title: Resveratrol treatment rescues hyperleptinemia and improves hypothalamic leptin signaling programmed by maternal high-fat diet in rats.
abstract: OBJECTIVE
  Perinatal high-fat diet is associated with obesity and metabolic diseases in adult offspring. Resveratrol has been shown to exert antioxidant and anti-obesity actions. However, the effects of resveratrol on leptinemia and leptin signaling are still unknown as well as whether resveratrol treatment can improve metabolic outcomes programmed by maternal high-fat diet. We hypothesize that resveratrol treatment in male rats programmed by high-fat diet would decrease body weight and food intake, and leptinemia with changes in central leptin signaling.
  
  
  METHODS
  Female Wistar rats were divided into two groups: control group (C), which received a standard diet containing 9 % of the calories as fat, and high-fat group (HF), which received a diet containing 28 % of the calories as fat. Dams were fed in C or HF diet during 8 weeks before mating and throughout gestation and lactation. C and HF male offspring received standard diet throughout life. From 150 until 180 days of age, offspring received resveratrol (30 mg/Kg body weight/day) or vehicle (carboxymethylcellulose).
  
  
  RESULTS
  HF offspring had increased body weight, hyperphagia and increased subcutaneous and visceral fat mass compared to controls, and resveratrol treatment decreased adiposity. HF offspring had increased leptinemia as well as increased SOCS3 in the arcuate nucleus of the hypothalamus, which suggest central leptin resistance. Resveratrol treatment rescued leptinemia and increased p-STAT3 content in the hypothalamus with no changes in SOCS3, suggesting improvement in leptin signaling.
  
  
  CONCLUSIONS
  Collectively, our data suggest that resveratrol could reverse hyperleptinemia and improve central leptin action in adult offspring from HF mothers attenuating obesity.
authors: Laboratório de Endocrinologia Molecular, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho, 373, sl G0-16, Cidade Universitária, Rio de Janeiro, RJ, 21941-902, Brazil.
authors: J G
authors: JG
authors: Franco
authors: Laboratório de Endocrinologia Molecular, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho, 373, sl G0-16, Cidade Universitária, Rio de Janeiro, RJ, 21941-902, Brazil.
authors: C P
authors: CP
authors: Dias-Rocha
authors: Laboratório de Endocrinologia Molecular, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho, 373, sl G0-16, Cidade Universitária, Rio de Janeiro, RJ, 21941-902, Brazil.
authors: T P
authors: TP
authors: Fernandes
authors: Laboratório de Fisiologia Endócrina, Departamento de Ciências Fisiológicas, Instituto de Biologia Roberto Alcântara Gomes, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil.
authors: L
authors: L
authors: Albuquerque Maia
authors: Laboratório de Fisiologia Endócrina, Departamento de Ciências Fisiológicas, Instituto de Biologia Roberto Alcântara Gomes, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil.
authors: P C
authors: PC
authors: Lisboa
authors: Laboratório de Fisiologia Endócrina, Departamento de Ciências Fisiológicas, Instituto de Biologia Roberto Alcântara Gomes, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil.
authors: E G
authors: EG
authors: Moura
authors: Laboratório de Endocrinologia Molecular, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho, 373, sl G0-16, Cidade Universitária, Rio de Janeiro, RJ, 21941-902, Brazil.
authors: C C
authors: CC
authors: Pazos-Moura
authors: Laboratório de Endocrinologia Molecular, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho, 373, sl G0-16, Cidade Universitária, Rio de Janeiro, RJ, 21941-902, Brazil. haraisis@biof.ufrj.br.
authors: I H
authors: IH
authors: Trevenzoli
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D001823:Body Composition; D059305:Diet, High-Fat / Q000009:adverse effects*; D005260:Female; D006963:Hyperphagia / Q000503:physiopathology; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism; D053614:Janus Kinase 2 / Q000235:genetics / Q000378:metabolism; D020738:Leptin / Q000097:blood*; D008297:Male; D039382:Maternal Nutritional Physiological Phenomena; D009765:Obesity / Q000503:physiopathology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000188:drug therapy*; D051381:Rats; D017208:Rats, Wistar; D000077185:Resveratrol; D050796:STAT3 Transcription Factor / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D013267:Stilbenes / Q000494:pharmacology*; D000071223:Suppressor of Cytokine Signaling 3 Protein / Q000235:genetics / Q000378:metabolism; D015430:Weight Gain
chemical_list: D020738:Leptin; D050796:STAT3 Transcription Factor; C491410:Socs3 protein, rat; C494088:Stat3 protein, rat; D013267:Stilbenes; D000071223:Suppressor of Cytokine Signaling 3 Protein; C507927:Jak2 protein, rat; D053614:Janus Kinase 2; D000077185:Resveratrol
keywords: Leptin; Obesity; Programming; Resveratrol