Renal insulin-like growth factor I and growth hormone receptor binding in experimental diabetes and after unilateral nephrectomy in the rat

1991 
We have measured specific binding of insulin-like growth factor I and growth hormone to renal plasma membranes from control, streptozotocin-diabetic, insulin-treated diabetic, uninephrectomised and combined diabetic-uninephrectomised male Wistar rats. Control, insulin-treated and uninephrectomised rats had similar body weights after 7 days (243±2 g), whereas diabetic and diabetic-uninephrectomised animals were significantly lighter (219±4 and 203±4 g, p<0.05). Blood glucose concentrations were similar in the diabetic and diabetic-uninephrectomised animals (around 26 mmol/l) but significantly lower in the insulin-treated group. Right kidney weight increased by 14% in the control, insulin-treated and sham-nephrectomised animals, by 33% in the diabetic group, 38% in the nephrectomised animals and 60% in the diabetic-nephrectomised group. The renal content of insulin-like growth factor I was similar and stable in the control, insulin-treated and sham-nephrectomised animals (208±14 ng/g wet weight) but rose to a peak of 669±35 ng/g in the diabetic group (p<0.001), 871±34 ng/g in the nephrectomised animals (p<0.001) and 1012±43 ng/g in the diabetic-uninephrectomised group (p<0.001). Maximum binding of insulin-like growth factor I fell on day 1 in the diabetic group (8.3±1.4 vs 5.2±0.71× 10− mol/l; p<0.01) but thereafter was identical to control animals. In the insulin-treated animals, maximum binding rose to 11.0±1.1×10−11 mol/l, significantly different from control and diabetic animals (p<0.01). Growth hormone binding fell acutely in both the diabetic and diabetic-nephrectomised animals (3.13±0.58 and 2.83±0.21 vs 7.77±0.68×10−12 mol/l; p<0.001 for both). Following uninephrectomy, maximum binding of insulin-like growth factor I and growth hormone was unchanged from control values. We conclude that the rise in renal content of insulin-like growth factor I which precedes the compensatory growth seen after induction of diabetes and uninephrectomy is not due to alterations in insulin-like growth factor I receptor binding and is independent of growth hormone binding.
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