Obesity Triggers Dysregulation of Essential ABC Transporters in Rat Testis and Sperm.
Source: PubMed, NCBI / U.S. National Library of Medicine
Obesity and the associated metabolic dysfunction influence fertility performance at molecular levels and ABC transporters are considered as potential molecular factors affecting fertility both in the testis and sperm; therefore, we aimed to examine the effect of a short-term diet-induced obesity on testicular and spermatic ABC transporters in a rat model focusing on the expressions of P-glycoprotein (P-gp, Abcb1) and breast cancer resistance protein (BCRP, Abcg2). The testicular androgen state involving aromatase enzyme (), androgen receptor (), and testosterone levels were also evaluated.Obesity was induced in male Sprague Dawley rats by feeding a high-fat, high-sugar diet (HFHSD) for 10 weeks, and metabolic status was evaluated using a glucose tolerance test. The weight and size of reproductive organs were measured, and Abcb1a/1b, Abcg2,, andexpression in testes or sperm was determined by RT-PCR and Western blotting. At the same time, testosterone levels were measured by ELISA.HFHSD successfully induced higher weight gain with glucose intolerance and reduced reproductive organ size. In obese rats, testicularandmRNA and P-gp protein expression were significantly higher, whereas testicularmRNA levels decreased. Spermatic,andmRNA expression also reduced in obesity. Neither testicular testosterone concentration norandmRNA expression levels changed after the 10-week obesogenic diet compared with controls.Overall, our study revealed infertility-related ABC transporter changes in
Abstract
Obesity and the associated metabolic dysfunction influence fertility performance at molecular levels and ABC transporters are considered as potential molecular factors affecting fertility both in the testis and sperm; therefore, we aimed to examine the effect of a short-term diet-induced obesity on testicular and spermatic ABC transporters in a rat model focusing on the expressions of P-glycoprotein (P-gp, Abcb1) and breast cancer resistance protein (BCRP, Abcg2). The testicular androgen state involving aromatase enzyme (), androgen receptor (), and testosterone levels were also evaluated.Obesity was induced in male Sprague Dawley rats by feeding a high-fat, high-sugar diet (HFHSD) for 10 weeks, and metabolic status was evaluated using a glucose tolerance test. The weight and size of reproductive organs were measured, and Abcb1a/1b, Abcg2,, andexpression in testes or sperm was determined by RT-PCR and Western blotting. At the same time, testosterone levels were measured by ELISA.HFHSD successfully induced higher weight gain with glucose intolerance and reduced reproductive organ size. In obese rats, testicularandmRNA and P-gp protein expression were significantly higher, whereas testicularmRNA levels decreased. Spermatic,andmRNA expression also reduced in obesity. Neither testicular testosterone concentration norandmRNA expression levels changed after the 10-week obesogenic diet compared with controls.Overall, our study revealed infertility-related ABC transporter changes in obese male rats, suggesting that these alterations may predispose obese males to fertility impairments, even before the obesity-induced androgen dysregulation.