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ABSTRACT
Two separate experiments were carried out to examine the effect of dietary protein intake on basal and GHstimulated plasma insulin-like growth factor-I (IGF-I) concentrations during either saline or glucose infusion into the jugular vein. In experiment 1, six castrated male lambs (27·1 ± 1·2 kg live weight (LW)) were fed a diet restricted in both metabolizable energy (ME; 0·18 MJ/kg LW per day) and nitrogen (2·0 g/kg LW per day) intakes, while in experiment 2 a further six lambs were fed a similar restricted ME intake but an increased nitrogen intake (3·0 g/kg LW per day). In both experiments glucose (experiment 1, 0·009 mmol/kg LW per min; experiment 2, 0·015 mmol/kg LW per min) or saline (0·25 ml/min) was infused for 6 days and plasma samples were obtained from the jugular vein at hourly intervals on day 4 (basal) or on days 5 and 6 after an i.v. GH challenge. In experiment 1 there was no increase in plasma IGF-I concentrations in response to the GH challenge during saline infusion, but during glucose infusion the plasma concentration of IGF-I increased to a peak after 24 h and declined over the next 20 h. Basal concentrations of IGF-I, insulin and glucose were significantly higher during glucose infusion. In experiment 2 the area under the IGF-I peak in response to the GH challenge was the same for the infusions of saline and glucose but the peak value for IGF-I was significantly higher during glucose infusion due to higher concentrations in the basal period. It is concluded that feeding a dietary intake of metabolisable energy and nitrogen which is only just sufficient to meet the requirements for maintenance of body tissues completely abolishes the increase in plasma IGF-I in response to GH challenge. Increasing the nitrogen supply in the diet or i.v. infusion of glucose re-establishes the IGF-I response to GH challenge as well as increasing basal IGF-I concentrations. The potential involvement of circulating concentrations of insulin, glucose and amino acids in the control of plasma IGF-I levels are discussed.
Journal of Endocrinology (1992) 132, 195–199