• Simone Ferreira Lemes, Anelise Cristina Parras de Souza, Tanyara Baliani Payolla, Milena Diorio Versutti, Albina de Fátima da Silva Ramalho, Cristiano Mendes-da-Silva, Camilla Mendes Souza, Marciane Milanski, Adriana Souza Torsoni, and Marcio Alberto Torsoni.
• Institute of Biology, University of Campinas, Campinas, Sao Paulo 13083-862, Brazil; Laboratory of Metabolic Disorders, School of Applied Sciences, University of Campinas, Sao Paulo 13484-350, Brazil.
• Neuroscience. 2018 Feb 10; 371: 1-15.

AbstractStudies show that maternal consumption of a high-fat diet (HFD) can impair the formation of hypothalamic neuronal circuits in mouse offspring. This damage can be mediated by Notch1/Hes5 signaling activation, leading to repression of proneural factors such as Mash1 and Ngn2/3, which are essential for neuronal differentiation and neurogenesis. Thus, we aimed to investigate the effects of maternal HFD consumption during gestation and lactation on the Notch1/Mash1 pathway in the hypothalamus and arcuate nucleus (ARC) of mouse offspring (neonates and 28 days old). Our results showed that maternal HFD consumption increases body weight and adiposity of mouse offspring, accompanied by increased levels of Il-1β mRNA compared to those in control offspring. We noticed high mRNA levels of Hes5 accompanied by diminished mRNA levels of Ascl1 (Mash1). The number of Mash1-labeled cells in the ARC was diminished in HFD-O. Additionally, the population of NPY neurons was increased in these animals. Mash1 is important for the development of POMC and NPY neurons in the ARC. Therefore, the reduction in Mash1-labeled cells could be related to modification of the NPY neuron population in the ARC. This scenario favors hyperphagia and weight gain, and could be responsible for the development of obesity in adulthood.Copyright © 2017 IBRO. Published by Elsevier Ltd. All rights reserved.

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