In vitro perfusion studies of the human placenta. VI. Evidence against active glucose transport.

Previous studies in our laboratory using "in vitro" perfusion have established that glucose transport across the human placenta is a carrier-mediated process. It is not known whether these carriers require the expenditure of metabolic energy to function. In the experiments presented here we demonstrate in the perfused placenta that there is not reduction in the rate of glucose transport or its analogue 3-O-methyl-alpha-D-glucopyranoside (3MG) in the presence of 10(-4) M dinitrophenol (DNP), an uncoupler of oxidative phosphorylation. The presence of DNP, however, does cause an increase in the glucose utilization rate as well as increased lactic acid production. In order to test whether glucose transport depends on the functioning of a sodium pump system, the sodium in the perfusion system was replaced with choline chloride. The final sodium content was 30 mEq/L. In the presence of a low sodium concentration there was no decrease in the rate of 3MG transport compared to the control experiments run at normal sodium levels. Also "counter transport" of glucose was observed, a further indication that the glucose carrier mechanism does not require a sodium gradient in order to function. Since the transport rate of glucose or its analogue 3MG across the placenta is not reduced in the presence of 10(-4)M DNP and is not reduced in the absence of a sodium gradient, it is unlikely that the mechanism of glucose transport is an active process requiring the expenditure of metabolic energy.