Department of Obstetrics and Gynecology, West China Second University Hospital, Chengdu, Sichuan, People's Republic of China; Reproductive Endocrinology and Regulation Laboratory, West China Second University Hospital, Sichuan, People's Republic of China; Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education, China.
Department of Obstetrics and Gynecology, West China Second University Hospital, Chengdu, Sichuan, People's Republic of China; Reproductive Endocrinology and Regulation Laboratory, West China Second University Hospital, Sichuan, People's Republic of China; Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education, China.
Obes Res Clin Pract. 2022 Nov-Dec;16(6):500-506. doi: 10.1016/j.orcp.2022.10.007. Epub 2022 Oct 21.
Maternal exposure to dibutyl phthalate (DBP) may result in obesity in female offspring. However, the underlying mechanisms remain elusive.
Sprague-Dawley rats were intraperitoneally injected with different doses of DBP and corn oil from gestational day 7 until the end of lactation. The weights, visceral fat percentage, serum lipid, insulin and glucose, protein levels of PI3K signal pathway in muscle were detected in F1 female offspring.
Although the birth weight of F1 female offspring was not different among groups, the weights were heavier in DBP groups from postnatal day 7 to adult (P < 0.001). The visceral adipose percentage in adult female offspring was increased by perinatal exposure to DBP (P < 0.001). Decreased serum level of triglyceride (P = 0.001) in F1 female offspring was found in DBP group as compared to control, especially in medium and high DBP. However, none difference was found for fasting glucose, prolactin, HOMA-IR, fasting insulin, total cholesterol, adiponectin. Different protein levels of GPR30 were observed in muscle of female offspring among four groups (P = 0.016). The protein level of AKT seemed higher in DBP group but without statistical significance (P = 0.05). None difference was observed for the protein levels of PI3K, p-AKT, pAKT/AKT, PTEN, GLUT4, InsR, IRS.
Maternal perinatal exposure to DBP might induce obesity and accumulation of visceral adipose tissue for the adult female offspring. Serum glucolipid and local signal transduction of PTEN/PI3K/AKT pathway in muscle were not adversely affected by perinatal exposure to DBP for adult female offspring.
母体暴露于邻苯二甲酸二丁酯(DBP)可能导致雌性后代肥胖。然而,其潜在机制尚不清楚。
从妊娠第 7 天到哺乳期结束,向 Sprague-Dawley 大鼠腹腔内注射不同剂量的 DBP 和玉米油。检测 F1 雌性后代肌肉中 PI3K 信号通路的体重、内脏脂肪百分比、血清脂质、胰岛素和葡萄糖、蛋白质水平。
尽管 F1 雌性后代的出生体重在各组之间没有差异,但从出生后第 7 天到成年,DBP 组的体重更重(P<0.001)。围产期接触 DBP 导致成年雌性后代内脏脂肪百分比增加(P<0.001)。与对照组相比,DBP 组 F1 雌性后代血清甘油三酯水平降低(P=0.001),尤其是中、高剂量 DBP 组。然而,空腹血糖、催乳素、HOMA-IR、空腹胰岛素、总胆固醇、脂联素均无差异。四组雌性后代肌肉中 GPR30 的蛋白水平不同(P=0.016)。DBP 组 AKT 蛋白水平似乎较高,但无统计学意义(P=0.05)。PI3K、p-AKT、pAKT/AKT、PTEN、GLUT4、InsR、IRS 蛋白水平无差异。
母体围产期暴露于 DBP 可能导致成年雌性后代肥胖和内脏脂肪组织堆积。血清糖脂和肌肉中 PTEN/PI3K/AKT 通路的局部信号转导未因围产期接触 DBP 而受到不利影响。