The impact of prenatal exposure to a single dose of testosterone on insulin resistance, glucose tolerance and lipid profile of female rat’s offspring in adulthood

• Published in: Journal of endocrinological investigation Vol. 38; no. 5; pp. 489 - 495
• Main Authors: Noroozzadeh, M., Ramezani Tehrani, F., Sedaghat, K., Godini, A., Azizi, F.
• Format: Journal Article
• Language: English
• Published: Cham Springer International Publishing 01.05.2015
• Subjects: Animals; Blood Glucose - metabolism; Disease Models, Animal; Endocrinology; Female; Insulin Resistance - physiology; Medicine; Medicine & Public Health; Metabolic Diseases; Metabolic Diseases - chemically induced; Metabolic Diseases - metabolism; Original Article; Polycystic Ovary Syndrome - chemically induced; Polycystic Ovary Syndrome - metabolism; Pregnancy; Prenatal Exposure Delayed Effects - chemically induced; Rats; Rats, Wistar; Testosterone - administration & dosage; Testosterone - pharmacology; Metabolic disturbances; Single dose of androgen; Rat model of PCOS; Prenatal androgen exposure
• ISSN: 1720-8386; 1720-8386
• DOI: 10.1007/s40618-014-0198-y

Purpose In our previous study, we introduced a rat model of polycystic ovary syndrome (PCOS) induced by prenatal exposure to a single dose of testosterone on embryonic day 20. In the current study, we aimed to investigate whether prenatal exposure to a single dose of testosterone could also induce metabolic disturbances, especially insulin resistance in adulthood (100–110 days of age) and also to make it as an appropriate rat model of PCOS (exhibiting both reproductive and metabolic disturbances with minimum morphological disorders in reproductive system) for further studies in PCOS. Methods Pregnant rats in the experimental group were subcutaneously injected with 5 mg free testosterone on the gestational day 20, while controls received only the solvent. Female offspring of both groups, prenatally androgenized (PNA) rats (PCOS models of rats) and controls were examined. Results Body weight measures showed significant increase in the PNA rats compared to controls on days 30, 45, 60 of age and in adulthood ( P  < 0.05). PNA rats showed insulin resistance compared to controls. Impaired glucose tolerance was not observed in the PNA rats compared to controls. There were no significant differences in lipid profile between the PNA and control rats ( P  > 0.05). Conclusion Our study suggests that metabolic disturbances in PCOS and their severity during adult life probably depend on the particular time and levels of prenatal androgen exposure.