Effects of exogenous insulin or vanadate on disposal of dietary triacylglycerols between mammary gland and adipose tissue in the lactating rat: insulin resistance in white adipose tissue.

The effects of exogenous insulin or vanadate (an insulin mimetic) on the disposal of dietary [14C]lipid between oxidation to 14CO2, deposition in adipose tissue or uptake by mammary gland and transfer to suckling pups were studied in virgin and lactating rats. After an oral load of [1-14C]triolein, virgin rats treated with a supraphysiological dose of insulin over 24 h showed a decrease (58%) in 14CO2 production and increased accumulation of [14C]lipid in carcass and white adipose tissue. There was a 2.5-fold increase in lipoprotein lipase activity in the latter. Chronic vanadate administration (12 days) had no effect on these parameters. In lactating rats, the stimulation of the deposition of [14C]lipid in adipose tissue by exogenous insulin was about 10% of that in virgin rats. In prolactin-deficient lactating rats there was no stimulation of [14C]lipid deposition in adipose tissue by insulin. However, both insulin and vanadate treatment increased the accumulation of [14C]lipid in mammary gland to the values seen in the mammary glands plus pups of normal lactating rats. Lipoprotein lipase activity in the gland was also restored to normal values. It is concluded that in lactation there is resistance to insulin stimulation of dietary lipid deposition in adipose tissue, and that this is not due to circulating prolactin. In addition, exogenous insulin plays a role in the regulation of lipoprotein lipase and hence of dietary lipid uptake into lactating mammary gland.