L. Madison, R. Unger
May 1, 1960
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33
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Journal
Diabetes
Abstract
Neither the precise biochemical mechanisms whereby phenethylbiguanide (DBI) lowers blood glucose concentration in human subjects nor its site of action, whether in the peripheral tissues and/or the liver, are known. In the absence of a urinary loss of glucose or glucose intermediaries, hypoglycemia can result only from an increase in peripheral glucose utilization or a decrease in hepatic output of glucose. Although many factors may be involved in either increased peripheral utilization or decreased hepatic production of glucose, the localization of the site of action of DBI might offer some insight into its possible mechanism of action. The present study was designed to determine the effect of DBI on peripheral glucose utilization in diabetic and normal human subjects. Changes in peripheral glucose utilization* were measured by following the changes in femoral arteriovenous glucose concentration difference after the administration of DBI.