Venci Renan de Oliveira, Ramos Gabriel Bortoli, Martins Isabela Peixoto, Matiusso Camila Cristina Ianoni, Saavedra Lucas Paulo Jacinto, Ribeiro Tatiane Aparecida, Pavanello Audrei, Prates Kelly Valério, Tófolo Laize Peron, Moraes Ana Maria Praxedes de, Fabricio Gabriel Sergio, de Oliveira Júlio Cezar, Franco Claudinéia Conationi da Silva, Palma-Rigo Kesia, Mathias Paulo Cezar de Freitas, Malta Ananda
Laboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil.
Institute of Health Sciences, Federal University of Mato Grosso, Sinop, Brazil.
Nutr Neurosci. 2020 Jun;23(6):432-443. doi: 10.1080/1028415X.2018.1516845. Epub 2018 Sep 6.
We aimed to assess the effects of a maternal protein-caloric restriction diet during late pregnancy on the metabolism of rat offspring fed a high-fat diet (HFD) during adulthood. During late pregnancy, rat dams received either a low-protein (4%; LP group) or normoprotein (23%; NP group) diet. After weaning, the offspring were fed a standard diet (Control; C). Male offspring (60 days old) from both groups were then fed either the C diet or HFD until they were 90 days old. The adult offspring and maternal metabolic parameters and autonomic nervous system (ANS) were then evaluated. Dams exhibited low body weight gain and food intake during the LP diet consumption. At lactation, these dams showed high body weight gain, hypoinsulinemia and hyperglycemia. The maternal LP diet resulted in low body weights for the pups. There were also no differences in the metabolic parameters between the adult LP offspring that were fed the C diet and the NP group. Adults of both groups that were fed the HFD developed obesity associated with altered insulin/ glucose homeostasis and altered ANS activity; however, the magnitudes of these parameters were higher in the LP group than in the NP group. Maternal protein malnutrition during the last third of pregnancy malprograms the metabolism of rat offspring, resulting in increased vulnerability to HFD-induced obesity, and the correlated metabolic impairment might be associated with lower sympathetic nerve activity in adulthood.
我们旨在评估妊娠晚期母体蛋白质 - 热量限制饮食对成年后喂食高脂饮食(HFD)的大鼠后代代谢的影响。在妊娠晚期,大鼠母鼠分别接受低蛋白(4%;LP组)或正常蛋白(23%;NP组)饮食。断奶后,后代喂食标准饮食(对照组;C)。然后,两组的雄性后代(60日龄)分别喂食C饮食或HFD直至90日龄。随后评估成年后代和母体的代谢参数以及自主神经系统(ANS)。母鼠在食用LP饮食期间体重增加和食物摄入量较低。在哺乳期,这些母鼠体重增加高,出现低胰岛素血症和高血糖症。母体LP饮食导致幼崽体重低。喂食C饮食的成年LP后代与NP组之间的代谢参数也没有差异。两组喂食HFD的成年大鼠均出现与胰岛素/葡萄糖稳态改变和ANS活性改变相关的肥胖;然而,这些参数的变化幅度在LP组高于NP组。妊娠最后三分之一期间母体蛋白质营养不良会使大鼠后代的代谢编程异常,导致对HFD诱导的肥胖易感性增加,并且相关的代谢损害可能与成年期较低的交感神经活动有关。