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Continuous administration of growth hormone does not prevent the decrease of IGF-I gene expression in zinc-deprived
1Diabetes and Nutrition Unit, University of Louvain School of Medicine, Brussels, Belgium.
Summary
Zinc deficiency impairs growth by reducing insulin-like growth factor I (IGF-I) and growth hormone binding (GHR). Restoring GHR in zinc-deficient rats did not restore IGF-I or growth, indicating zinc is essential for IGF-I synthesis.
Area of Science:
- Endocrinology
- Nutritional Science
- Molecular Biology
Background:
- Zinc deficiency is linked to reduced growth and impaired insulin-like growth factor I (IGF-I) levels.
- Reduced liver growth hormone receptor (GHR) expression is observed in zinc-deficient (ZD) animals.
- The precise role of GHR in mediating the effects of zinc deficiency on IGF-I remains unclear.
Purpose of the Study:
- To investigate the role of reduced liver GHR in the decreased IGF-I observed in zinc-deficient animals.
- To determine the effects of GHR restoration on growth, IGF-I, and its binding proteins (IGFBPs) in ZD rats.
Main Methods:
- Rats were fed zinc-deficient (ZD) or pair-fed (PF) diets for 4 weeks.
- ZD rats received continuous subcutaneous infusion of bovine growth hormone (bGH).
- Measurements included weight gain, serum and liver IGF-I, IGFBPs, GHR, and growth hormone binding protein (GHBP) and their respective mRNAs.
Main Results:
- Zinc deficiency significantly reduced weight gain, serum and liver IGF-I, IGFBPs, liver GHR, and GHBP compared to pair-fed rats.
- Exogenous bGH normalized liver GHR, GHBP, and IGFBPs in ZD rats.
- Despite normalized GHR and GHBP, GH infusion did not stimulate growth, serum IGF-I, or liver IGF-I mRNA in ZD rats.
Conclusions:
- IGF-I synthesis requires zinc in addition to growth hormone.
- The lack of growth promotion by GH in zinc-deprived rats is due to a defect beyond GH binding to its liver receptors.
- Zinc is essential for the growth-promoting effects of GH, independent of GHR levels.
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