Tumor growth and lipid metabolism during lactation in the rat.

Implantation of the Walker 256 carcinoma in lactating rats 2-3 days after parturition had no effect on maternal food intake or pup weight gain over the next 8-9 days. The rate of mammary gland lipogenesis in vivo, which is an index of glucose utilization by the gland, was similar in control and post-partum implanted rats. The accumulation of 14C-lipid in the mammary tissue after an oral load of [1-14C]triolein was also not altered by the presence of the tumor, nor was there evidence for hypertriglyceridaemia. This suggests that the activity of lipoprotein lipase in mammary tissue is not sensitive to the tumor as it appears to be in adipose tissue of non-lactating rats. In contrast, implantation of the tumor 1-2 days before parturition resulted in a faster rate of tumor growth, decreased maternal food intake and decreased pup weight gain compared to either control rats or rats with tumor implanted post-partum. In addition, the rate of mammary gland lipogenesis was decreased by 70% and that of the carcass by 50%. This decrease in lipogenesis is likely to be due to the relative hypophagia in the pre-partum implanted group. The 14C-lipid accumulation in mammary tissue after oral [1-14C]triolein tended to be lower in the pre-partum group but this was not statistically significant. It is concluded that the marked effects on lactation of pre-partum implantation of the tumor are due to effects of the tumor or its presence on the differentiation of the gland around parturition. The alternative explanation that the pre-partum tumor implantation suppresses the stimulus for physiological hyperphagia during lactation is less likely, because this does not occur with the post-partum implantation. The role of putative humoral factors in these effects of the Walker 256 carcinoma in lactation is discussed.