.48 g/100 g diet, respectively. Nutrient density was altered to compensate for reduced feed intake with pST, but diets were approximately isocaloric. Rate and efficiency of gain and whole-body protein accretion rate exhibited a dose-response improvement (P < 0.01) to increases in dietary protein for both excipient and pST-treated pigs. Pigs receiving pST grew more rapidly and more efficiently than control counterparts (P < 0.01). Treatment with pST improved the rate of protein accretion (P < 0.01) at all but the lowest level of dietary protein. The net lysine utilization for lysine accretion and maintenance was 0.46 for control pigs and 0.57 for pigs receiving pST, a 24% improvement in the efficiency. Thus, treatment with pST increased the maximum rate of protein accretion as well as the partial efficiency with which dietary lysine is used for protein accretion. Consequently, only a 9% increase in dietary lysine was required to maximize protein deposition in pST-treated pigs, because the metabolic efficiency of lysine utilization was improved.
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