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Influence of diet on basal and growth hormone-stimulated plasma concentrations of IGF-I in beef cattle
Authors:T H Elsasser  T S Rumsey  A C Hammond
Institution:ARS, Ruminant Nutr. Lab., U.S. Department of Agriculture, Beltsville, Maryland 20705.
Abstract:The effects of nutrition on plasma concentrations of insulin-like growth factor-I (IGF-I) were characterized in steers under basal conditions and following single i.m. injection of bovine growth hormone (bGH, .1 mg/kg BW). Nutritional effects on IGF-I were studied in three trials. In all trials steers were individually fed and penned Angus or Hereford x Angus (280 kg). In the first trial, two diets (LPLE1: 8% CP and 1.96 Mcal ME/kg, 4.5 kg.hd-1.d-1; MPHE1: 11% CP, 2.67 Mcal ME/kg, 6.5 kg.hd-1.d-1) were fed (n = 5/diet). Plasma IGF-I concentrations averaged 74 (LPLE1) and 152 (MPHE1) ng/ml (P less than .02). Following bGH injection, IGF-I increased to peak concentrations between 12 and 24 h (averaging 105 and 208 ng/ml at peak for LPLE and MPLE, respectively, P less than .01). In the second trial, steers were fed diets composed of 8, 11 or 14% CP and 1.96 or 2.67 Mcal ME/kg dry matter (6.35 kg.hd-1.d-1 in a factorial arrangement for 84 d, n = 4/diet). Within the low ME diet groups, plasma IGF-I was similar in steers fed 11 and 14% CP but greater at these two CP levels than in steers fed 8% CP (P less than .05). Within the high ME diet groups, plasma IGF-I increased linearly with CP (P less than .01). In the third trial, steers were fed diets to result in a negative N status. Insulin-like growth factor-I was lower (P less than .02) during feed restriction than when steers were full-fed. The IGF-I response to bGH was diminished or absent in underfed steers (P less than .01). These data are interpreted to suggest that diet composition and intake affect plasma concentrations of IGF-I in steers. In cattle, CP may be the primary nutritional determinant of basal IGF-I, but the IGF-I response to CP may be affected by the available ME. Undernutrition can attenuate the IGF-I response to GH and uncouple the regulation of IGF-I normally ascribed to GH.
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