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Júlio Cezar de Oliveira Laboratório de Biologia Celular da Secreção, Departamento de Biotecnologia, Genética e Biologia Celular, Universidade Estadual de Maringá, Maringá, Brazil
Departamento de Ciências Fisiológicas, Laboratório de Fisiologia Endócrina, Instituto de Biologia Roberto Alcântara Gomes, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil
Instituto de Ciências da Saúde, Universidade Federal de Mato Grosso, Sinop, Brazil

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Egberto Gaspar de Moura Departamento de Ciências Fisiológicas, Laboratório de Fisiologia Endócrina, Instituto de Biologia Roberto Alcântara Gomes, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil

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Rosiane Aparecida Miranda Laboratório de Biologia Celular da Secreção, Departamento de Biotecnologia, Genética e Biologia Celular, Universidade Estadual de Maringá, Maringá, Brazil
Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil

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Ana Maria Praxedes de Moraes Laboratório de Biologia Celular da Secreção, Departamento de Biotecnologia, Genética e Biologia Celular, Universidade Estadual de Maringá, Maringá, Brazil

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Luiz Felipe Barella Laboratório de Biologia Celular da Secreção, Departamento de Biotecnologia, Genética e Biologia Celular, Universidade Estadual de Maringá, Maringá, Brazil

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Ellen Paula Santos da Conceição Departamento de Ciências Fisiológicas, Laboratório de Fisiologia Endócrina, Instituto de Biologia Roberto Alcântara Gomes, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil

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Rodrigo Mello Gomes Departamento de Ciências Fisiológicas, Universidade Federal de Goiás, Goiânia, Brazil

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Tatiane Aparecida Ribeiro Laboratório de Biologia Celular da Secreção, Departamento de Biotecnologia, Genética e Biologia Celular, Universidade Estadual de Maringá, Maringá, Brazil

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Ananda Malta Laboratório de Biologia Celular da Secreção, Departamento de Biotecnologia, Genética e Biologia Celular, Universidade Estadual de Maringá, Maringá, Brazil

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Isabela Peixoto Martins Laboratório de Biologia Celular da Secreção, Departamento de Biotecnologia, Genética e Biologia Celular, Universidade Estadual de Maringá, Maringá, Brazil

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Claudinéia Conationi da Silva Franco Laboratório de Biologia Celular da Secreção, Departamento de Biotecnologia, Genética e Biologia Celular, Universidade Estadual de Maringá, Maringá, Brazil

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Patrícia Cristina Lisboa Departamento de Ciências Fisiológicas, Laboratório de Fisiologia Endócrina, Instituto de Biologia Roberto Alcântara Gomes, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil

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Paulo Cezar de Freitas Mathias Laboratório de Biologia Celular da Secreção, Departamento de Biotecnologia, Genética e Biologia Celular, Universidade Estadual de Maringá, Maringá, Brazil

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We examined the long-term effects of protein restriction during puberty on the function of hypothalamic–pituitary–adrenal (HPA) and hypothalamic–pituitary–gonadal (HPG) axes in male rats. Male Wistar rats from the age of 30 to 60 days were fed a low-protein diet (4%, LP). A normal-protein diet (20.5%) was reintroduced to rats from the age of 60 to 120 days. Control rats were fed a normal-protein diet throughout life (NP). Rats of 60 or 120 days old were killed. Food consumption, body weight, visceral fat deposits, lipid profile, glycemia, insulinemia, corticosteronemia, adrenocorticotropic hormone (ACTH), testosteronemia and leptinemia were evaluated. Glucose-insulin homeostasis, pancreatic-islet insulinotropic response, testosterone production and hypothalamic protein expression of the androgen receptor (AR), glucocorticoid receptor (GR) and leptin signaling pathway were also determined. LP rats were hypophagic, leaner, hypoglycemic, hypoinsulinemic and hypoleptinemic at the age of 60 days (P < 0.05). These rats exhibited hyperactivity of the HPA axis, hypoactivity of the HPG axis and a weak insulinotropic response (P < 0.01). LP rats at the age of 120 days were hyperphagic and exhibited higher visceral fat accumulation, hyperleptinemia and dyslipidemia; lower blood ACTH, testosterone and testosterone release; and reduced hypothalamic expression of AR, GR and SOCS3, with a higher pSTAT3/STAT3 ratio (P < 0.05). Glucose-insulin homeostasis was disrupted and associated with hyperglycemia, hyperinsulinemia and increased insulinotropic response of the pancreatic islets. The cholinergic and glucose pancreatic-islet responses were small in 60-day-old LP rats but increased in 120-day-old LP rats. The hyperactivity of the HPA axis and the suppression of the HPG axis caused by protein restriction at puberty contributed to energy and metabolic disorders as long-term consequences.

