Abstract

Previous studies have indicated that acute stress in vivo or ovine corticotropin releasing hormone (oCRH) in vitro, releases both β-lipotropin (β-LPH) and β-endorphin (β-END) from the anterior lobe, with β-END predominating over β-LPH by 2:1. However, repeated stress shifts this ratio to proportionately more β-LPH released with re-stress of oCRH in vitro. Alternative hypotheses were that the glucocorticoids released during stress altered the processing of proopiomelanocortin (POMC) or that the increased biosynthetic drive rresulted in an inability of the processing enzymes to keep pace with biosynthesis. To distinguish between these alternatives, adrenalectomy studies were performed. Following removal of glucocorticoid negative feedback there is greatly increased secretion of β-END-IR from anterior lobe corticotrophs with a subsequent increase in biosynthetic drive. Under these conditions of increased biosynthetic drive in the absence of steroids, the corticotroph secretes primarily β-LPH, suggesting that increased biosynthetic drive alters the post-translational processing rate of POMC.

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