Statistical evidence that endogenous reverse triiodothyronine (rT3) may affect oxygen consumption in food deprived chickens.

Exogenous rT3 decreases O2 consumption in mammals and birds. Until now a correlation coefficient and a regression equation have not been presented. Statistical evaluation seems to be requisite for verifying the answer to the question of whether endogenous rT3 may be able to reduce O2 consumption in birds where the normal level of plasma rT3 is 10 times less than the corresponding level of T3. Food deprived chickens (for 48 h) were used in this study because fasting enhances plasma rT3. The results revealed a reciprocal relation of T3 and rT3 in the circulation. Reverse T3 began to increase when T3 decreased to a plateau at 53.9% of initial level. As expected a reciprocal relationship was obtained (r = -0.749; n = 36) between plasma rT3 and O2 consumption. The regression line was calculated according to the equation: Y = -0.388X + 0.856. This relation differs from the linear relationship between T3 and O2 consumption (r = 0.796; Y = 0.107X + 0.449). The regression line lies in the range of 0.122-0.778 nmol rT3/l, which is found in some physiological conditions in birds where elevated plasma rT3 occurs. This suggests that endogenous rT3 may participate in modifying O2 consumption in birds. Using the rT3:T3 ratio the correlation coefficient was somewhat higher (r = -0.831; Y = -0.673X + 0.831) suggesting common involvement of both triiodothyronines in the reduction of O2 consumption during food deprivation. The drop in O2 consumption after 48 h of food deprivation was 28.4%; decreased T3 and increased rT3 may participate in 15.4% and 13.0% of this fall, respectively. The hypometabolic effectiveness of rT3 seems to be greater than the hypermetabolic effectiveness of T3, since a smaller increase of plasma rT3 was needed to reduce O2 consumption compared to the amount of T3 necessary to enhance it.

Serum pattern of thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) in fed and fasted cocks following TRH stimulation.

Food deprivation for 27 and 75h in cocks decreased serum levels of T3 maximally by 61.1% and increased the level of rT3 by 51.4% and that of T4 by 22.4%. Injection of a single dose of TRH (10 micrograms/kg b.w.) increased serum levels of all 3 iodothyronines in both fed and food-deprived animals. In fasted, TRH-treated birds the peak of serum rT3 was 80.5 and 73.3% above control levels in 27- and 75-hr food-deprived cocks, respectively (fed birds: 14.6 and 9.7%); the relevant data for T3 were: 78.3 and 40.4% (fed birds: 95.7 and 127.5%); for T4: 30.0 and 27.0% (fed birds: 9.2 and 6.1%). The greater relative increment of serum rT3 than T3 in food-deprived and TRH-treated cocks was supported by a fall of the serum T3/rT3 ratio to 78.7 and 27.9% in fed cocks and 27- and 75-hr fasted animals, respectively. We conclude, that food deprivation modifies the response of the hypophysis-thyroid axis to exogenous TRH in the sense that during fasting the production of rT3 is enhanced relative to T3.

Hypometabolic effect of 3,3',5'-triiodothyronine in chickens: interaction with hypermetabolic effect of 3,5,3'-triiodothyronine.

The effect of 3,3',5'-triiodothyronine (rT3) and 3,5,3'-triiodothyronine (T3) on O2 consumption in 1-day-old chickens was studied. The birds were divided into five groups, each of six chickens: (1) control--without injection; (2) control--injected with 100 microliters of solvent (0.01 N NaOH in saline); (3) injected with 10 micrograms rT3/chicken; (4) injected with 0.5 micrograms T3/chicken; and (5) injected with 10 micrograms rT3 + 0.5 microgram T3/chicken. O2 consumption was measured using a Kipp & Zonen diaferometer at neutral temperature (30 degrees) 0, 1, 2, 3, and 4 hr after injection of hormones. Corresponding groups of other chickens served only for blood collection. rT3 and T3 were measured by radioimmunoassay. Reverse T3 decreased O2 consumption by 10.87%. Contrary to this, T3 increased O2 consumption by 29.41%. Reverse T3, injected together with T3, interacted with the hypermetabolic effect of T3 up to 2 hr after injection; then, O2 consumption started to increase, and was about 16.7% higher compared with the basal level 3 hr after injection. The blood plasma level of rT3 increased about 29-fold at the first hour after injection, without changes in the basal level of T3. Administration of T3 increased its level 6-fold 2 hr after injection, which was accompanied by a gradual decrease in the basal level of rT3 (3.7-fold) 4 hr after injection. Administration of rT3 + T3 increased the rT3 level 30-fold at 2 hr and the T3 level 1.7-fold at the first hour after injection. Thus, rT3 acts hypometabolically and interacts with the hypermetabolic effect of T3; administration of T3 lowered the basal level of rT3; and the plasma level of T3 did not change after administration of rT3.