Key result
Human and bovine growth hormone similarly stimulate hepatic LDL receptors in rats independently of prolactin.
Why the study?
Does human growth hormone affect cholesterol metabolism via prolactin receptors in male rats?
Does human growth hormone affect cholesterol metabolism via prolactin receptors in male rats?
The effects of human growth hormone on cholesterol and lipoprotein metabolism in male rats are not mediated by prolactin receptors.
Answers are grounded in this paper and cite their sources.
Rat data do not inform human therapy; leaves open direct GH receptor roles in lipid metabolism.
Previous studies have established that growth hormone (GH) has many important effects on the regulation of cholesterol and lipoprotein metabolism. However, human GH (hGH) can also bind to prolactin receptors, eliciting prolactin receptor-mediated effects. In this study, we evaluated whether hGH can exert such responses in currently used animal models and whether prolactin affects lipoprotein and/or hepatic cholesterol metabolism. Normal and hypophysectomized (Hx) male rats were given either hGH or bovine GH, the latter unable to bind to the prolactin receptor. The hormones were continuously infused by use of subcutaneous osmotic mini-pumps for 7 days; blood and livers were collected after euthanasia. Both hormones stimulated hepatic LDL receptor expression and bile acid synthesis to a similar extent and normalized the altered plasma lipoprotein pattern in Hx rats. Prolactin, injected twice daily to Hx male rats, did not exert any effects on the plasma lipoprotein pattern or on cholesterol metabolism. We conclude that previously established effects of hGH on cholesterol metabolism are not mediated by prolactin in male rats.
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Matasconi et al. (2004) studied Lipoprotein and bile acid metabolism. Human growth hormone (hGH) vs. Bovine growth hormone (bGH) and prolactin was evaluated on Hepatic LDL receptor expression, bile acid synthesis, and plasma lipoprotein pattern. Human growth hormone and bovine growth hormone similarly stimulated hepatic LDL receptor expression and bile acid synthesis in male rats, indicating these effects are not mediated by prolactin.
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