Increase in hepatic mitochondrial α-glycerophosphate dehydrogenase activity after surgical stress in hyperthyroid rats

We have established a rat model to investigate the relationship among serum thyroid hormones, nuclear iodothyronine receptors, and biological responses in thyrotoxic and euthyroid rats after surgical stress. Euthyroid or hyperthyroid rate (1.0 Mg T₃/ml drinking water for 14 days) were subjected to surgical stress (ether anesthesia, laparotomy plus 50 mg talc, ip). Groups of control or stressed rats were killed 1, 2, and 3 days after surgical stress for measurement of thyroid hormone-responsive hepatic enzymes, α-glycerophosphate dehydrogenase (αGPD) and cytosol malic enzyme, serum T₃, T₃ nuclear receptors, and GH mRNA. Thyrotoxic rats had a 3.8-fold increase in αGPD compared to euthyroid rats before surgical stress; αGPD increased further to 5.9-fold the euthyroid value 1 day after surgery (P < 0.001) to 5.1-fold after 2 days (P < 0.05) and was similar to control after 3 days. Malic enzyme activity increased 10.5-fold before surgical stress and decreased slightly after surgical stress perhaps due to multifactorial regulation of that enzyme. No increases in T₃ nuclear receptor or GH mRNA occurred after surgery in hyperthyroid rats or in any of the above parameters after surgical stress in euthyroid rats. Our findings suggest that increased αGPD after surgical stress in thyrotoxic rats was not due to either increased serum total T₃ or free T₃ or to increased T₃-nuclear receptor complexes. Increased αGPD, therefore, appeared to be a consequence of postreceptor amplification of this thyroidal response.