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Pathophysiological differences between obese and non-obese spontaneously hypertensive rats

B C Wexler, S G Iams, J P McMurtry

    British Journal of Experimental Pathology
    |April 1, 1980
    PubMed
    Summary

    A new genetic rat model, Obese/SHR, exhibits obesity, hypertension, and diabetes, mirroring human Cushing's disease. This model shows hormonal imbalances and cardiovascular issues, offering insights into metabolic and endocrine disorders.

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    Area of Science:

    • Endocrinology
    • Cardiovascular Research
    • Genetics

    Background:

    • Spontaneously Hypertensive Rats (SHR) are a model for hypertension.
    • A genetic variant, Obese/SHR, exhibits both obesity and hypertension.
    • Obese/SHR present with metabolic and cardiovascular abnormalities.

    Purpose of the Study:

    • To characterize the Obese/SHR rat model.
    • To investigate the physiological and hormonal profiles of Obese/SHR.
    • To compare Obese/SHR to non-obese cohorts and standard SHR.

    Main Methods:

    • Phenotypic characterization of Obese/SHR.
    • Biochemical analysis of serum enzymes, lipids, glucose, and hormones (corticosterone, DOC, aldosterone, prolactin, insulin, growth hormone).
    • Histopathological examination of liver, pancreas, and kidneys.

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    Main Results:

    • Obese/SHR are significantly heavier (800g vs 300g) with elevated serum enzymes, myocardial necrosis, hyperlipidaemia, fatty liver, hyperglycaemia, enlarged islets, and beta-cell degranulation.
    • Despite elevated blood urea nitrogen (BUN), renal damage is minimal.
    • Obese/SHR show hyper-responsiveness to stress in corticosterone, DOC, aldosterone, and prolactin levels, alongside hyperinsulinaemia and subnormal growth hormone.
    • Vascular pathology includes early polyarteritis nodosa, but no atheromatous changes.

    Conclusions:

    • The Obese/SHR model displays a complex metabolic and endocrine phenotype resembling human Cushing's disease.
    • Genetically programmed hypertension and hyperglycaemia are linked to increased deoxycorticosterone (DOC), aldosterone, and corticosterone.
    • This model provides a valuable tool for studying the interplay of obesity, hypertension, diabetes, and hormonal dysregulation.