Abstract
Prostaglandin E1 (PGEi), T4, and epinephrine (Epi) were incubated with mammary tissue slices from normal and adrenalectomized (Adx) rats and Adx rats receiving cortisol (Adx + C). PGEi, T4 and the combination of Epi, T4, and PGEi increased mammary slice cAMP levels in all groups. No differences were observed among treatment groups in basal cAMP levels or responses to hormones. Glucose-l-14C oxidation and incorporation into lipids were stimulated by PGEi, T4, and the combination of Epi, T4, and PGEi in normal rats. Responses were depressed by adrenalectomy and reversed by cortisol. PGEi, T4, and the combination of Epi, T4, and PGEi depressed glucose-6-l4C oxidation. Fatty acid synthesis from glucose-6-14C was stimulated by Epi, PGEi, and T4 in tissues from normal and Adx + C rats, but not in those from Adx rats. Glycerol synthesis was unchanged. Pyruvate-l-14C and pyruvate-2-14C oxidation were uneffected by adrenalectomy or hormones. Fatty acid synthesis was depressed by adrenalectomy and reversed by cortisol. T4 and the combination of Epi, T4, and PGEi depressed triacylglycerol and fatty acid synthesis in all groups. Glycerol synthesis was unchanged. Hormonal effects were much more pronounced when glucose was the substrate. This suggests that cAMP effects on glucose metabolism are manifest at a site between hexose-P and pyruvate, and further, that a primary effect of adrenalectomy may be to reduce the responsiveness of this site to cAMP. Linear regression analyses comparing cAMP levels with glucose and pyruvate metabolic parameters further support this conclusion.