Neurogenesis is a process that occurs throughout the life of a vertebrate. Among the different factors that may affect the natural occurrence of neurogenesis, obesity seems to decrease the proliferation capacity of progenitor neuronal cells. Conversely, the phytoestrogen genistein is known to attenuate some obesity effects beyond its neuroprotective action.

Aiming to improve the understanding of how obesity and genistein trigger an impact on the neural and retinal progenitor competence of adult zebrafish, fish were exposed to genistein (GEN - 2 μg L⁻¹) alone or combined with two dietary groups (control and overfeed - OFD) for up to 9 weeks. Zebrafish were fed once per day with Artemia sp. in the control and GEN (2% of BW, control diet), and three times per day in the OFD and OFD + GEN groups (12% BW, overfeeding diet). To assess obesity induction, BMI, biometric parameters, and PPAR-γ protein were quantified. Afterwards, qRT-PCR and immunohistochemistry were performed to determine the cell proliferation and the presence of stem cells through PCNA and Sox-2. Our findings proved that overfeeding adult zebrafish increased the general growth and induced the development of fatty liver. However, for OFD + GEN, this effect was assuaged through the anti-adipogenic effect of GEN. This finding suggests that phytoestrogens could be beneficial to reduce the negative effects of obesity. Moreover, OF induced negative effects on retinal and brain homeostasis, decreasing the proliferation capacity of progenitor neuronal cells. With regard to retinal progenitor competence, genistein seems to mitigate the negative impacts of obesity, whereas the effects of obesity on the brain were exacerbated by this phytoestrogen which negatively influenced the homeostasis of zebrafish neural progenitor competence. This study highlighted the fact that the effects of phytoestrogens in adult neural progenitor competence are complex and could exhibit dissimilar effects depending on the tissue.

神经发生是一个贯穿脊椎动物一生的过程。在可能影响神经发生自然发生的不同因素中，肥胖似乎会降低祖神经元细胞的增殖能力。相反，已知植物雌激素染料木黄酮可以减轻一些超出其神经保护作用的肥胖效应。

为了加深对肥胖和染料木素如何触发对成年斑马鱼神经和视网膜祖细胞能力的影响的理解，鱼单独或与两个饮食组（对照和过量喂食^- OFD) 长达 9 周。斑马鱼每天喂一次卤虫sp。在对照组和 GEN（2% BW，对照饮食）中，每天 3 次在 OFD 和 OFD + GEN 组（12% BW，过度喂养饮食）。为了评估肥胖诱导，量化了 BMI、生物特征参数和 PPAR-γ 蛋白。之后，进行 qRT-PCR 和免疫组织化学，通过 PCNA 和 Sox-2 确定细胞增殖和干细胞的存在。我们的研究结果证明，过度喂养成年斑马鱼会增加总体生长并诱导脂肪肝的发展。然而，对于 OFD + GEN，这种影响通过 GEN 的抗脂肪形成作用得到缓解。这一发现表明植物雌激素可能有助于减少肥胖的负面影响。此外，OF 对视网膜和大脑稳态产生负面影响，降低祖神经元细胞的增殖能力。关于视网膜祖细胞能力，染料木素似乎减轻了肥胖的负面影响，而这种植物雌激素加剧了肥胖对大脑的影响，这种植物雌激素对斑马鱼神经祖细胞能力的稳态产生了负面影响。这项研究强调了这样一个事实，即植物雌激素对成人神经祖细胞能力的影响是复杂的，并且可能会根据组织表现出不同的影响。