Growth hormone receptors in rat liver membranes: effects of fasting and refeeding, and correlation with plasma somatomedin activity

MC Postel-Vinay, E Cohen-Tanugi, J Charrier - Molecular and Cellular …, 1982 - Elsevier
MC Postel-Vinay, E Cohen-Tanugi, J Charrier
Molecular and Cellular Endocrinology, 1982Elsevier
The effects of fasting and refeeding on hepatic growth hormone receptors, on insulin
receptors and on plasma somatomedin activity were studied. Female rats were either
subjected to fasting for 4 days, refed for 3 days after a 4-day fasting, or allowed free access
to food (controls). The specific binding of 125 I-labelled bovine growth hormone was low in
liver microsomal membranes (45% that of controls) and in plasma membranes (52% that of
controls) of fasted rats. The number of somatotropic sites rather than the affinity of the …
Abstract
The effects of fasting and refeeding on hepatic growth hormone receptors, on insulin receptors and on plasma somatomedin activity were studied. Female rats were either subjected to fasting for 4 days, refed for 3 days after a 4-day fasting, or allowed free access to food (controls). The specific binding of 125I-labelled bovine growth hormone was low in liver microsomal membranes (45% that of controls) and in plasma membranes (52% that of controls) of fasted rats. The number of somatotropic sites rather than the affinity of the binding was decreased. Lactogenic sites as judged by the binding of 125I-labelled human growth hormone were not significantly reduced in liver membranes of fasted rats. 125I-labelled insulin specific binding was enhanced in microsomal (184% that of controls) and plasma membranes (136% that of controls) of fasted rats; these modifications were associated with a decreased insulinaemia. But immunoreactive rat growth hormone levels were not different in plasma of fasted, refed and control animals. Decreased plasma bioassayable somatomedin was associated with the low number of somatotropic binding sites in liver membranes of fasted rats. Somatomedin activity of refed animals was comparable to controls. A significant correlation between the plasma bioassayable somatomedin and the hepatic level of somatotropic binding sites was found. It is proposed that, in fasting, the loss of somatotropic binding sites in the liver is one of the possible causes of the decreased plasma somatomedin bioactivity.
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