Neonatal stimulation of the thyroid gland with iodine or suppression during adolescence with triiodothyronine changes the prevalence of autoimmune thyroiditis in BB rats.
OBJECTIVE
Changes in the functional state of beta cells by neonatal stimulation or adolescent suppression have reduced the incidence of type 1 diabetes mellitus in animal models. The aim of this study was to evaluate the effect of manipulation of the activity of the thyroid gland by neonatal stimulation or by adolescent suppression on the prevalence of spontaneous autoimmune thyroiditis (AIT) in rats.


METHODS
Bio-Breeding/Worcester (BB) rats were treated neonatally with sodium iodine (NaI) or thyroid stimulating hormone (TSH), or during adolescence by triiodothyronine (T(3)), and the lymphocytic infiltration in the thyroid gland was evaluated.


RESULTS
Neonatal treatment with NaI decreased the prevalence of AIT to 32+/-9% compared with 66+/-5% in the controls (P<0.002), mainly caused by a reduction among the female rats (13+/-9% vs 52+/-8%, P<0.006). TSH had no effect. Post neonatal suppression of the thyroid gland by T(3) had a biphasic response. Early in adolescence the overall prevalence was 14+/-7% compared with 66+/-5% in the controls (P<10(-5)); for female rats AIT was prevented (0+/-0%) compared with 52+/-8% in the controls (P<0.0003) and in male rats the values were 29+/-13% compared with 80+/-6% in the controls (P<0.001). Treatment with T(3) later in adolescence increased the overall prevalence to 81+/-7% compared with 66+/-5% in the controls (not significant). For female rats the prevalence increased to 78+/-9% compared with 52+/-8% in the controls (P=0.04). The degree of thyroiditis among the affected animals was similar in all groups.


CONCLUSIONS
Neonatal stimulation of the thyroid gland by iodine or early adolescent suppression by T(3) reduced the prevalence of AIT whereas T(3) given later increased the prevalence of thyroiditis in rats. Thyroid activity at various ages seems to be of importance for the development of autoimmune thyroiditis.
Hartoft-Nielsen
M-L
ML
Department of Endocrinology PE-2131, Copenhagen University Hospital, Copenhagen, Denmark. ma-lars@dadlnet.dk
Rasmussen
A K
AK
Kaas
A
A
Feldt-Rasmussen
U
U
Buschard
K
K
D000367:Age Factors; D000818:Animals; D000831:Animals, Newborn; D001835:Body Weight; D005260:Female; D008297:Male; D015995:Prevalence; D051381:Rats; D011919:Rats, Inbred Strains; D012974:Sodium Iodide / Q000494:pharmacology*; D013961:Thyroid Gland / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D013967:Thyroiditis, Autoimmune / Q000453:epidemiology* / Q000209:etiology / Q000473:pathology; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000494:pharmacology*
D014284:Triiodothyronine; D013972:Thyrotropin; D012974:Sodium Iodide; D013974:Thyroxine