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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mild cold exposure (22 degrees C, with reference to 28 degrees C, thermoneutral) was studied by overnight whole-body indirect calorimetry in euthyroid women. Basal, sleeping, energy expenditure (EE) was significantly increased (+3.8%, P less than 0.05) in six normal weight women but reduced (-3.5%, P less than 0.05) in five obese type II diabetic women. Mixed responses were found in five women with simple obesity. Biochemical measurements were made on fasting blood samples taken at 0900 h after 12 h exposure to the two temperatures. Serum T4, free T3 and TSH were within the normal reference range in all subjects. Serum T4 did not show any differences between the groups, nor any effect from temperature. There was a significant increase in free T3 (P less than 0.05) at 22 degrees C in the control subjects, but no differences in the obese diabetic women. Serum thyroglobulin fell significantly in the diabetic group. Both TSH and free T3 responses to mild cold were significantly different between the groups, but both correlated positively (P less than 0.05) with the changes in sleeping energy expenditure at 22 degrees C with reference to 28 degrees C. Changes in TSH and free T3 were themselves significantly correlated within individuals (P less than 0.01). The normal physiological non-shivering thermogenesis of adult humans on exposure to a cool environment may thus be mediated by a pituitary-thyroid mechanism. The abnormal response of obese diabetic women was associated with impaired TSH and thyroid hormone responses, and may be a factor contributing to weight gain.
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PMID:Metabolic and thyroidal responses to mild cold are abnormal in obese diabetic women. 325 62

Cornell Obese (OS) (B13B13), Special C (Sp.C) (B13B13) and K-strain White Leghorn chickens (B15B15) were examined for both naturally occurring and induced autoantibodies directed against erythroid fetal antigens. Obese chickens have been reported to produce high levels of autoantibodies to thyroglobulin and to occasionally produce antinuclear autoantibodies specific for erythrocytes. Despite producing high levels of antithyroglobulin autoantibodies and antibodies cross-reactive with erythrocytes, no OS chickens were found to possess naturally occurring autoantibodies to fetal-specific antigens on erythrocytes. However, such antibodies were induced following immunization with fetal erythrocytes derived from a strain allogeneic for the major histocompatibility complex (MHC), the B-complex. Challenge with both intact erythrocytes and erythroid membranes in Freund's complete adjuvant resulted in production of antibodies specific for fetal antigens. The ability to induce autoantibodies to fetal erythrocytes was not restricted to the OS-strain; similar antibodies were detected in the Cornell K-strain and Special C-strain chickens even when intrastrain immunizations were employed. These results suggest that antibodies can be induced to fetal antigens on chicken erythrocytes in both autoimmune and normal chickens given the appropriate antigen presentation.
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PMID:Induced autoantibodies to fetal erythroid antigens in the chicken. 369 24

In Obese strain (OS) chickens the role of maternal antibodies, passively transferred through the egg to the developing chick, was evaluated as a causative factor in the early development of spontaneous autoimmune thyroiditis (SAT). In the egg, passive antibody titers were highest in the yolk and lower in the allantoic fluid and sera of developing embryos. This passage of antibodies was documented by use of radiolabeled antibodies. In dams with high antibody titers, antibodies could be found in the sera of chicks at the time of hatch. Thyroglobulin was absent in the yolk of OS eggs during embryonal life, as compared with its detection in normal eggs. Immune complexes (thyroglobulin-autoantibody) detected in the thyroids of OS, but not CS, chicks at the time of hatch, or earlier, appear to reflect the presence of the maternally transferred antibodies. A pair of crosses between OS chickens, with thyroiditis, and the C strain (CS), without thyroiditis, was made to evaluate the role of transferred antibodies in the pathogenesis of autoimmune disease. When an OS chicken was the dam, maternal antibodies could be passively transferred; when a CS chicken was the dam, no maternal antibodies were present to be transferred. Nevertheless, both hybrids developed full-blown thyroiditis, demonstrating that binding of transferred maternal antibody to thyroglobulin is not a prerequisite for the induction of SAT. However, presence of maternal antibodies precipitated the onset of disease. Immune complexes formed in the embryonic thyroid are likely to participate in early autoimmune disease, although the development of full-blown thyroiditis may await the competency of the chick's immune system to provide the characteristic cellular infiltrate.
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PMID:Materno-embryonally transferred antibodies precipitate autoimmune thyroiditis in obese strain (OS) chickens. 372 17

This report reveals a surprisingly high incidence of thyroid hormone (T3 and T4) autoantibodies (THA) and thyroglobulin autoantibodies in a closed flock of untreated Cornell strain (CS) White Leghorn chickens. This flock is closely related to the Obese strain chicken, which develops a severe spontaneous autoimmune thyroiditis. A sensitive electrophoretic autoradiographic assay for THA was developed. This assay was applied to the study of autoantibodies to T3 and T4 in the sera of adult female CS chickens. Of 109 females, 29.4% had antibodies to T3 and 18.4% had antibodies to T4. The incidence of thyroglobulin antibodies, determined by passive hemagglutination, was 15.6%. The presence of THA affected RIA measurements because serum T3 and T4 hormone concentrations appeared elevated in those birds with moderate to high antibody levels. There was major variance in the electrophoretic heterogeneity of the THA from individual chickens; i.e., some of the sera contained antibodies to T3 or T4 that appeared to be monoclonal, whereas other sera exhibited polyclonal multi-banded patterns. To determine if antibodies reactive with T3 and T4 (which are haptens) were generated by antibody responses to the T3/T4 sites on the thyroglobulin molecule, competitive binding assays were performed to determine the relative binding affinities of the antibodies for the haptens (T3/T4) and the "hapten-conjugate" (thyroglobulin). In these assays, thyroglobulin competed with the haptens, thus supporting the above hypothesis.
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PMID:Analysis of triiodothyronine and thyroxine-binding autoantibodies in chickens susceptible to autoimmune thyroiditis. 398 98

