title: Adiponectin Deficiency Impairs Maternal Metabolic Adaptation to Pregnancy in Mice.
abstract: Hypoadiponectinemia has been widely observed in patients with gestational diabetes mellitus (GDM). To investigate the causal role of hypoadiponectinemia in GDM, adiponectin gene knockout (Adipoq-/-) and wild-type (WT) mice were crossed to produce pregnant mouse models with or without adiponectin deficiency. Adenoviral vector-mediated in vivo transduction was used to reconstitute adiponectin during late pregnancy. Results showed thatAdipoq-/-dams developed glucose intolerance and hyperlipidemia in late pregnancy. Increased fetal body weight was detected inAdipoq-/-dams. Adiponectin reconstitution abolished these metabolic defects inAdipoq-/-dams. Hepatic glucose and triglyceride production rates ofAdipoq-/-dams were significantly higher than those of WT dams. Robustly enhanced lipolysis was found in gonadal fat ofAdipoq-/-dams. Interestingly, similar levels of insulin-induced glucose disposal and insulin signaling in metabolically active tissues inAdipoq-/-and WT dams indicated that maternal adiponectin deficiency does not reduce insulin sensitivity. However, remarkably decreased serum insulin concentrations were observed inAdipoq-/-dams. Furthermore, β-cell mass, but not glucose-stimulated insulin release, inAdipoq-/-dams was significantly reduced compared with WT dams. Together, these results demonstrate that adiponectin plays an important role in controlling maternal metabolic adaptation to pregnancy.
authors.affiliation: Department of Pediatrics, University of California, San Diego, La Jolla, CA.
authors.forename: Liping
authors.initials: L
authors.lastname: Qiao
authors.affiliation: Department of Pediatrics, University of California, San Diego, La Jolla, CA.
authors.forename: Jean-Sebastien
authors.initials: JS
authors.lastname: Wattez
authors.affiliation: Department of Pediatrics, University of California, San Diego, La Jolla, CA.
authors.forename: Samuel
authors.initials: S
authors.lastname: Lee
authors.affiliation: Department of Pediatrics, University of California, San Diego, La Jolla, CA.
authors.forename: Amanda
authors.initials: A
authors.lastname: Nguyen
authors.affiliation: Department of Microbiology, University of Colorado School of Medicine, Aurora, CO.
authors.forename: Jerome
authors.initials: J
authors.lastname: Schaack
authors.affiliation: Department of Pediatrics, University of Colorado School of Medicine, Aurora, CO.
authors.forename: William W
authors.initials: WW
authors.lastname: Hay
authors.affiliation: Department of Pediatrics, University of California, San Diego, La Jolla, CA jishao@ucsd.edu.
authors.forename: Jianhua
authors.initials: J
authors.lastname: Shao
mesh_terms: D000222:Adaptation, Physiological / Q000235:genetics*; D052242:Adiponectin / Q000172:deficiency* / Q000235:genetics / Q000378:metabolism; D052436:Adipose Tissue, White / Q000378:metabolism; D000818:Animals; D015153:Blotting, Western; D001835:Body Weight; D016640:Diabetes, Gestational / Q000235:genetics* / Q000378:metabolism; D005260:Female; D005333:Fetus; D005947:Glucose / Q000378:metabolism*; D015309:Glucose Clamp Technique; D018149:Glucose Intolerance / Q000235:genetics* / Q000378:metabolism; D006949:Hyperlipidemias / Q000235:genetics* / Q000378:metabolism; D007150:Immunohistochemistry; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance / Q000235:genetics; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000378:metabolism / Q000473:pathology; D008066:Lipolysis / Q000235:genetics; D008099:Liver / Q000378:metabolism; D008661:Metabolism, Inborn Errors / Q000235:genetics* / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D009929:Organ Size; D011247:Pregnancy; D060888:Real-Time Polymerase Chain Reaction; D014280:Triglycerides / Q000378:metabolism
chemical_list: D052242:Adiponectin; C499919:Adipoq protein, mouse; D007328:Insulin; D014280:Triglycerides; D005947:Glucose