Normalizing adiponectin levels in obese pregnant mice prevents adverse metabolic outcomes in offspring

Megan E. Paulsen, Fredrick J. Rosario, Stephanie R. Wesolowski, Theresa L. Powell, Thomas Jansson

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

Infants of obese mothers have an increased risk of developing obesity, insulin resistance, and type 2 diabetes. The underlying mechanisms remain elusive, and no effective interventions to limit the transmission of metabolic disease from the obese mother to her infant are currently available. Obese pregnant women have decreased circulating levels of adiponectin, which is associated with increased placental nutrient transport and fetal overgrowth. We have reported that normalization of adiponectin levels during late gestation reversed placental dysfunction and fetal overgrowth in a mouse model of maternal obesity in pregnancy. In the current study, we hypothesized that adiponectin supplementation during pregnancy in obese mice attenuates the adverse metabolic outcomes in adult offspring. Adult male offspring of obese mice developed obesity, fatty liver, and insulin resistance, with adult female offspring of obese mice having a less pronounced metabolic phenotype. These metabolic abnormalities in offspring born to obese mice were largely prevented by normalization of maternal adiponectin levels in late pregnancy. We provide evidence that low circulating maternal adiponectin is a critical mechanistic link between maternal obesity and the development of metabolic disease in offspring. Strategies aimed at improving maternal adiponectin levels may prevent long-term metabolic dysfunction in offspring of obese mothers.-Paulsen, M. E., Rosario, F. J., Wesolowski, S. R., Powell, T. L., Jansson, T. Normalizing adiponectin levels in obese pregnant mice prevents adverse metabolic outcomes in offspring.

Original languageEnglish (US)
Pages (from-to)2899-2909
Number of pages11
JournalFASEB Journal
Volume33
Issue number2
DOIs
StatePublished - 2019

Bibliographical note

Funding Information:
The authors thank A. Kramer and N. Anderson (University of Colorado) for providing technical assistance in the acquisition of data, and the Mouse Metabolic Phenotyping Center at the University of Cincinnati (Cincinnati, OH, USA) [U.S. National Institutes of Health (NIH) National Institute of Diabetes and Digestive and Kidney Diseases; Grant DK59630] for performing colorimetric assay of serum triglycerides. This work was supported by NIH Office of the Director Grant R24OD016724, and NIH Eunice Kennedy Shriver National Institute of Child Health and Human Development Grants R01HD065007 and T32HD07186. The authors declare no conflicts of interest.

Publisher Copyright:
© 2019 FASEB.

Keywords

  • Fatty liver
  • Fetal programming
  • Insulin resistance
  • Animals, Newborn
  • Adiponectin/metabolism
  • Mice, Inbred C57BL
  • Insulin Resistance
  • Male
  • Pregnancy
  • Blood Glucose/analysis
  • Animals
  • Metabolic Diseases/etiology
  • Obesity/complications
  • Female
  • Glucose Intolerance/etiology
  • Mice, Obese
  • Pregnancy Complications/etiology
  • Mice

PubMed: MeSH publication types

  • Journal Article
  • Research Support, N.I.H., Extramural

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