In several pathophysiologic states, i.e., cirrhosis of liver, protein calorie malnutrition, starvation, carbohydrate deprivation, etc., thyroid hormone metabolism is reported to be altered with a decrease in serum T3 and a reciprocal increase in TR3. Uncontrolled diabetes mellitus is a similar state in which glucose does not enter the cells causing cellular starvation and hyperglycemia ensues. Therefore, serum T4, T3, RT3, T3-resin uptake, TSH, and glucose were determined after an overnight fast in 94 male diabetics (aged 28 to 85 years) during a routine follow-up visit to the outpatient clinic and 24 healthy male adults (aged 24 to 81 years). Glycosylated hemoglobin concentrations were measured as well in normal subjects and 16 newly discovered diabetics. In normal subjects, no significant relationships between fasting plasma glucose and T3 and RRT3 levels were observed. In diabetics there was a significant positive (r = 0.611; p less than 0.001) correlation between glucose and RT3. Similarly, a significant negative relationship was observed between glucose and T3 (r = 0.491; p less than 0.001). T4, free T4, T3-resin uptake, and TSH were normal in diabetics. In 16 newly discovered diabetics, with fasting plasma glucose greater than 200 mg/dl, serum T3 rose (96 +/- 5 to 128 +/- 5 ng/dl) and RT3 declined (26.3 +/- 10.4 +/- 1.4 ng/dl) on improvement of hyperglycemia (fasting plasma glucose less than 140 mg/dl) after intensive therapy for 6 to 8 weeks. Glycosylated hemoglobin levels declined as well (14.6 +/- 0.9% to 9.3 +/- 0.7%). These data indicate: (1) thyroid hormone metabolism may be altered in diabetes mellitus with a fall in serum T3 and a reciprocal rise in RT3; and (2) T3 and RT3 concentrations may serve as indicators of metabolic control in diabetes mellitus.

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PubMedDate not supplied

Effect of pregnancy on thyroxine binding globulin (TBG) in partial TBG deficiency.

An unusual opportunity was afforded to study the effect of endogenous increase in estrogen on thyroxine binding globulin (TBG) throughout pregnancy in a partially TBG-deficient female who conceived subsequent to initial examination. TBG binding of 125I-thyroxine (T4) before and up to four months of pregnancy was low in comparison to normal. Starting from six months and up to the end of pregnancy, TBG activity showed a definite increase although still below normal. TBG binding capacity increased from a low value of 4.2 microgram T4/100 ml ,efore pregnancy to a value 9.3 microgram T4/100 ml in the last month of pregnancy. This was accompanied by an increase in immunoassayable TBG from less than 1 mg/100 ml in the second month of pregnancy to 1.9 mg/100 ml in the last month, and an increase of T4 from 3.1 microgrom/100 ml to 4.3 microgram/100 ml. Two weeks after delivery, TBG binding of 125I-T4 showed a precipitous decline to the abnormally low distribution noted prior to and during the early months of pregnancy. TBG binding activity was normal in the cord blood of the infant. These studies provide the first direct evidence that increase in endogenous estrogen results in detectable increases in TBG concentration in the human with partial TBG deficiency.

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