Abnormal Thyroid Regulation in Chickens with Autoimmune Thyroiditis*

Abstract

The obese strain of chicken (OS) in which virtually all individuals spontaneously develop autoimmune thyroiditis was developed by selection from the Cornell strain (CS). Lymphocytes start infiltrating the thyroid gland 1 week after hatching. One possibility explaining this infiltration postulates preexisting abnormalities or defects of the target organ. The present study examines one parameter of thyroid function, uptake of ¹³¹I^- under conditions in which TSH secretion is minimized. This was accomplished by supplementation of feed with T₄ from hatching until sacrifice. Serum T₄ levels were monitored by RIA. Twenty-hour thyroidal iodide uptakes were determined at autopsy by counting the radioactivity in the extirpated thyroid lobes. Dietary T₄ supplementation increased serum T₄ levels many times above normal. This drastically decreased thyroid function in four normal chicken strains; thyroidal uptake of ¹³¹I^- was suppressed 97.5-99.2%. OS chickens were incompletely suppressed; mean values ranged between 80.9-94.2% suppression. CS chickens were the most poorly suppressible, with values ranging between 62.3-68.5%. The incomplete suppression of the OS and CS is probably not due to a thyroid-stimulating immunoglobulin, since pretreatment with cyclophosphamide had no effect on thyroid suppression. An analysis of the intrathyroidal coupling reaction to form iodothyronines from iodotyrosines likewise revealed a marked resistance to suppression induced by T₄ feeding in the OS and CS chickens. Thus, the OS chicken and its progenitor CS strain have an abnormality of thyroid function reflected by significant thyroidal uptakes and iodotyrosine coupling in the presence of serum T₄ levels which are adequate for suppression in control chickens. The poor suppressibility is not likely due to persistent TSH secretion by the pituitary, since OS and CS chickens have normal serum and thyroidal T₄ and T₃ values on a regular feed. An abnormality of the thyroid gland is more likely to cause this dysfunction.