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The MCR and secretion rate of rat TSH have been measured to determine whether altered rates of TSH metabolism could account for the lower plasma TSH concentration in streptozotocin-diabetic rats. The MCR of TSH in diabetics, (0.57 ± 0.04 ml/min) was similar to that of control animals (0.55 ± 0.08 ml/min). So was the t.A (19.5 ± 0.6 min) for controls and (20.0 ± 0.8 min) for diabetics. The secretion rate in controls (0.17 ± 0.01 μg/min) was higher than in diabetic rats (0.10 ± 0.01 Mg/min) (P < 0.01). Furthermore, plasma TSH concentration was measured before and after an iv injection of 50 or 100 ng of TRH. The basal plasma TSH levels in diabetic rats (0.26 ± 0.07 μg/ml) w e r e lower than those in control rats (0.40 ± 0.09 μg/ml). The maximal TSH response to 50 ng TRH in diabetics (0.60 ± 0.10 μg/ml) w a s significantly lower than that in the control group (1.2 ± 0.15 μg/ml; P < 0.01). Similar differences in response of the two groups were found in the plasma TSH concentrations after 100 ng TRH (1.75 ± 0.20 vs. 1.0 ± 0.1 Mg/ml, P < 0.01). The total amount of TSH released by 50 ng TRH in diabetics (7.0 ±0.1 μg/ml) was lower than in control rats (18.1 ± 0.1 μg/ml; P < 0.001). Mean values of 13.3 ± 0.1 and 29.5 ± 0.3 μg/ml were obtained for diabetic and control rats, respectively, after injection of 100 ng TRH. The results indicate that diabetic rats have a lower TSH secretion rate, lower TSH response to TRH, and thus lower plasma TSH levels than control animals. These data appear to be compatible with the hypothesis that these alterations may be induced as a consequence of decreased pituitary TSH content, an alteration in the pituitary sensitivity to TRH, or an increased sensitivity to the feedback-inhibitory effect of thyroid hormones.
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Pastor et al. (1983) studied this question.
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