GLUCOSE AND ACETATE METABOLISM AND LIPOGENESIS IN MAMMARY GLANDS OF HYPOPHYSECTOMIZED RATS IN WHICH LACTATION WAS HORMONALLY INDUCED1

Abstract

Rats which had been hypophysectomized in midpregnancy were injected daily during the postpartum period with either a) mammotrophin, [DELTA]1-hydrocortisone acetate, and somatotrophin, or b) mammotrophin and [DELTA]1-hydrocortisone acetate or c) [DELTA]1-hydrocortisone acetate and somatotrophin or d) one of these hormones alone. The pattern of glucose and acetate metabolism in slices of their mammary glands was evaluated by the following criteria: 1) the extent and relative conversion of glucose carbons 1, 2, and 6 to CO2 and fatty acids; 2) the relative participation of the Embden-Meyerhof and the hexosemonophosphate oxidative pathways of glycolysis in the conversion of glucose to fatty acids; and 3) the stimulating effect of glucose on lipogenesis from acetate. Lactation was established and maintained in rats injected with hormones listed under a) and b) above. The metabolic behavior of their mammary glands was identical in all respects with that observed in mammary tissue of normal lactating rats. A metabolic feature of the hormonally-maintained, lactating mammary glands of the hypophysectomized rats was the participation of a non-Embden-Meyerhof pathway in the conversion of glucose to fatty acids. The appearance of this pathway seemed to be related to milk formation and secretion and not to gland growth and development.