HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

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.
AuthorsAndressa Reginato, Thaís de Fante, Mariana Portovedo, Natália Ferreira da Costa, Tanyara Baliani Payolla, Josiane Érica Miyamotto, Laís Angélica Simino, Letícia M Ignácio-Souza, Márcio A Torsoni, Adriana S Torsoni, Marciane Milanski
JournalThe Journal of nutritional biochemistry (J Nutr Biochem) Vol. 34 Pg. 30-41 (08 2016) ISSN: 1873-4847 [Electronic] United States
PMID27180121 (Publication Type: Comparative Study, Journal Article)
CopyrightCopyright © 2016 Elsevier Inc. All rights reserved.
Chemical References
  • Map1lc3b protein, mouse
  • Microtubule-Associated Proteins
  • Nerve Tissue Proteins
  • Sequestosome-1 Protein
  • Sqstm1 protein, mouse
Topics
  • Animals
  • Animals, Newborn
  • Diet, High-Fat (adverse effects)
  • Female
  • Fetal Development
  • Gene Expression Regulation, Developmental
  • Hypothalamus (metabolism)
  • Lactation
  • Liver (metabolism)
  • Male
  • Maternal Nutritional Physiological Phenomena
  • Mice
  • Microtubule-Associated Proteins (genetics, metabolism)
  • Nerve Tissue Proteins (metabolism)
  • Neurons (metabolism)
  • Obesity (etiology, physiopathology)
  • Organ Specificity
  • Pediatric Obesity (etiology, metabolism, pathology)
  • Pregnancy
  • Pregnancy Complications (etiology, physiopathology)
  • Random Allocation
  • Sequestosome-1 Protein (genetics, metabolism)
  • Weaning

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: