Reproductive Biology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
CONACyT-Cátedras, Reproductive Biology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
J Physiol. 2019 Dec;597(23):5549-5563. doi: 10.1113/JP278232. Epub 2019 Nov 11.
Maternal obesity predisposes to metabolic dysfunction in male and female offspring Maternal high-fat diet consumption prior to and throughout pregnancy and lactation accelerates offspring metabolic ageing in a sex-dependent manner This study provides evidence for programming-ageing interactions ABSTRACT: Human epidemiological studies show that maternal obesity (MO) shortens offspring life and health span. Life course cellular mechanisms involved in this developmental programming-ageing interaction are poorly understood. In a well-established rat MO model, female Wistar rats ate chow (controls (C)) or high energy, obesogenic diet to induce MO from weaning through pregnancy and lactation. Females were bred at postnatal day (PND) 120. Offspring (F ) of mothers on control diet (CF ) and MO diet (MOF ) delivered spontaneously at terms. Both CF and MOF ate C diet from weaning throughout the study. Offspring were killed at PND 36, 110, 450 and 650. We determined body and liver weights, liver and serum metabolite concentrations, hormones and oxidative stress biomarkers. Male and female CF body weight, total fat, adiposity index, serum leptin, insulin, insulin resistance, and liver weight, fat, triglycerides, malondialdehyde, reactive oxygen species and nitrotyrosine all rose with differing ageing trajectories. Female CF triglycerides were unchanged with age. Age-related increases were greater in MOF than CF in both sexes for all variables except glucose in males and females and cholesterol in males. Cholesterol fell in CF females but not MOF . Serum corticosterone levels were higher in male and female MOF than CF and declined with age. DHEA serum levels were lower in male and female MOF than CF . Liver antioxidant enzymes decreased with age (CF and MOF ).
exposure to the developmental challenge of MO accelerates progeny ageing metabolic and endocrine profiles in a sex specific manner, providing evidence for programming-ageing interactions.
母体肥胖使雄性和雌性后代易发生代谢功能障碍。
在妊娠和哺乳期之前和期间，母体高脂肪饮食的消耗会以性别依赖的方式加速后代的代谢衰老。
本研究为编程衰老相互作用提供了证据。
人体流行病学研究表明，母体肥胖（MO）会缩短后代的寿命和健康寿命。
在一个成熟的大鼠 MO 模型中，雌性 Wistar 大鼠从断奶到妊娠和哺乳期一直吃高能量、肥胖诱导的饮食来诱导 MO。
雌性在产后第 120 天繁殖。
来自控制饮食（CF）和 MO 饮食（MOF）母亲的后代（F）在足月时自然分娩。
出生后，CF 和 MOF 均从断奶开始一直吃 C 饮食。
在 PND36、110、450 和 650 处死后代。
测定体重和肝脏重量、肝脏和血清代谢物浓度、激素和氧化应激生物标志物。
雄性和雌性 CF 的体重、总脂肪、肥胖指数、血清瘦素、胰岛素、胰岛素抵抗以及肝脏重量、脂肪、甘油三酯、丙二醛、活性氧和硝基酪氨酸均随着不同的衰老轨迹而增加。
雌性 CF 的甘油三酯随年龄而增加。
MOF 的所有变量均高于 CF，除了雄性和雌性的葡萄糖和雄性的胆固醇。
CF 女性的胆固醇下降，但 MOF 女性的胆固醇没有下降。
血清皮质酮水平在 MOF 男性和女性中高于 CF，且随年龄下降。
DHEA 血清水平在 MOF 男性和女性中低于 CF。
肝脏抗氧化酶随年龄而下降（CF 和 MOF）。
