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Alison Mostyn UP 2012.10.101 EGEAL, School of Veterinary Medicine and Science, INRA UMR 703, INRA, Unité de Recherche 04UR08/03, The Hebrew University of Jerusalem, Unité NOPA, Early Life Research Unit, Institut Polytechnique LaSalle, Beauvais, France

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Linda Attig UP 2012.10.101 EGEAL, School of Veterinary Medicine and Science, INRA UMR 703, INRA, Unité de Recherche 04UR08/03, The Hebrew University of Jerusalem, Unité NOPA, Early Life Research Unit, Institut Polytechnique LaSalle, Beauvais, France

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Thibaut Larcher UP 2012.10.101 EGEAL, School of Veterinary Medicine and Science, INRA UMR 703, INRA, Unité de Recherche 04UR08/03, The Hebrew University of Jerusalem, Unité NOPA, Early Life Research Unit, Institut Polytechnique LaSalle, Beauvais, France

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Samir Dou UP 2012.10.101 EGEAL, School of Veterinary Medicine and Science, INRA UMR 703, INRA, Unité de Recherche 04UR08/03, The Hebrew University of Jerusalem, Unité NOPA, Early Life Research Unit, Institut Polytechnique LaSalle, Beauvais, France

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Pascale Chavatte-Palmer UP 2012.10.101 EGEAL, School of Veterinary Medicine and Science, INRA UMR 703, INRA, Unité de Recherche 04UR08/03, The Hebrew University of Jerusalem, Unité NOPA, Early Life Research Unit, Institut Polytechnique LaSalle, Beauvais, France

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Monia Boukthir UP 2012.10.101 EGEAL, School of Veterinary Medicine and Science, INRA UMR 703, INRA, Unité de Recherche 04UR08/03, The Hebrew University of Jerusalem, Unité NOPA, Early Life Research Unit, Institut Polytechnique LaSalle, Beauvais, France

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Arieh Gertler UP 2012.10.101 EGEAL, School of Veterinary Medicine and Science, INRA UMR 703, INRA, Unité de Recherche 04UR08/03, The Hebrew University of Jerusalem, Unité NOPA, Early Life Research Unit, Institut Polytechnique LaSalle, Beauvais, France

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Jean Djiane UP 2012.10.101 EGEAL, School of Veterinary Medicine and Science, INRA UMR 703, INRA, Unité de Recherche 04UR08/03, The Hebrew University of Jerusalem, Unité NOPA, Early Life Research Unit, Institut Polytechnique LaSalle, Beauvais, France

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Michael E Symonds UP 2012.10.101 EGEAL, School of Veterinary Medicine and Science, INRA UMR 703, INRA, Unité de Recherche 04UR08/03, The Hebrew University of Jerusalem, Unité NOPA, Early Life Research Unit, Institut Polytechnique LaSalle, Beauvais, France

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Latifa Abdennebi-Najar UP 2012.10.101 EGEAL, School of Veterinary Medicine and Science, INRA UMR 703, INRA, Unité de Recherche 04UR08/03, The Hebrew University of Jerusalem, Unité NOPA, Early Life Research Unit, Institut Polytechnique LaSalle, Beauvais, France

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Intrauterine growth restriction (IUGR) may be accompanied by inadequate thermoregulation, especially in piglets that are not considered to possess any brown adipose tissue (BAT) and are thus entirely dependent on shivering thermogenesis in order to maintain body temperature after birth. Leptin can stimulate heat production by promoting non-shivering thermogenesis in BAT, but whether this response occurs in piglets is unknown. Newborn female piglets that were characterised as showing IUGR (mean birth weight of approximately 0.98 kg) were therefore administered injections of either saline or leptin once a day for the first 5 days of neonatal life. The dose of leptin was 0.5 mg/kg, which is sufficient to increase plasma leptin by approximately tenfold and on the day of birth induced a rapid increase in body temperature to values similar to those of normal-sized ‘control’ piglets (mean birth weight of ∼1.47 kg). Perirenal adipose tissue was then sampled from all offspring at 21 days of age and the presence of the BAT-specific uncoupling protein 1 (UCP1) was determined by immunohistochemistry and immunoblotting. UCP1 was clearly detectable in all samples analysed and its abundance was significantly reduced in the IUGR piglets that had received saline compared with controls, but was raised to the same amount as in controls in those IUGR females given leptin. There were no differences in gene expression between primary markers of brown and white adipose tissues between groups. In conclusion, piglets possess BAT that when stimulated exogenously by leptin can promote increased body temperature.

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Ananda Malta
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Júlio Cezar de Oliveira
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Tatiane Aparecida da Silva Ribeiro
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Laize Peron Tófolo
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Luiz Felipe Barella
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Kelly Valério Prates
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Rosiane Aparecida Miranda
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Ghada Elmhiri Laboratory of Secretion Cell Biology, UPSP‐EGEAL Institut Polytechnique LaSalle de Beauvais, Department of Cell Biology and Genetics, Block H67, Room 19, State University of Maringá, Colombo Avenue 5970, 87020-900 Maringá, Parana, Brazil

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Claudinéia Conationi da Silva Franco
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Aryane Rodrigues Agostinho
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Amanda Bianchi Trombini
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Audrei Pavanello
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Clarice Gravena
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Latifa Abdennebi-Najar Laboratory of Secretion Cell Biology, UPSP‐EGEAL Institut Polytechnique LaSalle de Beauvais, Department of Cell Biology and Genetics, Block H67, Room 19, State University of Maringá, Colombo Avenue 5970, 87020-900 Maringá, Parana, Brazil

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Paulo Cezar de Freitas Mathias
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Nutritional insults during developmental plasticity have been linked with metabolic diseases such as diabetes in adulthood. We aimed to investigate whether a low-protein (LP) diet at the beginning of adulthood is able to program metabolic disruptions in rats. While control rats ate a normal-protein (23%; NP group) diet, treated rats were fed a LP (4%; LP group) diet from 60 to 90 days of age, after which an NP diet was supplied until they were 150 days old. Plasma levels of glucose and insulin, autonomous nervous system (ANS), and pancreatic islet function were then evaluated. Compared with the NP group, LP rats exhibited unchanged body weight and reduced food intake throughout the period of protein restriction; however, after the switch to the NP diet, hyperphagia of 10% (P<0.05), and catch-up growth of 113% (P<0.0001) were found. The LP rats showed hyperglycemia, insulin resistance, and higher fat accretion than the NP rats. While the sympathetic tonus from LP rats reduced by 28%, the vagus tonus increased by 21% (P<0.05). Compared with the islets from NP rats, the glucose insulinotropic effect as well as cholinergic and adrenergic actions was unaltered in the islets from LP rats. Protein restriction at the beginning of adulthood induced unbalanced ANS activity and fat tissue accretion later in life, even without functional disturbances in the pancreatic islets.

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