title: Maternal high-fat diets cause insulin resistance through inflammatory changes in fetal adipose tissue.
abstract: OBJECTIVE
  Epidemiological and animal studies have shown that maternal obesity predisposes the offspring to obesity and the metabolic syndrome, possibly via late-onset metabolic programming of the fetus. Little is known, however, about the metabolic effect of maternal obesity on the fetus. This study investigated the effect of a maternal high-fat diet (HFD) on fetal growth and glucose metabolism using a diet-induced obesity mouse model.
  
  
  METHODS
  Female mice (6 weeks old; C57BL/6N) were fed either a normal chow diet (NCD, 10 kcal% fat) or an HFD (60 kcal% fat) for 4 weeks before mating and throughout pregnancy. At 17 days of gestation, gene expression of inflammatory markers and adipokines in fetal subcutaneous adipose tissue was analyzed by quantitative real-time polymerase chain reaction.
  
  
  RESULTS
  HFD mice were overweight, glucose intolerant and insulin resistant compared with NCD mice of the same gestational age. Although fetal body weight was not significantly different, fetal plasma glucose and insulin levels were higher in the HFD group than the NCD group. Furthermore, examination of fetal subcutaneous adipose tissue in the HFD group revealed hypertrophy with an increase in the levels of cluster of differentiation-68, chemokine receptor-2 and tumor necrosis factor-α mRNA, but a decrease in the level of glucose transporter-4 mRNA.
  
  
  CONCLUSIONS
  Maternal HFD causes inflammatory changes in the adipose tissue of offspring.
authors: Department of Obstetrics and Gynaecology, Mie University Graduate School of Medicine, Mie, Japan.
authors: N
authors: N
authors: Murabayashi
authors: T
authors: T
authors: Sugiyama
authors: L
authors: L
authors: Zhang
authors: Y
authors: Y
authors: Kamimoto
authors: T
authors: T
authors: Umekawa
authors: N
authors: N
authors: Ma
authors: N
authors: N
authors: Sagawa
mesh_terms: D000273:Adipose Tissue; D000818:Animals; D015703:Antigens, CD / Q000096:biosynthesis; D015214:Antigens, Differentiation, Myelomonocytic / Q000096:biosynthesis; D059305:Diet, High-Fat; D005260:Female; D047109:Fetal Development; D005333:Fetus / Q000378:metabolism*; D051275:Glucose Transporter Type 4 / Q000096:biosynthesis; D007249:Inflammation / Q000473:pathology*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000503:physiopathology; D012333:RNA, Messenger / Q000378:metabolism; D054390:Receptors, CCR2 / Q000096:biosynthesis; D050151:Subcutaneous Fat / Q000378:metabolism* / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D051275:Glucose Transporter Type 4; D007328:Insulin; D012333:RNA, Messenger; D054390:Receptors, CCR2; D014409:Tumor Necrosis Factor-alpha; C081026:CD68 protein, mouse; D000097382:CD68 Molecule; C515335:Ccr2 protein, mouse; C495693:Slc2a4 protein, mouse