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Jocemara Patrícia Silva de Souza Parrela Research Group on Perinatal Programming of Metabolic Diseases: DOHaD Paradigm, Laboratory of Metabolic and Cardiovascular Diseases, Health Education and Research Center (NUPADS), Institute of Health Sciences, Federal University of Mato Grosso, University Campus of Sinop, Sinop, Mato Grosso, Brazil

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Ingridys Regina Borkenhagen Research Group on Perinatal Programming of Metabolic Diseases: DOHaD Paradigm, Laboratory of Metabolic and Cardiovascular Diseases, Health Education and Research Center (NUPADS), Institute of Health Sciences, Federal University of Mato Grosso, University Campus of Sinop, Sinop, Mato Grosso, Brazil

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Sarah Ramany Faria Salmeron Research Group on Perinatal Programming of Metabolic Diseases: DOHaD Paradigm, Laboratory of Metabolic and Cardiovascular Diseases, Health Education and Research Center (NUPADS), Institute of Health Sciences, Federal University of Mato Grosso, University Campus of Sinop, Sinop, Mato Grosso, Brazil

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Thalyne Aparecida Leite Lima Research Group on Perinatal Programming of Metabolic Diseases: DOHaD Paradigm, Laboratory of Metabolic and Cardiovascular Diseases, Health Education and Research Center (NUPADS), Institute of Health Sciences, Federal University of Mato Grosso, University Campus of Sinop, Sinop, Mato Grosso, Brazil

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Ginislene Dias Souza Miranda Research Group on Perinatal Programming of Metabolic Diseases: DOHaD Paradigm, Laboratory of Metabolic and Cardiovascular Diseases, Health Education and Research Center (NUPADS), Institute of Health Sciences, Federal University of Mato Grosso, University Campus of Sinop, Sinop, Mato Grosso, Brazil

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Hercules de Oliveira Costermani Research Group on Perinatal Programming of Metabolic Diseases: DOHaD Paradigm, Laboratory of Metabolic and Cardiovascular Diseases, Health Education and Research Center (NUPADS), Institute of Health Sciences, Federal University of Mato Grosso, University Campus of Sinop, Sinop, Mato Grosso, Brazil

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Camila Luiza Rodrigues dos Santos Ricken Research Group on Perinatal Programming of Metabolic Diseases: DOHaD Paradigm, Laboratory of Metabolic and Cardiovascular Diseases, Health Education and Research Center (NUPADS), Institute of Health Sciences, Federal University of Mato Grosso, University Campus of Sinop, Sinop, Mato Grosso, Brazil

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Ester Vieira Alves Research Group on Perinatal Programming of Metabolic Diseases: DOHaD Paradigm, Laboratory of Metabolic and Cardiovascular Diseases, Health Education and Research Center (NUPADS), Institute of Health Sciences, Federal University of Mato Grosso, University Campus of Sinop, Sinop, Mato Grosso, Brazil

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Rodrigo Mello Gomes Laboratory of Endocrine Physiology and Metabolism, Institute of Biological Sciences, Federal University of Goiás, Goiânia, Goiás, Brazil

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Júlio Cezar de Oliveira Research Group on Perinatal Programming of Metabolic Diseases: DOHaD Paradigm, Laboratory of Metabolic and Cardiovascular Diseases, Health Education and Research Center (NUPADS), Institute of Health Sciences, Federal University of Mato Grosso, University Campus of Sinop, Sinop, Mato Grosso, Brazil

