Maternal obesity and western-style diet impair fetal and juvenile offspring skeletal muscle insulin-stimulated glucose transport in nonhuman primates

William Campodonico-Burnett, Byron Hetrick, Stephanie R. Wesolowski, Simon Schenk, Diana L. Takahashi, Tyler A. Dean, Elinor L. Sullivan, Paul Kievit, Maureen Gannon, Kjersti Aagaard, Jacob E. Friedman, Carrie E. McCurdy

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

Infants born to mothers with obesity have a greater risk for childhood obesity and metabolic diseases; however, the underlying biological mechanisms remain poorly un-derstood. We used a Japanese macaque model to investigate whether maternal obesity combined with a Western-style diet (WSD) impairs offspring muscle insulin action. Adult females were fed a control or WSD prior to and during pregnancy through lactation, and offspring subsequently weaned to a control or WSD. Muscle glucose uptake and signaling were measured ex vivo in fetal (n = 5–8/group) and juvenile (n = 8/group) offspring. In vivo signaling was evaluated after an insulin bolus just prior to weaning (n = 4–5/group). Maternal WSD reduced insulin-stimulated glucose uptake and impaired insulin signaling at the level of Akt phosphor-ylation in fetal muscle. In juvenile offspring, insulin-stimulated glucose uptake was similarly reduced by both maternal and postweaning WSD and corresponded to modest reductions in insulin-stimulated Akt phosphory-lation relative to controls. We conclude that maternal WSD leads to a persistent decrease in offspring muscle insulin-stimulated glucose uptake even in the absence of increased offspring adiposity or markers of systemic insulin resistance. Switching offspring to a healthy diet did not reverse the effects of maternal WSD on muscle insulin action, suggesting earlier interventions may be warranted.

Original languageEnglish (US)
Pages (from-to)1389-1400
Number of pages12
JournalDiabetes
Volume69
Issue number7
DOIs
StatePublished - Jul 2020

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

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