Short Communication

International Journal of Obesity advance online publication 18 April 2017; doi: 10.1038/ijo.2017.82

Prenatal steroid administration leads to adult pericardial and hepatic steatosis in male baboons

A H Kuo1, J Li2,3, C Li3,4, H F Huber4, M Schwab5, P W Nathanielsz3,4 and G D Clarke1,3

  1. 1Department of Radiology and Research Imaging Institute, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA
  2. 2Xiangya School of Medicine, Central South University, Changsha, Hunan, China
  3. 3Southwest National Primate Research Center, Texas Biomedical Research Institute, San Antonio, TX, USA
  4. 4Department of Animal Science, University of Wyoming, Laramie, WY, USA
  5. 5Department of Neurology, Jena University Hospital, Jena, Germany

Correspondence: Dr AH Kuo, Department of Radiology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, MC 7800, San Antonio, TX 78229-3900, USA. E-mail: kuoa@uthscsa.edu

Received 15 January 2017; Revised 18 February 2017; Accepted 15 March 2017
Accepted article preview online 24 March 2017; Advance online publication 18 April 2017

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Abstract

Developmental programming studies indicate that glucocorticoids modify fetal development. We hypothesized that administration of the synthetic glucocorticoid (sGC) betamethasone to pregnant baboons at doses and stages of fetal life equivalent to human obstetric practice to decrease premature offspring morbidity and mortality, programs lipid metabolism. In 10-year-old male baboons (human equivalent 40) exposed in fetal life to betamethasone or saline, we quantified pericardial fat and hepatic lipid content with magnetic resonance imaging and spectroscopy. sGC offspring delivered at term as do most sGC-exposed human neonates. Pericardial fat thickness (7.7±3.6mm vs 3.1±1.1mm, M±s.d.; P=0.022; n=5) and hepatic fatty acids (13.3±11.0% vs 2.5±2.2%; P=0.046; n=5) increased following sGC without birth weight or current body morphometric differences. Our results indicate that antenatal sGC therapy caused abnormal fat deposition and adult body composition in mid-life primate offspring. The concern raised is that this degree of pericardial and hepatic lipid accumulation can lead to harmful local lipotoxicity. In summary, developmental programing by sGC produces a mid-life metabolically obese but normal weight phenotype. Prior studies show sexually dimorphic responses to some programming challenges thus female studies are necessary.

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