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Overview of Structural and Functional Lesions in Endocrine Organs of Animals

Charles C. Capen

Department of Veterinary Biosciences, The Ohio State University, Columbus, Ohio 43210, capen.2{at}osu.edu

The objective of this review is to summarize the pathogenic mechanisms responsible for perturbations of endocrine function and development of structural lesions that result in important diseases in domestic and laboratory animals. For each major category, several specifi c disease problems have been selected to illustrate the functional and morphologic lesions that are characteristic for either a naturally occurring endocrinopathy or endocrine disturbances induced by the administration of large doses of xenobiotic chemicals. The major pathogenic mechanisms responsible for disruption of endocrine function include primary hyperfunction, secondary hyperfunction, primary hypofunction, secondary hypofunction, endocrine hyperactivity secondary to other conditions, hypersecretion of hormones by nonendocrine tumors, failure of target cells to respond to a hormone, failure of fetal endocrine function, abnormal degradation (increased or decreased rate) of hormone, and iatrogenic syndromes of hormone excess (direct and indirect). Disorders of the endocrine system are encountered in a wide variety of domestic and laboratory animal species and often present challenging diagnostic problems. The development of proliferative lesions, usually hyperplasia and benign tumors, in endocrine organs and hormone-responsive tissues are common findings in chronic studies with high doses of many nongenotoxic xenobiotic chemicals administered to sensitive rodent species and may have limited significance for human safety assessment.

Key Words: Endocrine lesions • hormonal imbalances • hyperthyroidism • hyperparathyroidism • congenital goiter • hypothyroidism • panhypopituitarism • testicular Leydig cell adenomas • tubulostromal tumors of ovary • humoral hypercalcemia of malignancy • parathyroid hormone—related protein • prolonged gestation • hormone degradation • iatrogenic syndromes of hormone excess

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Toxicologic Pathology, Vol. 29, No. 1, 8-33 (2001)
DOI: 10.1080/019262301301418829
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K. P. Keenan, C.-M. Hoe, L. Mixson, C. L. Mccoy, J. B. Coleman, B. A. Mattson, G. A. Ballam, L. A. Gumprecht, and K. A. Soper
Diabesity: A Polygenic Model of Dietary-Induced Obesity from Ad Libitum Overfeeding of Sprague-Dawley Rats and Its Modulation by Moderate and Marked Dietary Restriction
Toxicol Pathol, October 1, 2005; 33(6): 650 - 674.
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Y. Tani, R. R. Maronpot, J. F. Foley, J. K. Haseman, N. J. Walker, and A. Nyska
Follicular Epithelial Cell Hypertrophy Induced by Chronic Oral Administration of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin in Female Harlan Sprague--Dawley Rats
Toxicol Pathol, January 1, 2004; 32(1): 41 - 49.
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G. M. Williams and M. J. Iatropoulos
Alteration of Liver Cell Function and Proliferation: Differentiation Between Adaptation and Toxicity
Toxicol Pathol, January 1, 2002; 30(1): 41 - 53.
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R. T. Miller, L. A. Scappino, S. M. Long, and J. C. Corton
Role of Thyroid Hormones in Hepatic Effects of Peroxisome Proliferators
Toxicol Pathol, January 1, 2001; 29(1): 149 - 155.
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