The effects of insulin deficiency (streptozotocin-induced) or insulin plus prolactin deficiency on the disposal of orally administered [1-C-14]triolein between oxidation to (CO2)-C-14, uptake by mammary gland and transfer to suckling pups were studied. Insulin deficiency decreased mammary-gland total weight (by 40%), but caused no change in total tissue DNA. A greater proportion of the [1-C-14]triolein was oxidized to (CO2)-C-14 (120 % increase) in the insulin-deficient rats, and there was a tendency for total transfer of [C-14]lipid to mammary gland and suckling pups to be decreased. A parallel decrease in total mammary-tissue lipoprotein lipase activity occurred. Combined hormone deficiency caused more dramatic changes in all parameters measured. Replacement of insulin (24 h) in insulin-deficient rats decreased (CO2)-C-14 production, increased the uptake of [C-14]lipid into the mammary gland and tended to increase total lipoprotein lipase activity. In contrast, administration of prolactin to insulin-deficient rats had no effect on any of the parameters measured. Replacement of insulin (24 h) in the combined hormone-deficient rats increased uptake of [C-14]lipid and lipoprotein lipase approx. 3-fold, whereas prolactin again had no significant effects. Replacement of both hormones increased (6-fold) transfer of [C-14]lipid to the pups, but did not increase overall uptake of [C-14]lipid (mammary gland, milk clot and pups) above the value for insulin alone. It is concluded that insulin is the primary regulator of triacylglycerol uptake and of lipoprotein lipase activity in the lactating mammary gland of the rat and that the action of prolactin on these processes is indirect. Prolactin, but not insulin, appears to have a direct effect on milk lipid transfer to pups.
