Thyroxine Turnover and Transport in Diabetes Mellitus

Abstract

In 27 adult-type diabetics, determinations were made of the free thyroxine fractions and free thyroxine iodine concentrations in serum, as well as the maximal binding capacities of thyroxine binding alpha-globulin (TBG) and thyroxine binding prealbumin (TBPA) by reverse flow paper electrophoresis in a glycine acetate system at pH 8.6. In addition, rapidly exchangeable cellular thyroxine was estimated from the serum disappearance curves of simultaneously administered 131I-thyroxine and 125I-albumin. Slightly diminished PBI values were found in all diabetics, especially in sulfonylurea-treated diabetics. Free thyroxine fractions were slightly elevated in patients with diabetes mellitus. The calculated free thyroxine iodine concentrations, representing the products of PBI values and free thyroxine fractions, were almost normal in patients with diabetes mellitus described in the present paper. The total distribution space of thyroxine was slightly higher in diabetics than in the control group. The expansions of total distribution space of thyroxine found in diabetic patients were due mainly to the elevation of intracellular distribution space of thyroxine. Moreover, the diabetic patients had almost normal intracellular pools of thyroxine, while they had somewhat reduced extracellular pools of thyroxine. The findings indicated a redistribution of thyroxine into the cellular compartment in diabetics. Furthermore, highly significant correlation was evident in the computation of multiple correlation coefficient of thyroxine turnover against free thyroxine fraction and maximal percent of 131I-thyroxine within the cellular compartment, whereas simple correlation coefficient between the halftime and free thyroxine fraction was not significant. The results suggested that cellular factors may play a major role in regulating thyroxine turnover. The demonstrated variation in thyroxine distribution, thyroxine binding, and serum thyroxine concentrations were considered sufficient to explain the maintenance of the constancy of absolute hormone disposal rate in patients with diabetes mellitus.