A
parasitic disease model (
sarcocystosis) was used to study the effects of
infection and associated plane of nutrition on GH and
somatomedin-C (SM-C) patterns in plasma, and SM-C
binding protein patterns in plasma from 4-month-old male Holstein calves. Calves, matched by age and rate of growth before the experiment, were divided into three treatment groups (n = 7). In the first (control), animals were uninfected and food was available ad libitum; in the second, animals were infected with Sarcocystis cruzi and food was available ad libitum. The third group consisted of uninfected animals pair-fed to the level of feed intake of the infected animals. Blood samples were obtained at various times after
infection for analysis of the secretory patterns of GH (day 27 after
infection, samples every 10 min for 6 h), SM-C (days 27, 35 and 58 after
infection) or
binding protein (day 42 after
infection). Samples were analysed for GH and SM-C by radioimmunoassay. Relative molecular weights of
binding proteins were assessed by elution patterns from gel permeation columns. Clinical signs of
infection were manifest abruptly on day 26 after
infection. Voluntary feed intakes of infected calves as a per cent of control calves were 18, 46 and 78 on days 27, 35 and 58 after
infection respectively. Plasma GH concentrations were lower in infected and pair-fed than in control calves (P less than 0.05). Plasma SM-C concentrations were reduced in calves with diminished feed intakes and lower still in infected calves (P less than 0.05). Plasma SM-C was positively correlated with
nitrogen retention across treatment groups (r = 0.81). Two classes of
binding proteins differing in molecular weight were identified. The relative amounts of each
binding protein in plasma were reduced during low feed intake with some differences in the endogenous saturation affected by
infection. These data suggest that altered growth and metabolism in parasitized calves may arise in part from both nutritional and
infection-mediated effects on the regulation of GH, SM-C and SM-C
binding proteins.