Abstract
Abstract
Nonpregnant female rats and pregnant rats were fed ad libitum. Diabetes was induced by a single intravenous injection of streptozotocin. Pregnant rats received streptozotocin on Day 17 of gestation. The diabetic rats were used 3 days after treatment with streptozotocin. Protamine zinc insulin and crystalline insulin were administered to diabetic rats subcutaneously 24 hr prior to removal of the livers for perfusion. Livers were removed and perfused in vitro in a recirculating liver perfusion apparatus.
Diabetes in nonpregnant and pregnant animals decreased the output of triacylglycerol and increased ketogenesis by the isolated perfused liver in comparison to the corresponding nondiabetic group. In agreement with previous data, pregnancy increased output of triacylglycerol and decreased ketogenesis. Livers from pregnant diabetic rats secreted more triacylglycerol and fewer ketones than did livers from nonpregnant diabetic rats. Pretreatment of diabetic rats with insulin reduced ketogenesis toward normal values and increased output of triacylglycerol to values exceeding corresponding control values. Total net synthesis of triacylglycerol was increased by pregnancy and was decreased in livers from pregnant diabetic rats, when compared to their corresponding controls. The data suggest that certain hormonal changes induced by pregnancy act antagonistically to experimental insulin deficiency.
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