title: Impaired glucose metabolism in response to high fat diet in female mice conceived by in vitro fertilization (IVF) or ovarian stimulation alone.
abstract: Individuals conceived by in vitro fertilization (IVF) may be at increased risk of cardio-metabolic disorders. We recently reported that IVF conceived male mice displayed impaired glucose metabolism at normal and high body weights. In this study, we examined glucose metabolism in mature female C57BL/6J mice that were conceived by natural conception (NC), by ovarian stimulation (OS) or by IVF following chow or high-fat diet (HFD) for 8 weeks. By design, litter size was comparable between groups, but interestingly the birth weight of IVF and OS females was lower than NC females (p ≤ 0.001). Mature IVF female mice displayed increased fasting glucose as compared to NC and OS mice, irrespective of diet. Mature IVF and OS mice were also more susceptible to the metabolic consequences of high fat diet as compared with NC females, with impaired glucose tolerance (p ≤ 0.01), whereas peripheral insulin resistance and increased hepatic expression of gluconeogenic genes Ppargc1α, Pck1 and G6pc was observed in IVF mice only (p<0.05). This study suggests that ovarian stimulation alone and IVF program distinct metabolic effects in females, but that high fat diet may be required to unmask these effects. This study adds to the growing body of literature that assisted reproduction procedures may increase the risk of developing type 2 diabetes in an obesity prone environment.
authors.affiliation: Robinson Research Institute, School of Paediatrics and Reproductive Health, The University of Adelaide, Adelaide, Australia, 5005; Department of Obstetrics and Gynaecology, The Affiliated Hospital of Guiyang Medical College, Guiyang, China, 550004; Discipline of Medicine, The University of Adelaide, Adelaide, Australia, 5005.
authors.forename: Miaoxin
authors.initials: M
authors.lastname: Chen
authors.affiliation: Robinson Research Institute, School of Paediatrics and Reproductive Health, The University of Adelaide, Adelaide, Australia, 5005.
authors.forename: Linda
authors.initials: L
authors.lastname: Wu
authors.affiliation: Discipline of Medicine, The University of Adelaide, Adelaide, Australia, 5005; Department of Emergency, The Affiliated Hospital of Guiyang Medical College, Guiyang, China, 550004.
authors.forename: Fang
authors.initials: F
authors.lastname: Wu
authors.affiliation: Discipline of Medicine, The University of Adelaide, Adelaide, Australia, 5005.
authors.forename: Gary A
authors.initials: GA
authors.lastname: Wittert
authors.affiliation: Robinson Research Institute, School of Paediatrics and Reproductive Health, The University of Adelaide, Adelaide, Australia, 5005.
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Norman
authors.affiliation: Robinson Research Institute, School of Paediatrics and Reproductive Health, The University of Adelaide, Adelaide, Australia, 5005.
authors.forename: Rebecca L
authors.initials: RL
authors.lastname: Robker
authors.affiliation: Robinson Research Institute, School of Paediatrics and Reproductive Health, The University of Adelaide, Adelaide, Australia, 5005; Discipline of Medicine, The University of Adelaide, Adelaide, Australia, 5005.
authors.forename: Leonie K
authors.initials: LK
authors.lastname: Heilbronn
mesh_terms: D000818:Animals; D001724:Birth Weight; D015153:Blotting, Western; D004272:DNA, Mitochondrial / Q000235:genetics; D059305:Diet, High-Fat / Q000009:adverse effects*; D004734:Energy Metabolism / Q000502:physiology*; D005260:Female; D005307:Fertilization in Vitro / Q000009:adverse effects*; D005943:Gluconeogenesis / Q000235:genetics; D044882:Glucose Metabolism Disorders / Q000139:chemically induced*; D007333:Insulin Resistance / Q000502:physiology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010062:Ovulation Induction / Q000009:adverse effects*; D060888:Real-Time Polymerase Chain Reaction
chemical_list: D004272:DNA, Mitochondrial