Abstract

The mammary gland of the lactating rat utilizes glucose, triglycerides and nonesterified fatty acids as its main substrates for lipogenesis [ 11. Ketone bodies are also used as substrates both for de novo fatty acid synthesis and for oxidation [2]. Utilization of ketone bodies by the gland inhibits glucose uptake by the gland invivo [3] and in vitro [2]. It has been suggested [2] that a possible explanation for this interrelationship between ketone body and glucose utilization by rat mammary gland is the inhibition of glycolysis at the phosphofructokinase (PFK) (EC 2.7.1 .l 1) step by elevated concentrations of citrate as a result of ketone body metabolism. This suggestion assumes that PFK from the secretory epithelial cells of mammary tissue is sensitive to inhibition by citrate. Although several studies have been conducted on the effects of citrate on this enzyme from other tissues (see, e.g. [4,5]) none have been performed on PFK from mammary gland and it is not known whether the enzyme from this tissue is sensitive to citrate [6]. In the present study PFK was extracted from rat mammary gland acini and found to be inhibited by concentrations of citrate that are present in the gland in vivo under conditions characterized by reduced glucose utilization.

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