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Overweight and obesity during critical periods, gestation and/or lactation, can harm offspring metabolic health. Maternal obesogenic diets may program offspring long-term, impairing physiology and increasing risk for insulin resistance. A key mechanism is the reduced expression/activity of insulin signaling proteins in peripheral glucose-metabolizing tissues. This systematic review examined the impact of maternal obesogenic diets on insulin resistance in the offspring of rats, through modulation of insulin signaling proteins in skeletal muscle, liver, and white adipose tissue. Searches in LILACS, PubMed, Web of Science, Scopus, and Sigle via Opera Gray yielded 2212 studies; 43 met inclusion criteria, following a PROSPERO-registered protocol. Findings showed reduced expression and activity of IRS-1, PI3K, AKT and GLUTs in peripheral tissues, alongside increased body weight, glucose intolerance, and insulin resistance. Thus, maternal obesogenic diets impair insulin signaling and related metabolic outcomes in offspring.
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http://dx.doi.org/10.1016/j.lfs.2025.123947 | DOI Listing |
Mol Hum Reprod
September 2025
Department of Veterinary Sciences, Laboratory of Veterinary Physiology and Biochemistry, Gamete Research Centre, University of Antwerp, Antwerp, Belgium.
Maternal diet-induced obesity (DIO) may affect adult offspring oocyte quality due to mitochondrial dysfunction. Here, we investigated whether offspring of DIO mothers exhibit mitochondrial abnormalities in their primordial follicle oocytes (PFOs) already at birth, and if (further) alterations can be detected at weaning. Female Swiss mice were fed a control or obesogenic diet for 7 weeks before mating, and throughout pregnancy and lactation.
View Article and Find Full Text PDFLife Sci
August 2025
Department of Nutrition, Center of Health Sciences, Federal University of Pernambuco, 55670-901 Recife, Brazil; Postgraduate Program in Nutrition, Universidade Federal de Pernambuco, 55670-901, Recife, PE, Brazil; Multicenter Postgraduate Program in Physiological Sciences - UFPE/SBFis, 55608-680, Vi
Overweight and obesity during critical periods, gestation and/or lactation, can harm offspring metabolic health. Maternal obesogenic diets may program offspring long-term, impairing physiology and increasing risk for insulin resistance. A key mechanism is the reduced expression/activity of insulin signaling proteins in peripheral glucose-metabolizing tissues.
View Article and Find Full Text PDFJAMA Netw Open
August 2025
Center for Childhood Obesity Research, The Pennsylvania State University, University Park.
Importance: Parents influence young children's diet, sleep, and physical activity behaviors. Pediatric primary care practitioners (PCPs) are uniquely positioned to identify obesogenic behaviors from infancy, yet few screening tools assess these behaviors in clinical settings.
Objective: To explore the association between parent-reported obesogenic behaviors and infant weight outcomes.
Med Sci Monit
August 2025
Department of Obstetrics and Gynaecology, Medical College, University of Rzeszów, Rzeszów, Poland.
The increasing prevalence of gestational diabetes mellitus (GDM) is a pressing global public health concern. Despite extensive identification of GDM risk factors and the implementation of screening programs, there has been a notable lack of significant reduction in maternal, fetal, and neonatal complications. It is vital to recognize that the health trajectory of future generations begins before birth, during intrauterine life and even before conception.
View Article and Find Full Text PDFJ Dev Orig Health Dis
August 2025
Unidad de Investigación en Obesidad, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, México.
The obesogenic maternal environment can lead to cardiac hypertrophy in the offspring. The aim of this study was to investigate whether (-)-epicatechin (Epi) modify the expression of genes related to pathological cardiac hypertrophy (CH), and its physiological pathway, in offspring obese by programing. Four groups of eight male offspring Wistar rats of 110 days were randomly selected to control groups [C and offspring of maternal obesity (MO)] or to Epi groups (C + Epi or MO + Epi).
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