Experimentally induced metabolic syndrome in rats: the pathogenesis of the development of benign prostatic hyperplasia and urination disorders

Introduction. Benign prostatic hyperplasia and associated diseases develop significantly more often in patients with metabolic syndrome (MS) in comparison with a general male population of the same age. The pathogenesis of these conditions requires a special research. Materials and methods. MS was modelled using 10 white thoroughbred male rats kept on hypercaloric feeding (with the excess of fats and carbohydrates) during three months. 10 intact rats constituted a control group. Histological examination of the prostate and the urinary bladder and determination of blood levels of insulin, androgens and estrogens, and prostate tissue androgens and estrogens was performed. Functional condition of the urinary bladder was analyzed by Fourier transform impedancemetry coupled with infusion cystometry. Results. The development of MS was confirmed by the data obtained from biochemical tests of blood and urine which have identified the development of glycaemia, glycosuria, triglyceridemia, hyperuricemia, increase in uric acid excretion and disrupted ratio of cholesterol derived from high-density and low-density lipoproteins. Increased body weight and prostate was found in rats with MS in comparison with the control group. Histological examination has confirmed the development of glandular and stromal forms of benign prostatic hyperplasia and had found detrusor hypertrophy in 60% of rats which was the evidence for urination difficulties. Infusion cystometry has identified the signs of detrusor hyperactivity. A study on the blood supply of the prostate and urinary bladder by conducting Fourier transform impedancemetry has revealed a significant impairment of microcirculation in both organs. The levels of testosterone and dihydrotestosterone has lowered in the blood but their concentration has significantly increased in prostate tissue of mice with MS. The level of estradiol in the blood of mice with MS was below the norm, which has led to an increased androgens/estrogens ratio. Hyperglycemia was combined with an increase in serum insulin concentration, which indicated a development of insulin resistance. Conclusion. The increase in the concentration of androgens in prostate tissue, chronic pelvic ischemia and development of insulin resistance play a major role in the pathogenesis of benign prostatic hyperplasia associated with metabolic syndrome. Urinary bladder dysfunction might be accounted by its chronic ischemia.