Williamson D H, Evans R D, Wood S C
Nuffield Department of Clinical Medicine, Radcliffe Infirmary, Oxford, U.K.
Adv Enzyme Regul. 1988;27:93-104. doi: 10.1016/0065-2571(88)90011-8.
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.
在分娩后2 - 3天将Walker 256癌植入哺乳期大鼠体内，在接下来的8 - 9天内对母体食物摄入量或幼崽体重增加没有影响。乳腺体内脂肪生成率是该腺体葡萄糖利用率的指标，在对照大鼠和产后植入肿瘤的大鼠中相似。口服[1 - 14C]甘油三酯后，乳腺组织中14C - 脂质的积累也不受肿瘤存在的影响，也没有高甘油三酯血症的证据。这表明乳腺组织中脂蛋白脂肪酶的活性对肿瘤不敏感，而在非哺乳期大鼠的脂肪组织中似乎是敏感的。相比之下，在分娩前1 - 2天植入肿瘤，与对照大鼠或产后植入肿瘤的大鼠相比，肿瘤生长速度更快，母体食物摄入量减少，幼崽体重增加减少。此外，乳腺脂肪生成率降低了70%，胴体脂肪生成率降低了50%。脂肪生成的这种降低可能是由于产前植入组相对摄食过少。产前组口服[1 - 14C]甘油三酯后乳腺组织中14C - 脂质积累倾向于较低，但这在统计学上不显著。结论是，产前植入肿瘤对泌乳的显著影响是由于肿瘤或其存在对分娩前后腺体分化的影响。产前肿瘤植入抑制泌乳期间生理性摄食亢进刺激的另一种解释可能性较小，因为产后植入不会出现这种情况。讨论了假定的体液因子在Walker 256癌对泌乳的这些影响中的作用。
