PITUITARY-THYROID FUNCTION IN THE C57 BL/KSJ DB/DB DIABETIC MOUSE.

Persistent Link:
http://hdl.handle.net/10150/187617
Title:
PITUITARY-THYROID FUNCTION IN THE C57 BL/KSJ DB/DB DIABETIC MOUSE.
Author:
FEHN, RICHARD.
Issue Date:
1983
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
The C57 BL/KsJ db/db mouse is obese, hyperglycemic, hyperinsulinemic and serves as a model for noninsulin dependent diabetes mellitus (NIDDM). This study reports a dysfunction in the pituitary-thyroid axis and apparent peripheral resistence to thyroid hormones due to a reduction in T3 receptor binding. Diabetic mice have subnormal serum T4 concentrations and supranormal T3 concentrations which are most pronounced between 8 and 10 weeks of age. Thyroid glands of diabetic animals appear hypoactive histologically. Serum TSH concentrations approximate those found in normal mice. In vitro studies show that thryroid glands from diabetic animals are responsive to TSH. Pituitary glands from the same animals hypersecrete TSH and are responsive to TRH. Ultrastructural analysis of pituitary thyrotropes from diabetic mice indicate that these cells are hypersecretory and may be under chronic stimulation by TRH. Diet restriction maintains diabetic mice at a normal total body weight but these animals still possess abnormally large fat deposits. The thyroid hormone profile of these mice appears normal as does the histological appearance of the thyroid gland. Similarly, the blockade of peripheral deiodination by daily injection of iopanoic acid returns the thyroid hormone profile to normal.
Type:
text; Dissertation-Reproduction (electronic)
Keywords:
Diabetes -- Research.; Mice -- Physiology.; Pituitary gland.; Thyroid gland.; Thyroid hormones.
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Graduate College
Degree Grantor:
University of Arizona
Advisor:
Chiasson, Robert

Full metadata record

DC FieldValue Language
dc.language.isoenen_US
dc.titlePITUITARY-THYROID FUNCTION IN THE C57 BL/KSJ DB/DB DIABETIC MOUSE.en_US
dc.creatorFEHN, RICHARD.en_US
dc.contributor.authorFEHN, RICHARD.en_US
dc.date.issued1983en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractThe C57 BL/KsJ db/db mouse is obese, hyperglycemic, hyperinsulinemic and serves as a model for noninsulin dependent diabetes mellitus (NIDDM). This study reports a dysfunction in the pituitary-thyroid axis and apparent peripheral resistence to thyroid hormones due to a reduction in T3 receptor binding. Diabetic mice have subnormal serum T4 concentrations and supranormal T3 concentrations which are most pronounced between 8 and 10 weeks of age. Thyroid glands of diabetic animals appear hypoactive histologically. Serum TSH concentrations approximate those found in normal mice. In vitro studies show that thryroid glands from diabetic animals are responsive to TSH. Pituitary glands from the same animals hypersecrete TSH and are responsive to TRH. Ultrastructural analysis of pituitary thyrotropes from diabetic mice indicate that these cells are hypersecretory and may be under chronic stimulation by TRH. Diet restriction maintains diabetic mice at a normal total body weight but these animals still possess abnormally large fat deposits. The thyroid hormone profile of these mice appears normal as does the histological appearance of the thyroid gland. Similarly, the blockade of peripheral deiodination by daily injection of iopanoic acid returns the thyroid hormone profile to normal.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.subjectDiabetes -- Research.en_US
dc.subjectMice -- Physiology.en_US
dc.subjectPituitary gland.en_US
dc.subjectThyroid gland.en_US
dc.subjectThyroid hormones.en_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorChiasson, Roberten_US
dc.contributor.committeememberLee, Stanleyen_US
dc.contributor.committeememberHadley, Macen_US
dc.contributor.committeememberHewlett, Martinezen_US
dc.contributor.committeememberKeck, Konraden_US
dc.identifier.proquest8405496en_US
dc.identifier.oclc690667051en_US
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