Further observations on the in vitro stimulation by insulin of fat synthesis by lactating mammary gland slices

Abstract

Insulin added in vitro markedly increased QO2, acetate and glucose utilization, and especially R.Q. and "extra CO2" (CO2 produced in excess of that required for R.Q. = 1) of lactating rat mammary gland slices in glucose plus acetate. This suggests a stimulatory action of insulin on net fat synthesis. Similar but less marked effects were obtained in glucose, but in acetate the tissue was inert to insulin. Rat mammary gland slices were unresponsive to insulin, both in glucose plus acetate and in glucose, at the end of pregnancy (19-20 days) and after 2 days'' weaning at days 20-21 of lactatipn. Lactating rabbit mammary tissue was similarly responsive to insulin in glucose plus acetate. Insulin had no effect on the metabolism of lactating mouse mammary gland in glucose alone. In the absence of insulin, the R.Q. of this tissue was lower in glucose plus acetate than in glucose, but the acid production was somewhat depressed, indicating a slight utilization of acetate. In glucose plus acetate the tissue responded to insulin by moderate increases in QO2 and acetate uptake and marked increases in R.Q. and "extra CO2" Udder slices from lactating ewes were inert to insulin both in glucose plus acetate and in acetate. Glycerol exerted a qualitatively similar effect to insulin, though less marked as regards the increases in R.Q. and "extra CO2," on the metabolism of lactating rat mammary tissue, except that the glucose uptake was not increased. The effects of glycerol and insulin were not additive. Udder slices from lactating ewes responded to glycerol in acetate alone, but in glucose plus acetate glycerol exerted a slight inhibitory effect. The stimulating effect of insulin on fat synthesis by mammary tissue may be due, partly at any rate, to stimulation of glycerol formation from glucose. Since mammary tissue can synthesize and secrete glycerides, the supply of glycerol may be a critical, rate-limiting factor in fat synthesis by this tissue, though the insulin effect may be related to glucose utilization as an energy source for fat synthesis.