title: Cardiovascular autonomic dysfunction and oxidative stress induced by fructose overload in an experimental model of hypertension and menopause.
abstract: BACKGROUND
  Metabolic syndrome is characterized by the association of 3 or more risk factors, including: abdominal obesity associated with an excess of abdominal fat, insulin resistance, type 2 diabetes, dyslipidemia and hypertension. Moreover, the prevalence of hypertension and metabolic dysfunctions sharply increases after the menopause. However, the mechanisms involved in these changes are not well understood. Thus, the aim of this study was to assess the effects of fructose overload on cardiovascular autonomic modulation, inflammation and cardiac oxidative stress in an experimental model of hypertension and menopause.
  
  
  METHODS
  Female SHR rats were divided into (n = 8/group): hypertensive (H), hypertensive ovariectomized (HO) and hypertensive ovariectomized undergoing fructose overload (100 g/L in drinking water) (FHO). Arterial pressure (AP) signals were directly recorded. Cardiac autonomic modulation was evaluated by spectral analysis. Oxidative stress was evaluated in cardiac tissue.
  
  
  RESULTS
  AP was higher in the FHO group when compared to the other groups. Fructose overload promoted an increase in body and fat weight, triglyceride concentration and a reduction in insulin sensitivity. IL-10 was reduced in the FHO group when compared to the H group. TNF-α was higher in the FHO when compared to all other groups. Lipoperoxidation was higher and glutathione redox balance was reduced in the FHO group when compared to other groups, an indication of increased oxidative stress. A negative correlation was found between IL-10 and adipose tissue.
  
  
  CONCLUSIONS
  Fructose overload promoted an impairment in cardiac autonomic modulation associated with inflammation and oxidative stress in hypertensive rats undergoing ovarian hormone deprivation.
authors.forename: Filipe Fernandes
authors.initials: FF
authors.lastname: Conti
authors.forename: Janaina de Oliveira
authors.initials: Jde O
authors.lastname: Brito
authors.forename: Nathalia
authors.initials: N
authors.lastname: Bernardes
authors.forename: Danielle da Silva
authors.initials: Dda S
authors.lastname: Dias
authors.forename: Iris Callado
authors.initials: IC
authors.lastname: Sanches
authors.forename: Christiane
authors.initials: C
authors.lastname: Malfitano
authors.forename: Susana Francisca
authors.initials: SF
authors.lastname: Llesuy
authors.forename: Maria-Claudia
authors.initials: MC
authors.lastname: Irigoyen
authors.affiliation: Laboratory of Translational Physiology, Universidade Nove de Julho (UNINOVE), São Paulo, SP, Brasil. prof.kangelis@uninove.br.
authors.forename: Kátia
authors.initials: K
authors.lastname: De Angelis
mesh_terms: D050154:Adiposity; D000818:Animals; D001341:Autonomic Nervous System / Q000503:physiopathology*; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D004195:Disease Models, Animal; D005260:Female; D005632:Fructose; D006321:Heart / Q000294:innervation*; D006439:Hemodynamics; D006973:Hypertension / Q000503:physiopathology*; D007249:Inflammation / Q000503:physiopathology; D008593:Menopause / Q000502:physiology*; D024821:Metabolic Syndrome / Q000139:chemically induced / Q000503:physiopathology*; D018384:Oxidative Stress / Q000502:physiology*; D011918:Rats, Inbred SHR; D014280:Triglycerides / Q000097:blood
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D014280:Triglycerides; D005632:Fructose