Instituto de Biofísica Carlos Chagas Filho,Universidade Federal do Rio de Janeiro,RJ,Brazil.
Instituto de Bioquímica Médica Leopoldo de Meis,Universidade Federal do Rio de Janeiro,RJ,Brazil.
Br J Nutr. 2019 Jun;121(12):1345-1356. doi: 10.1017/S0007114519000771. Epub 2019 Apr 3.
Perinatal maternal high-fat diet (HFD) increases susceptibility to obesity and fatty liver diseases in adult offspring, which can be attenuated by the potent hypolipidaemic action of fish oil (FO), an n-3 PUFA source, during adult life. Previously, we described that adolescent HFD offspring showed resistance to FO hypolipidaemic effects, although FO promoted hepatic molecular changes suggestive of reduced lipid accumulation. Here, we investigated whether this FO intervention only during the adolescence period could affect offspring metabolism in adulthood. Then, female Wistar rats received isoenergetic, standard (STD: 9 % fat) or high-fat (HFD: 28·6 % fat) diet before mating, and throughout pregnancy and lactation. After weaning, male offspring received the standard diet; and from 25 to 45 d old they received oral administration of soyabean oil or FO. At 150 d old, serum and hepatic metabolic parameters were evaluated. Maternal HFD adult offspring showed increased body weight, visceral adiposity, hyperleptinaemia and decreased hepatic pSTAT3/STAT3 ratio, suggestive of hepatic leptin resistance. FO intake only during the adolescence period reduced visceral adiposity and serum leptin, regardless of maternal diet. Maternal HFD promoted dyslipidaemia and hepatic TAG accumulation, which was correlated with reduced hepatic carnitine palmitoyl transferase-1a content, suggesting lipid oxidation impairment. FO intake did not change serum lipids; however, it restored hepatic TAG content and hepatic markers of lipid oxidation to STD offspring levels. Therefore, we concluded that FO intake exclusively during adolescence programmed STD offspring and reprogrammed HFD offspring male rats to a healthier metabolic phenotype in adult life, reducing visceral adiposity, serum leptin and hepatic TAG content in offspring adulthood.
围产期母体高脂肪饮食（HFD）会增加成年后代肥胖和脂肪肝疾病的易感性，而鱼油（FO）作为 n-3PUFA 的来源，在成年期具有强大的降血脂作用，可以减轻这种易感性。此前，我们描述了青春期 HFD 后代对 FO 降血脂作用表现出抵抗，尽管 FO 促进了肝脏分子变化，提示脂质积累减少。在这里，我们研究了仅在青春期进行 FO 干预是否会影响成年后代的代谢。然后，雌性 Wistar 大鼠在交配前、怀孕期间和哺乳期接受等热量、标准（STD：9%脂肪）或高脂肪（HFD：28.6%脂肪）饮食。断奶后，雄性后代接受标准饮食；从 25 到 45 天龄，他们接受口服大豆油或 FO。在 150 天龄时，评估血清和肝脏代谢参数。母体 HFD 成年后代表现出体重增加、内脏肥胖、高瘦素血症和肝 pSTAT3/STAT3 比值降低，提示肝瘦素抵抗。仅在青春期摄入 FO 可减少内脏肥胖和血清瘦素，而与母体饮食无关。母体 HFD 促进血脂异常和肝 TAG 积累，这与肝肉碱棕榈酰转移酶-1a 含量减少有关，提示脂质氧化受损。FO 摄入不会改变血清脂质；然而，它恢复了肝 TAG 含量和肝脂质氧化标志物，使其达到 STD 后代的水平。因此，我们得出结论，仅在青春期摄入 FO 可使 STD 后代程序化，并使 HFD 后代雄性大鼠在成年期向更健康的代谢表型转变，减少成年后代的内脏肥胖、血清瘦素和肝 TAG 含量。