Obese strain chickens develop severe spontaneous autoimmune thyroiditis several weeks after hatching, characterized by mononuclear cell infiltration and antibodies to thyroglobulin (Tg). The presence of antibodies to Tg suggests that Tg is an important antigen in this disease, but it does not provide definitive evidence. To clarify this point, Obese strain chicks were tolerized at hatching with Tg and then examined up to 6 wk later for antibodies to Tg, thyroid pathology, and function. Various tolerance regimens were tested. The optimal conditions were i.v. injection of Tg within 24 hr of hatching, and injection of at least 1 mg. Tg isolated from normal thyroid glands was satisfactory, and it did not have to be deaggregated. Tolerance induced by the above procedure significantly retarded all parameters of autoimmunity, although by 6 wk of age some of the tolerized chicks had severe thyroiditis. Multiple weekly injections of Tg were no more effective than a single injection at hatching. Interestingly, a single injection at hatching was very effective, yet it was cleared from the circulation within 24 hr. In summary, tolerance induced with Tg had a profound effect on the disease and thus provides good evidence for the role of Tg in this disease.
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PMID:The induction of tolerance to thyroglobulin significantly reduces the severity of thyroiditis in obese strain chickens. 399 65

The effects of dietary thyroxine (T4) supplementation for specific periods on the early development of the primary lymphoid organs and spontaneous autoimmune thyroiditis (SAT) was examined in the Obese (OS) strain of chicken. Effects of the treatments on concentrations of serum growth hormone (GH) and testosterone were also determined. All treatment groups were examined at 6 weeks. T4 supplementation did not affect serum testosterone or GH concentrations. However T4 given for the first three weeks resulted in significantly increased bursa weights, no change in thymic weights, significantly decreased lymphoid infiltration of the thyroid and reduced thyroglobulin autoantibody levels (TgAAb). T4 supplementation for the full six weeks resulted in no change in bursal weight, significantly increased thymic weight, significantly decreased lymphoid infiltration of the thyroid, and reduced TgAAb. These results suggest that the effects of T4 supplementation on SAT and immune development are dependent on the interval during which it is administered and that testosterone and GH probably do not mediate these effects.
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PMID:Differential effects of thyroxine on immune development and autoimmune thyroiditis in the obese strain chicken. 404 83

In this study we investigated the genetic background of primary abnormalities found in the thyroid gland of Obese strain (OS) chickens with spontaneous autoimmune thyroiditis (SAT), i.e., susceptibility to passively transferred antibodies to thyroglobulin (TgAb) and incomplete suppression of iodine uptake by thyroxine (T4). Several crosses between the B15/B15 subline of OS chickens and the inbred CB line (B12/B12) were done and the progeny was analyzed for thyroiditis after injection of OS serum containing high titers of TgAb. It was found that passive transfer of TgAb increased the lymphoid infiltration in the thyroids of OS chickens, but had no effect on CB birds. A genetic analysis of backcrosses revealed that this trait is, in the case of simple Mendelian inheritance, encoded by at least three recessive genes. The thyroidal 131I uptake of these crosses under T4 was also determined and we found that this trait is most probably encoded by only one recessive gene.
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PMID:Spontaneous autoimmune thyroiditis in obese strain chickens: a genetic analysis of target organ abnormalities. 405 27

Obese strain chickens develop circulating autoantibodies to thyroglobulin and lymphocytic infiltration of their thyroids during aging. Two alleles, B(1) and B(4), are found with high gene frequency at the major histocompatibility (B) locus. Greater pathology and higher antibody titers are observed in B(1)B(1) and B(1)B(4) birds than in their B(4)B(4) siblings.
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PMID:Relation between the major histocompatibility (B) locus and autoimmune thyroiditis in obese chickens. 441 30

This study demonstrates immune complexes in thyroid glands of Obese strain (OS) chickens, that consist of thyroglobulin (Tg) and antibodies to Tg. In IIF tests it was shown that these complexes fix complement with an age-dependent increase from 12% in 19-day-old embryos up to 100% in 6-week-old animals. This finding and the observation that the deposition of complement-binding immune complexes precede cellular infiltration of the thyroid gland and correlate with the serum titer of Tg-Ab (as one parameter of the disease) points towards a role as one initial effector mechanism for the development of spontaneous autoimmune thyroiditis (SAT).
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PMID:Immunofluorescence studies on the codistribution immune deposits and complement in the thyroid glands of Obese strain (OS) chickens. 622 80

In addition to thyroglobulin autoantibodies, some Obese strain (OS) chickens gave organ-specific reactions with the cytoplasm of thyroid acinar cells when the sera were tested by immunofluorescence. The staining pattern was similar to that seen with human antibodies to thyroid microsomes. A proportion stained the proventricular glands of the chicken stomach in a manner indistinguishable from that of pernicious anaemia sera containing parietal cell antibodies. Isolated examples of organ-specific reactions with adrenal and exocrine pancreas were also recorded. These findings strengthen the notion that the OS chicken represents an authentic model for human organ-specific autoimmune disease. The high incidence of non-organ specific reactions complicates but does not necessarily invalidate this view since normal chickens show a propensity to develop such antibodies. However the OS chicken appears to differ from the human in being hyper-responsive to antigens in general.
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PMID:Predisposition to organ-specific autoimmunity in Obese strain (OS) chickens: reactivity to thyroid, gastric, adrenal and pancreatic cytoplasmic antigens. 675 35


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