title: Overnourishment during lactation induces metabolic and haemodynamic heart impairment during adulthood.
abstract: OBJECTIVE
  In this study, the effects of postnatal overfeeding on heart energy homoeostasis and cardiac haemodynamics in adult male Swiss mice were examined.
  
  
  RESULTS
  During the suckling period, the mice were divided into four groups of control or overfed pups in combination with baseline or ischaemia/reperfusion treatments (control group baseline, CGBL; overfed group baseline, OGBL; control group ischaemia/reperfusion, CGIR; and overfed group ischaemia/reperfusion, OGIR). End diastolic pressure (EDP), heart contraction speed (Max dP/dt), relaxation speed (Min dP/dt), isovolumetric relaxation time (Tau) and frequency by beats per minute (BPM) were measured. During baseline and ischaemia/reperfusion, key proteins such as AKT1, AKT2, AKT3, pAKT, adenosine monophosphate-activated protein kinase (AMPK), pAMPK, insulin receptor beta (IRβ), protein tyrosine phosphatase 1B (PTP1B), insulin receptor substrate 1 (IRS1), fatty acid binding protein (FABP), CD36, phosphoinositide 3-kinase (PI3K) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) were studied. The expression of atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), carnitine palmitoyltransferase 1 (CPT1) and uncoupling protein 3 (UCP3) was studied as a marker of cardiac hypertrophy and energetic metabolism. Cardiac fibrosis was analyzed by quantifying collagen deposition, which is increased in the OGBL and OGIR groups compared with the control groups.
  
  
  CONCLUSIONS
  The OGBL group showed reduced EDP compared with the CGBL group and high Max dP/dt compared with the OGBL group. Ischaemia/reperfusion increased EDP and Min dP/dt in the intragroup comparison. By contrast, Tau and frequency were not significantly different among groups. The OGIR mice showed significant alterations in heart metabolism proteins, including AKT2, pAKT/AKT1, pAKT/AKT2, AMPK, pAMPK/AMPK, PTP1B, IRS1, FABP and CD36. Furthermore, alterations in ANP, BNP, CPT1 and UCP3 messenger RNA (mRNA) expression indicated hypertrophy and reduction in their efficiency, such that exclusive overnutrition in childhood induces a long-term effect on haemodynamics, metabolism and heart remodelling.
authors: Laboratory of Physiology of Nutrition and Development, Department of Physiological Sciences, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
authors: A K G
authors: AK
authors: Vieira
authors: Laboratory of Physiology of Nutrition and Development, Department of Physiological Sciences, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
authors: V M
authors: VM
authors: Soares
authors: Laboratory of Physiology of Nutrition and Development, Department of Physiological Sciences, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
authors: A F
authors: AF
authors: Bernardo
authors: Laboratory of Physiology of Nutrition and Development, Department of Physiological Sciences, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
authors: F A
authors: FA
authors: Neves
authors: Laboratory of Physiology of Nutrition and Development, Department of Physiological Sciences, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
authors: A B M
authors: AB
authors: Mattos
authors: Laboratory of Physiology of Nutrition and Development, Department of Physiological Sciences, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
authors: R M
authors: RM
authors: Guedes
authors: Laboratory of Cell Culture, Department of Histology and Embryology, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
authors: E
authors: E
authors: Cortez
authors: Laboratory of Cell Culture, Department of Histology and Embryology, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
authors: D C
authors: DC
authors: Andrade
authors: Laboratory of Physiology of Nutrition and Development, Department of Physiological Sciences, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
authors: G
authors: G
authors: Lacerda-Miranda
authors: Laboratory of Physiology of Nutrition and Development, Department of Physiological Sciences, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
authors: E P
authors: EP
authors: Garcia-Souza
authors: Laboratory of Physiology of Nutrition and Development, Department of Physiological Sciences, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil. Electronic address: anibal.nebin@gmail.com.
authors: A S
authors: AS
authors: Moura
mesh_terms: D000818:Animals; D009320:Atrial Natriuretic Factor / Q000235:genetics / Q000378:metabolism; D001794:Blood Pressure; D005260:Female; D006333:Heart Failure / Q000209:etiology* / Q000378:metabolism; D006439:Hemodynamics; D055504:Insulin Receptor Substrate Proteins / Q000235:genetics / Q000378:metabolism; D050152:Intra-Abdominal Fat / Q000378:metabolism; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism; D007774:Lactation; D008297:Male; D051379:Mice; D024101:Mitochondrial Proteins / Q000235:genetics / Q000378:metabolism; D009200:Myocardial Contraction; D032383:Myocytes, Cardiac / Q000378:metabolism; D044343:Overnutrition / Q000150:complications* / Q000378:metabolism; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics / Q000378:metabolism; D011181:Postnatal Care; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1 / Q000235:genetics / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011972:Receptor, Insulin / Q000235:genetics / Q000378:metabolism; D000071247:Uncoupling Protein 3
chemical_list: D055504:Insulin Receptor Substrate Proteins; D007473:Ion Channels; C526295:Irs1 protein, mouse; D024101:Mitochondrial Proteins; D047495:PPAR gamma; D012333:RNA, Messenger; C000604393:Ucp3 protein, mouse; D000071247:Uncoupling Protein 3; D009320:Atrial Natriuretic Factor; D019869:Phosphatidylinositol 3-Kinases; D011972:Receptor, Insulin; C514862:Akt1 protein, mouse; C494922:Akt2 protein, mouse; D051057:Proto-Oncogene Proteins c-akt; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; C516609:Ptpn1 protein, mouse
keywords: Fatty acid; Heart metabolism; Insulin; Ischaemia/reperfusion injury; Postnatal overfeeding