Altered glucose metabolism in mouse and humans conceived by in-vitro fertilization (IVF)

  1. Leonie K. Heilbronn2,3
  1. 1Department of Obstetrics and Gynaecology, The Affiliated Hospital of Guiyang Medical College, Guiyang, China, 550004
  2. 2Robinson Institute, School of Paediatrics and Reproductive Health, The University of Adelaide, SA, 5005
  3. 3Discipline of Medicine, The University of Adelaide, SA, 5005
  4. 4Reproductive Medicine Center, The General Hospital of Ningxia Medical University, Yinchuan, China, 750004
  5. 5Department of Emergency, The Affiliated Hospital of Guiyang Medical College, Guiyang, China, 550004
  1. Corresponding author: Leonie Heilbronn, Email: leonie.heilbronn{at}adelaide.edu.au

Abstract

In-vitro fertilization (IVF) may influence the metabolic health of children. However, in humans, it is difficult to separate out the relative contributions of genetics, environment, or the process of IVF, which includes ovarian stimulation and embryo culture. Therefore, we examined glucose metabolism in young adult humans and in adult male C57BL/6J mice conceived by IVF versus naturally, under energy balanced and high-fat overfeeding conditions. In humans, peripheral insulin sensitivity, as assessed by hyperinsulinemic-euglycemic clamp (80mU/m2/min), was lower in IVF (n=14) versus controls (n=20) after 3 days of an energy-balanced diet (30% fat). In response to 3-days of overfeeding (+1250 kcal/day, 45% fat), there was a greater increase in systolic blood pressure in IVF versus controls (P=0.02). Mice conceived following either ovarian stimulation alone or IVF weighed significantly less at birth versus controls (P<0.01). However, only mice conceived by IVF displayed increased fasting glucose, impaired glucose tolerance and reduced insulin-stimulated Akt phosphorylation in liver following 8 weeks of either chow or high-fat diet (60% fat). Thus, ovarian stimulation impaired fetal growth in mouse, but only embryo culture resulted in changes in glucose metabolism that may increase the risk of developing metabolic diseases later in life, and in both mouse and humans.

  • Received January 22, 2014.
  • Accepted April 14, 2014.

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