Abstract

We have investigated whether the low serum levels of somatomedin-C (SM-C) observed in protein malnutrition could be related to changes in liver growth hormone and prolactin binding. Growing female rats were fasted for 3 days and subsequently refed for 14 days with isocaloric diets containing 5% (low) or 25% (normal) protein. Control rats were fed a normal protein diet during the entire study. The numbers and affinity constants of somatogenic (GH) and lactogenic (PRL) binding sites were determined by analysis of saturation curves using liver homogenates incubated with 125I-labelled bovine growth hormone and 125I-labelled ovine prolactin. Serum SM-C and growth hormone concentrations were measured by radioimmunoassay. After fasting for 3 days body weight dropped by 21% ( P < 0.01 vs. controls) and serum SM-C by 53% ( P < 0.01), while GH and PRL binding capacities decreased respectively by 63% ( P < 0.01) and 62% ( P < 0.01). On refeeding with a normal protein diet, body weight, serum SM-C, GH and PRL binding capacities returned to control values. In contrast, with low protein intake, body weight, SM-C, GH and PRL binding capacities remained respectively 16%, 55%, 49% and 81% lower than controls ( P < 0.01). No significant changes in serum growth hormone concentrations occurred with fasting or refeeding. Only in the fasted rats were the affinity constants of GH and PRL binding sites significantly ( P < 0.01) lower ( GH 0.63 ± 0.06 × 10 9 M −1 vs. 0.86 ± 0.04 × 10 9 M −1; PRL 0.90 ± 0.04 × 10 9 M −1 vs. 1.34 ± 0.07 × 10 9 M −1 ). These findings indicate that adequate protein intake is an essential regulator of liver somatogenic and lactogenic binding sites. In addition, the data suggest that the low serum SM-C levels in protein deficiency might be due to the reduction in hepatic GH and PRL binding capacities and that this reduction may, in turn, be responsible for the liver insensitivity to growth hormone.

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