Maternal high-fat diet (HFD) consumption can promote a systemic inflammatory condition that may impair the offspring brain development, damaging memory and learning, when it reaches the hippocampus. This study aims to evaluate maternal HFD effects, during pregnancy and lactation, upon dams/mice offspring nutritional status, protein and gene expression of inflammatory pathway (JNK, pJNK and TNF-α), serotonin system molecules (Tryptophan Hydroxylase 2 (TPH2), key-enzyme of serotonin synthesis, serotonin transporter (SERT); 5-HT1A serotonergic receptor (5-HT1A)) and brain derived neurotrophic factor (BDNF) on recently weaned mice offspring hippocampus. Female Swiss mice were fed a control diet (CD, 11,5% fat) or a HFD (45.0% fat) from pre-mating to lactation. After weaning, the offspring received CD up to 28 post-natal days (PND28). Body weight and visceral adiposity (retroperitoneal and gonadal adipose tissue) of dams and offspring were measured. After euthanasia, the offspring hippocampus was dissected for evaluations of BDNF, inflammatory pathway and serotonergic system molecules protein and gene expression, through the techniques of Western Blotting, RTqPCR and ELISA. Our findings show that, during pregnancy, HFD-dams and HFD-offspring exhibited an increase in body weight gain and visceral adipose tissue compared to control animals. The hippocampus of HFD-offspring showed increased protein expression of TPH2, BDNF, pJNK and increased mRNA levels of TNF-α. However, the TPH2 increase in HFD-offspring did not alter hippocampal serotonin levels quantified through ELISA. Maternal HFD promoted an obesity phenotype in its offspring with increased body weight and visceral adiposity, increased protein and gene expression of the pro-inflammatory proteins pJNK and TNF-α. These changes were accompanied by increased TPH2 and BDNF protein expression. Thus, our findings show that maternal HFD during gestation and lactation increased pJNK and TNF-α expression in their offspring hippocampus indicating a pro-inflammatory state, with increased BDNF expression and alterations in its serotonergic system reflected by increased TPH2 expression.

母亲食用高脂肪饮食 (HFD) 会促进全身炎症，当它到达海马体时，可能会损害后代的大脑发育，损害记忆和学习。本研究旨在评估母体 HFD 在怀孕和哺乳期间对母鼠/小鼠后代营养状况、炎症途径（JNK、pJNK 和 TNF-α）、血清素系统分子（色氨酸羟化酶 2 (TPH2)、血清素合成的关键酶，血清素转运蛋白 (SERT)；5-HT1A 血清素受体 (5-HT1A)) 和最近断奶小鼠后代海马的脑源性神经营养因子 (BDNF)。从交配前到哺乳期，雌性瑞士小鼠被喂食对照饮食（CD，11.5% 脂肪）或 HFD（45.0% 脂肪）。断奶后，后代接受 CD 至产后 28 天 (PND28)。测量了大坝和后代的体重和内脏脂肪（腹膜后和性腺脂肪组织）。安乐死后，通过Western Blotting、RTqPCR和ELISA技术对后代海马体进行解剖以评估BDNF、炎症通路和5-羟色胺能系统分子蛋白和基因表达。我们的研究结果表明，在怀孕期间，与对照动物相比，HFD-dams 和 HFD-后代表现出体重增加和内脏脂肪组织的增加。HFD 后代的海马显示出 TPH2、BDNF、pJNK 蛋白表达增加和 TNF-α mRNA 水平增加。然而，HFD 后代中 TPH2 的增加并没有改变通过 ELISA 量化的海马血清素水平。母体 HFD 促进其后代的肥胖表型，增加体重和内脏肥胖，增加促炎蛋白 pJNK 和 TNF-α 的蛋白质和基因表达。这些变化伴随着 TPH2 和 BDNF 蛋白表达的增加。因此，我们的研究结果表明，妊娠和哺乳期间母体 HFD 增加了其后代海马中 pJNK 和 TNF-α 的表达，表明其处于促炎状态，BDNF 表达增加，其 5-羟色胺能系统的改变由 TPH2 表达增加反映。