title: Running Exercise in Obese Pregnancies Prevents IL-6 Trans-signaling in Male Offspring.
abstract: OBJECTIVE
  Maternal obesity is known to predispose the offspring to impaired glucose metabolism and obesity associated with low-grade inflammation and hypothalamic dysfunction. Because preventive approaches in this context are missing to date, we aimed to identify molecular mechanisms in the offspring that are affected by maternal exercise during pregnancy.
  
  
  METHODS
  Diet-induced obese mouse dams were divided into a sedentary obese (high-fat diet [HFD]) group and an obese intervention (HFD-running intervention [RUN]) group, which performed voluntary wheel running throughout gestation. Male offspring were compared with the offspring of a sedentary lean control group at postnatal day 21.
  
  
  RESULTS
  HFD and HFD-RUN offspring showed increased body weight and white adipose tissue mass. Glucose tolerance testing showed mild impairment only in HFD offspring. Serum interleukin-6 (IL-6) levels, hypothalamic and white adipose tissue IL-6 gene expressions, and phosphorylation of signal transducer and activator of transcription 3 in HFD offspring were significantly increased, whereas HFD-RUN was protected against these changes. The altered hypothalamic global gene expression in HFD offspring showed partial normalization in HFD-RUN offspring, especially with respect to IL-6 action.
  
  
  CONCLUSIONS
  Maternal exercise in obese pregnancies effectively reduces IL-6 trans-signaling and might be the underlying mechanism for the amelioration of glucose metabolism at postnatal day 21 independent of body composition.
authors.affiliation: 1Department of Pediatrics, University Hospital of Cologne, Cologne, GERMANY; 2Department of Ophthalmology, University Hospital of Cologne, Cologne, GERMANY; 3Cologne Centre for Prevention in Childhood and Youth, Heart Centre Cologne, University Hospital of Cologne, Cologne, GERMANY; and 4Department for Physical Activity in Public Health, Institute of Movement and Neurosciences, German Sport University Cologne, Cologne, GERMANY.
authors.forename: Inga
authors.initials: I
authors.lastname: Bae-Gartz
authors.forename: Ruth
authors.initials: R
authors.lastname: Janoschek
authors.forename: Cora-Sophia
authors.initials: CS
authors.lastname: Kloppe
authors.forename: Christina
authors.initials: C
authors.lastname: Vohlen
authors.forename: Frederik
authors.initials: F
authors.lastname: Roels
authors.forename: Andre
authors.initials: A
authors.lastname: Oberthür
authors.forename: Miguel Angel
authors.initials: MA
authors.lastname: Alejandre Alcazar
authors.forename: Gregor
authors.initials: G
authors.lastname: Lippach
authors.forename: Philipp S
authors.initials: PS
authors.lastname: Muether
authors.forename: Katharina
authors.initials: K
authors.lastname: Dinger
authors.forename: Nina
authors.initials: N
authors.lastname: Ferrari
authors.forename: Christine
authors.initials: C
authors.lastname: Graf
authors.forename: Jörg
authors.initials: J
authors.lastname: Dötsch
authors.forename: Eva
authors.initials: E
authors.lastname: Hucklenbruch-Rother
mesh_terms: D052436:Adipose Tissue, White / Q000378:metabolism; D050154:Adiposity; D000818:Animals; D001835:Body Weight; D059305:Diet, High-Fat; D005260:Female; D005947:Glucose / Q000378:metabolism; D005951:Glucose Tolerance Test; D007031:Hypothalamus / Q000378:metabolism; D007328:Insulin / Q000097:blood; D015850:Interleukin-6 / Q000097:blood / Q000378:metabolism*; D020738:Leptin / Q000097:blood; D008297:Male; D051379:Mice; D009043:Motor Activity; D009765:Obesity / Q000503:physiopathology*; D010641:Phenotype; D010805:Physical Conditioning, Animal; D011247:Pregnancy; D050796:STAT3 Transcription Factor / Q000378:metabolism; D015398:Signal Transduction; D059467:Transcriptome
chemical_list: D007328:Insulin; D015850:Interleukin-6; D020738:Leptin; D050796:STAT3 Transcription Factor; C494087:Stat3 protein, mouse; D005947:Glucose