title: Autophagy proteins are modulated in the liver and hypothalamus of the offspring of mice with diet-induced obesity.
abstract: Nutritional excess during pregnancy and lactation has a negative impact on offspring phenotype. In adulthood, obesity and lipid overload represent factors that compromise autophagy, a process of lysosomal degradation. Despite knowledge of the impact of obesity on autophagy, changes in offspring of obese dams have yet to be investigated. In this study, we tested the hypothesis that maternal obesity induced by a high fat diet (HFD) modulates autophagy proteins in the hypothalamus and liver of the offspring of mice. At birth (d0), offspring of obese dams (HFD-O) showed an increase in p62 protein and a decrease in LC3-II, but only in the liver. After weaning (d18), the offspring of HFD-O animals showed impairment of autophagy markers in both tissues compared to control offspring (SC-O). Between day 18 and day 42, both groups received a control diet and we observed that the protein content of p62 remained increased in the livers of the HFD-O offspring. However, after 82days, we did not find any modulation in offspring autophagy proteins. On the other hand, when the offspring of obese dams that received an HFD from day 42 until day 82 (OH-H) were compared with the offspring from the controls that only received an HFD in adulthood (OC-H), we saw impairment in autophagy proteins in both tissues. In conclusion, this study describes that HFD-O offspring showed early impairment of autophagy proteins. Although the molecular mechanisms have not been explored, it is possible that changes in autophagy markers could be associated with metabolic disturbances of offspring.
authors.affiliation: Faculdade de Ciências Aplicadas, Universidade Estadual de Campinas, UNICAMP, Limeira, SP, Brazil.
authors.forename: Andressa
authors.initials: A
authors.lastname: Reginato
authors.affiliation: Faculdade de Ciências Aplicadas, Universidade Estadual de Campinas, UNICAMP, Limeira, SP, Brazil.
authors.forename: Thaís
authors.initials: T
authors.lastname: de Fante
authors.affiliation: Faculdade de Ciências Aplicadas, Universidade Estadual de Campinas, UNICAMP, Limeira, SP, Brazil.
authors.forename: Mariana
authors.initials: M
authors.lastname: Portovedo
authors.affiliation: Faculdade de Ciências Aplicadas, Universidade Estadual de Campinas, UNICAMP, Limeira, SP, Brazil.
authors.forename: Natália Ferreira
authors.initials: NF
authors.lastname: da Costa
authors.affiliation: Faculdade de Ciências Aplicadas, Universidade Estadual de Campinas, UNICAMP, Limeira, SP, Brazil.
authors.forename: Tanyara Baliani
authors.initials: TB
authors.lastname: Payolla
authors.affiliation: Faculdade de Ciências Aplicadas, Universidade Estadual de Campinas, UNICAMP, Limeira, SP, Brazil.
authors.forename: Josiane Érica
authors.initials: JÉ
authors.lastname: Miyamotto
authors.affiliation: Faculdade de Ciências Aplicadas, Universidade Estadual de Campinas, UNICAMP, Limeira, SP, Brazil.
authors.forename: Laís Angélica
authors.initials: LA
authors.lastname: Simino
authors.affiliation: Faculdade de Nutrição, Universidade Federal do Mato Grosso, UFMT, Cuiabá, MT, Brazil.
authors.forename: Letícia M
authors.initials: LM
authors.lastname: Ignácio-Souza
authors.affiliation: Faculdade de Ciências Aplicadas, Universidade Estadual de Campinas, UNICAMP, Limeira, SP, Brazil.
authors.forename: Márcio A
authors.initials: MA
authors.lastname: Torsoni
authors.affiliation: Faculdade de Ciências Aplicadas, Universidade Estadual de Campinas, UNICAMP, Limeira, SP, Brazil.
authors.forename: Adriana S
authors.initials: AS
authors.lastname: Torsoni
authors.affiliation: Faculdade de Ciências Aplicadas, Universidade Estadual de Campinas, UNICAMP, Limeira, SP, Brazil. Electronic address: marciane.milanski@fca.unicamp.br.
authors.forename: Marciane
authors.initials: M
authors.lastname: Milanski
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D059305:Diet, High-Fat / Q000009:adverse effects; D005260:Female; D047109:Fetal Development; D018507:Gene Expression Regulation, Developmental; D007031:Hypothalamus / Q000378:metabolism*; D007774:Lactation; D008099:Liver / Q000378:metabolism*; D008297:Male; D039382:Maternal Nutritional Physiological Phenomena; D051379:Mice; D008869:Microtubule-Associated Proteins / Q000235:genetics / Q000378:metabolism*; D009419:Nerve Tissue Proteins / Q000378:metabolism; D009474:Neurons / Q000378:metabolism; D009765:Obesity / Q000209:etiology / Q000503:physiopathology; D009928:Organ Specificity; D063766:Pediatric Obesity / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D011247:Pregnancy; D011248:Pregnancy Complications / Q000209:etiology / Q000503:physiopathology; D011897:Random Allocation; D000071456:Sequestosome-1 Protein / Q000235:genetics / Q000378:metabolism*; D014886:Weaning
chemical_list: C480860:Map1lc3b protein, mouse; D008869:Microtubule-Associated Proteins; D009419:Nerve Tissue Proteins; D000071456:Sequestosome-1 Protein; C101343:Sqstm1 protein, mouse
keywords: Autophagy; High-fat diet; Hypothalamus; Liver; Obesity; Offspring