We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Exposure to Obesogenic Environments during Perinatal Development Modulates Offspring Energy Balance Pathways in Adipose Tissue and Liver of Rodent Models.
- Authors
Sousa, Diana; Rocha, Mariana; Amaro, Andreia; Ferreira-Junior, Marcos Divino; Cavalcante, Keilah Valéria Naves; Monteiro-Alfredo, Tamaeh; Barra, Cátia; Rosendo-Silva, Daniela; Saavedra, Lucas Paulo Jacinto; Magalhães, José; Caseiro, Armando; Freitas Mathias, Paulo Cezar de; Pereira, Susana P.; Oliveira, Paulo J.; Gomes, Rodrigo Mello; Matafome, Paulo
- Abstract
Obesogenic environments such as Westernized diets, overnutrition, and exposure to glycation during gestation and lactation can alter peripheral neuroendocrine factors in offspring, predisposing for metabolic diseases in adulthood. Thus, we hypothesized that exposure to obesogenic environments during the perinatal period reprograms offspring energy balance mechanisms. Four rat obesogenic models were studied: maternal diet-induced obesity (DIO); early-life obesity induced by postnatal overfeeding; maternal glycation; and postnatal overfeeding combined with maternal glycation. Metabolic parameters, energy expenditure, and storage pathways in visceral adipose tissue (VAT) and the liver were analyzed. Maternal DIO increased VAT lipogenic [NPY receptor-1 (NPY1R), NPY receptor-2 (NPY2R), and ghrelin receptor], but also lipolytic/catabolic mechanisms [dopamine-1 receptor (D1R) and p-AMP-activated protein kinase (AMPK)] in male offspring, while reducing NPY1R in females. Postnatally overfed male animals only exhibited higher NPY2R levels in VAT, while females also presented NPY1R and NPY2R downregulation. Maternal glycation reduces VAT expandability by decreasing NPY2R in overfed animals. Regarding the liver, D1R was decreased in all obesogenic models, while overfeeding induced fat accumulation in both sexes and glycation the inflammatory infiltration. The VAT response to maternal DIO and overfeeding showed a sexual dysmorphism, and exposure to glycotoxins led to a thin-outside-fat-inside phenotype in overfeeding conditions and impaired energy balance, increasing the metabolic risk in adulthood.
- Subjects
MATERNAL health services; ENERGY metabolism; RODENTS; WESTERN diet; MOTHERS; LIVER; ANIMAL experimentation; NUTRITION disorders; NUTRITIONAL requirements; RATS; METABOLIC disorders; OBESITY risk factors; RESEARCH funding; ADIPOSE tissues; ADULTS
- Publication
Nutrients, 2023, Vol 15, Issue 5, p1281
- ISSN
2072-6643
- Publication type
Article
- DOI
10.3390/nu15051281