Neonatal Overnutrition-Induced Adiposity and Glucose Intolerance are Associated with Impaired Lipolytic and Insulin Signaling in Adipose Tissue.

Authors

Camila F de Souza, Larissa Rugila S Stopa, Andressa B Martins, Ana Luiza M Wunderlich, Flaviane de Fatima Silva, Ayumi Cristina Medeiros Komino, Fábio Goulart de Andrade, Cristiane Mota Leite, Cassia Thaïs Bv Zaia, Fabio Bessa Lima, Ernane Torres Uchoa

Published in

Archives of medical research. Volume 57. Issue 7. Pages 103499. Jul 20, 2026. Epub Jul 20, 2026.

Abstract

Neonatal overnutrition induced by litter size reduction leads to obesity from childhood until adulthood. Increased adiposity in white adipose tissue (WAT) and glucose intolerance are obesity-related comorbidities. In this context, adiposity is regulated by lipogenesis and lipolysis, and glucose intolerance can result from insulin resistance and/or impaired insulin secretion by pancreatic β cells. Thus, this study assessed the lipolytic and insulin signaling pathways in the WAT in adult male rats overfed during lactation.
Male rats were reared in either a small litter (SL) or a normal litter (NL). On postnatal day (PND) 73, the animals underwent a glucose tolerance test. The following day, they were euthanized by decapitation to collect retroperitoneal and epididymal WAT.
SL rats exhibited increased body weight, adipocyte area in both fat depots, and glucose intolerance. These animals also exhibited reduced expression of proteins involved in lipolytic regulation, such as adrenergic receptors β1, β3, Ser563pHSL, and FABP4, as well as proteins in the insulin signaling pathway, PI3Kp85 and GLUT4, in the retroperitoneal WAT, but not in the epididymal adipose tissue.
This study demonstrates that neonatal overnutrition leads to adult adiposity and glucose intolerance, which are associated with depot-specific molecular alterations in proteins involved in the lipolytic and insulin signaling pathways, particularly in retroperitoneal WAT.

PMID:
42475779
Bibliographic data and abstract were imported from PubMed on 21 Jul 2026.

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