title: In vivo oocyte developmental competence is reduced in lean but not in obese superovulated dairy cows after intraovarian administration of IGF1.
abstract: The present study investigated the role of IGF1 in lactating lean and non-lactating obese dairy cows by injecting 1 μg IGF1 into the ovaries prior to superovulation. This amount of IGF1 has been linked with pregnancy loss in women with the polycystic ovary syndrome (PCOS) and was associated with impaired bovine oocyte competence in vitro. Transcript abundance and protein expression of selected genes involved in apoptosis, glucose metabolism, and the IGF system were analyzed. Plasma concentrations of IGF1 and leptin, and IGF1 in uterine luminal fluid (ULF), were also measured. IGF1 treatment decreased embryo viability in lean cows to the levels observed in obese cows. Obese cows were not affected by IGF1 treatment and showed elevated levels of IGF1 (in both plasma and ULF) and leptin. Blastocysts from lean cows treated with IGF1 showed a higher abundance of SLC2A1 and IGFBP3 transcripts. IGF1 treatment reduced protein expression of tumor protein 53 in blastocysts of lean cows, whereas the opposite was observed in obese cows. IGF1 in plasma and ULF was correlated only in the control groups. Blastocyst transcript abundance of IGF1 receptor and IGFBP3 correlated positively with IGF1 concentrations in both plasma and ULF in lean cows. The detrimental microenvironment created by IGF1 injection in lean cows and the lack of effect in obese cows resemble to a certain extent the situation observed in PCOS patients, where IGF1 bioavailability is increased in normal-weight women but reduced in obese women, suggesting that this bovine model could be useful for studying IGF1 involvement in PCOS.
authors.affiliation: Department of Biotechnology, Friedrich-Loeffler-Institut (FLI), Neustadt, Germany.
authors.forename: Miguel A
authors.initials: MA
authors.lastname: Velazquez
authors.forename: Klaus-Gerd
authors.initials: KG
authors.lastname: Hadeler
authors.forename: Doris
authors.initials: D
authors.lastname: Herrmann
authors.forename: Wilfried A
authors.initials: WA
authors.lastname: Kues
authors.forename: Susanne E
authors.initials: SE
authors.lastname: Ulbrich
authors.forename: Susanne
authors.initials: S
authors.lastname: Ulbrich
authors.forename: Heinrich H D
authors.initials: HH
authors.lastname: Meyer
authors.forename: Benoît
authors.initials: B
authors.lastname: Rémy
authors.forename: Jean-François
authors.initials: JF
authors.lastname: Beckers
authors.forename: Helga
authors.initials: H
authors.lastname: Sauerwein
authors.forename: Heiner
authors.initials: H
authors.lastname: Niemann
mesh_terms: D000818:Animals; D001755:Blastocyst / Q000166:cytology / Q000378:metabolism; D002417:Cattle; D004195:Disease Models, Animal; D020964:Embryo Loss / Q000209:etiology; D005260:Female; D018507:Gene Expression Regulation, Developmental; D051272:Glucose Transporter Type 1 / Q000235:genetics / Q000378:metabolism; D018972:Insulin-Like Growth Factor Binding Protein 3 / Q000235:genetics / Q000378:metabolism; D007334:Insulin-Like Growth Factor I / Q000008:administration & dosage / Q000032:analysis / Q000378:metabolism*; D007774:Lactation / Q000187:drug effects; D020738:Leptin / Q000097:blood; D009765:Obesity / Q000150:complications*; D009866:Oogenesis; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D011247:Pregnancy; D012333:RNA, Messenger / Q000378:metabolism; D017526:Receptor, IGF Type 1 / Q000235:genetics / Q000378:metabolism; D013480:Superovulation; D013851:Thinness / Q000150:complications*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D014599:Uterus / Q000378:metabolism
chemical_list: D051272:Glucose Transporter Type 1; D018972:Insulin-Like Growth Factor Binding Protein 3; D020738:Leptin; D012333:RNA, Messenger; D016159:Tumor Suppressor Protein p53; D007334:Insulin-Like Growth Factor I; D017526:Receptor, IGF Type 1