title: Interaction between maternal obesity and post-natal over-nutrition on skeletal muscle metabolism.
abstract: OBJECTIVE
  Maternal obesity and post-natal over-nutrition play an important role in programming glucose and lipid metabolism later in life. The aim of this study was to decipher the contributions of maternal obesity and post-natal over-nutrition on glucose and lipid metabolism in skeletal muscle.
  
  
  RESULTS
  Male offspring of Sprague Dawley rat mothers fed either chow or high fat diet (HFD) for 5 weeks prior to mating were subsequently fed either chow or HFD until 18 weeks of age. Collection of plasma and skeletal muscle was performed at weaning (20 days) and 18 weeks. At weaning, offspring from obese mothers showed increased body weight, plasma insulin and lactate concentrations associated with reduced skeletal muscle glucose transporter 4 (GLUT4) and increased monocarboxylate transporter 1 (MCT1) protein. In 18-week old offspring, post-weaning HFD further exacerbated the elevated body weight caused by maternal obesity. Surprisingly this additive effect on body weight was not reflected in plasma glucose, insulin, lactate and MCT1; these markers were only increased by post-weaning HFD consumption. However, an additive effect of maternal obesity and post-weaning HFD led to decreased muscle GLUT4 levels, as well as mRNA levels of carnitine palmitoyl transferase-1, myogenic differentiation protein and myogenin.
  
  
  CONCLUSIONS
  Post-weaning HFD exerted an additive effect to that of maternal obesity on body weight and skeletal muscle markers of glucose and lipid metabolism but not on plasma glucose and insulin levels, suggesting that maternal obesity and post-natal over-nutrition impair skeletal muscle function via different mechanisms.
authors.affiliation: School of Medical Sciences, University of New South Wales, Sydney NSW 2052, Australia. d.simar@unsw.edu.au
authors.forename: D
authors.initials: D
authors.lastname: Simar
authors.forename: H
authors.initials: H
authors.lastname: Chen
authors.forename: K
authors.initials: K
authors.lastname: Lambert
authors.forename: J
authors.initials: J
authors.lastname: Mercier
authors.forename: M J
authors.initials: MJ
authors.lastname: Morris
mesh_terms: D000367:Age Factors; D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D001835:Body Weight; D059305:Diet, High-Fat; D004734:Energy Metabolism; D005260:Female; D051275:Glucose Transporter Type 4 / Q000378:metabolism; D007328:Insulin / Q000097:blood; D019344:Lactic Acid / Q000097:blood; D008297:Male; D027501:Monocarboxylic Acid Transporters / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000503:physiopathology; D009765:Obesity / Q000378:metabolism* / Q000503:physiopathology; D044343:Overnutrition / Q000378:metabolism* / Q000503:physiopathology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D027981:Symporters / Q000378:metabolism; D014886:Weaning; D000099233:Monocarboxylate Transport Protein 1
chemical_list: D051275:Glucose Transporter Type 4; D007328:Insulin; D019344:Lactic Acid; D027501:Monocarboxylic Acid Transporters; D027981:Symporters; D000099233:Monocarboxylate Transport Protein 1; C495694:Slc2a4 protein, rat