Sep 2026· Journal of Developmental Origins of Health and Disease· Vol 17· 0 citations· 37 references
Medicine
TL;DR
It is hypothesized that maternal obesity during pregnancy results in reduced expression of proteins associated with pancreatic β cell function and increased expression of proteins associated with apoptosis in the offspring.
Abstract
Abstract Maternal obesity, resulting from high caloric intake during pregnancy, can impair pancreatic development in the offspring and lead to an increased risk of diabetes. We hypothesized that maternal obesity during pregnancy results in reduced expression of proteins associated with pancreatic β cell function and increased expression of proteins associated with apoptosis. C57BL/6J (N = 6) female mice were fed either a control (CON; n = 3) or a high-fat (HFD; n = 3) diet for fourteen weeks prior to pregnancy, diets were continued throughout gestation and lactation. Offspring were weaned at four weeks and then maintained on a control diet. At eight weeks of age, the offspring were euthanized (N = 20; 4–6/treatment/sex) and pancreas tissue samples were collected. Protein was isolated and analyzed using ultra-high performance liquid chromatography and tandem mass spectrometry. A total of 2,329 proteins were identified across both male and female mice in the comparison between the control and HFD groups, with 165 differentially expressed (DE) proteins (CON vs HFD males: 145; CON vs HFD females: 20; P ≤ 0.05). In male offspring, 131 DE proteins were down regulated, and 14 were upregulated, while in females 13 were upregulated and seven were down regulated. Four DE proteins (Mgat2, Lama2, Isyna1, Got2) were common to both sexes. However, only Lama2 exhibited a similar pattern of expression, with both HFD males and females having greater expression than CON. Alternatively, HFD males exhibited reduced expression of Mgat2, Got2, and Isyna1 when compared with CON. HFD females exhibited increased gene expression for the DEPs.
OBJECTIVES
The objective of this study was to examine whether offspring postnatal prebiotic fiber (Pre) intake could mitigate metabolic risks associated with a maternal obesogenic diet plus aspartame (APM) consumed during pregnancy and lactation.
METHODS
Following 11 weeks of obesity induction, female Sprague-Dawley...
Gabriel A. Venegas Silva, Erin W. Noye Tuplin, Vibha M. Kumar et al.· Nutrition (Burbank, Los Ange...· 0 citations
BACKGROUND
Maternal diabetes and exposure to a high‑fat diet (HFD) disrupt pancreatic development and glucose homeostasis, potentially inducing transgenerational metabolic changes.
OBJECTIVE
Investigate how maternal diabetes and HFD exposure impact the endocrine pancreas across generations. Elucidate their effects on...
F. Q. Gallego, V. S. Barco, Y. Sinzato et al.· Archives of Medical Research· 0 citations
Background/Objective: Pediatric obesity represents a paramount problem for global health that affects children’s actual quality of life, dramatically compromising their future health. Obesity has been demonstrated to alter skeletal muscle, a highly plastic tissue with dimorphic characteristics, which changes during dev...
Emiliana Giacomello, P. Giraudi, N. Rosso et al.· Nutrients· 0 citations
Abstract Maternal protein restriction during lactation is associated with stunted growth and hyperphagia in adult offspring, yet its long-term effects on mitochondrial uncoupling-related proteins in interscapular brown adipose tissue (iBAT) remain unknown. This study investigated how postnatal protein undernutrition af...
Willian Do Nascimento de Souza Rodrigues, L. Saavedra, Paulo Cezar de Freitas Mathias· Journal of Developmental Ori...· 0 citations
Abstract Fetal in-utero exposures are known to impact the long-term metabolic health of offspring. Insulin is the primary treatment to manage glucose concentrations in mothers with gestational diabetes. However, adverse offspring outcomes persist, such as macrosomia and increased risk of early obesity in offspring with...
Tracy K. Her, Grace Chung, Ron Regal et al.· Journal of Developmental Ori...· 0 citations
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