title: Adverse cardiac remodeling due to maternal low protein diet is associated with alterations in expression of genes regulating glucose metabolism.
abstract: OBJECTIVE
  We have previously shown that a maternal low protein (LP) diet during pregnancy in the rat results in adverse ventricular remodeling and contractile deficiencies of the neonatal rat heart. Since pathological cardiac hypertrophy is associated with increased expression of genes involved in glucose handling, this study was undertaken to examine if maternal LP diet alters the expression of genes encoding for some key components of glucose metabolism and uptake, and of the insulin receptor (IR) signal transduction in the heart of male offspring.
  
  
  RESULTS
  We determined the effect of maternal LP and normal diet (90 and 180 g/casein/kg respectively) on IR β-subunit, insulin receptor substrate (IRS)-1, phosphotyrosyl protein phosphatase (PTP) 1B, GLUT4 and phosphatidylinositol (PI) 3-kinase in male rat offspring at 24 h and at 1, 4 and 8 wks post-partum. Quantitative real-time RT-PCR revealed significant age-dependent increases in the expression of IR β-subunit, IRS-1, PTP1B, GLUT4 and PI3-kinase in the LP group with concomitant increases in corresponding protein abundance at 4 wks of age. These changes were associated with increases in left ventricular (LV) internal diameters as well as increases in LV wall thickness.
  
  
  CONCLUSIONS
  A maternal LP diet can induce increases in the gene expression and protein levels of key components of glucose metabolism and the IR signal transduction pathway in the neonatal rat heart, which may be related to accelerated energy supply, demand and utilization for ventricular remodeling due to compromised contractile performance during early life.
authors.affiliation: I.H. Asper Clinical Research Institute, St. Boniface Hospital Research Centre, Canada. ptappia@sbrc.ca
authors.forename: P S
authors.initials: PS
authors.lastname: Tappia
authors.forename: C
authors.initials: C
authors.lastname: Guzman
authors.forename: L
authors.initials: L
authors.lastname: Dunn
authors.forename: N
authors.initials: N
authors.lastname: Aroutiounova
mesh_terms: D000818:Animals; D015153:Blotting, Western; D006332:Cardiomegaly / Q000503:physiopathology; D018753:Diet, Protein-Restricted / Q000009:adverse effects*; D004195:Disease Models, Animal; D004452:Echocardiography; D005260:Female; D015870:Gene Expression; D005947:Glucose / Q000378:metabolism*; D051275:Glucose Transporter Type 4 / Q000235:genetics / Q000378:metabolism; D006321:Heart / Q000503:physiopathology*; D055504:Insulin Receptor Substrate Proteins / Q000235:genetics / Q000378:metabolism; D008297:Male; D044342:Malnutrition / Q000378:metabolism; D039382:Maternal Nutritional Physiological Phenomena; D058539:Phosphatidylinositol 3-Kinase / Q000235:genetics / Q000378:metabolism; D011247:Pregnancy; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1 / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D060888:Real-Time Polymerase Chain Reaction; D011972:Receptor, Insulin / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D051275:Glucose Transporter Type 4; D055504:Insulin Receptor Substrate Proteins; C526296:Irs1 protein, rat; C495694:Slc2a4 protein, rat; D058539:Phosphatidylinositol 3-Kinase; D011972:Receptor, Insulin; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; C516610:Ptpn1 protein, rat; D005947:Glucose