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Herein, we assessed milk hormones, the biochemical composition of milk, and its association with neonatal body weight gain and metabolic homeostasis in weaned rats whose mothers were undernourished in the last third of pregnancy. From the 14th day of pregnancy until delivery, undernourished mothers had their food restricted by 50% (FR50), whereas control mothers were fed ad libitum. The litter size was adjusted to eight pups, and rats were weaned at 22 days old. Milk and blood from mothers, as well as blood and tissues from pups, were collected for further analyses. At birth, FR50 pups were smaller than control pups, and they exhibited hyperphagia and rapid catch-up growth during the suckling period. On day 12, the milk from FR50 mothers had higher energy content, glucose, total cholesterol, triglycerides, and acylated ghrelin but lower leptin and corticosterone levels. Interestingly, FR50 mothers were hypoglycemic and hyperleptinemic at the end of the nursing period. Weaned FR50 pups had an obese phenotype and exhibited insulin resistance, which was associated with hyperglycemia and hypertriglyceridemia; they also had high blood levels of total cholesterol, leptin, and acylated ghrelin. In addition, the protein expression of growth hormone secretagogue receptor (GHSR) in the hypothalamus was increased by almost 4-fold in FR50 pups. In summary, maternal calorie restriction during the last third of pregnancy disrupts energy and metabolic hormones in milk, induces pup hyperleptinemia and hyperghrelinemia, and upregulates their hypothalamic GHSR, thus suggesting that the hypothalamic neuroendocrine circuitry may be working to address the early onset of obesity.

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Alexia Barroso Department of Cell Biology, Physiology, and Immunology, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), University of Cordoba, Reina Sofia University Hospital, Cordoba, Spain
CIBER Fisiopatologia de la Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain

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Jose Antonio Santos-Marcos CIBER Fisiopatologia de la Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
Lipids and Atherosclerosis Research Unit, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba, Cordoba, Spain

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Cecilia Perdices-Lopez Department of Cell Biology, Physiology, and Immunology, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), University of Cordoba, Reina Sofia University Hospital, Cordoba, Spain
CIBER Fisiopatologia de la Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain

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Ana Vega-Rojas CIBER Fisiopatologia de la Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
Lipids and Atherosclerosis Research Unit, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba, Cordoba, Spain

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Miguel Angel Sanchez-Garrido Department of Cell Biology, Physiology, and Immunology, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), University of Cordoba, Reina Sofia University Hospital, Cordoba, Spain
CIBER Fisiopatologia de la Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain

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Yelizabeta Krylova CIBER Fisiopatologia de la Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
Lipids and Atherosclerosis Research Unit, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba, Cordoba, Spain

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Helena Molina-Abril Department of Applied Mathematics I, University of Seville, Seville, Spain

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Claes Ohlsson Centre for Bone and Arthritis Research, Institute of Medicine, The Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden

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Pablo Perez-Martinez CIBER Fisiopatologia de la Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
Lipids and Atherosclerosis Research Unit, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba, Cordoba, Spain

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Matti Poutanen Centre for Bone and Arthritis Research, Institute of Medicine, The Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden
Institute of Biomedicine, Research Centre for Integrative Physiology and Pharmacology, University of Turku, Turku, Finland

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Jose Lopez-Miranda CIBER Fisiopatologia de la Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
Lipids and Atherosclerosis Research Unit, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba, Cordoba, Spain

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Manuel Tena-Sempere Department of Cell Biology, Physiology, and Immunology, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), University of Cordoba, Reina Sofia University Hospital, Cordoba, Spain
CIBER Fisiopatologia de la Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
Institute of Biomedicine, Research Centre for Integrative Physiology and Pharmacology, University of Turku, Turku, Finland

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Antonio Camargo CIBER Fisiopatologia de la Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
Lipids and Atherosclerosis Research Unit, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba, Cordoba, Spain

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al. 2019 ). Early metabolic programming by sex steroids also contributes to define differences in susceptibility to later development of the metabolic disease. Inappropriate exposures to sex steroids during early maturational periods (e

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Júlio Cezar de Oliveira
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Patrícia Cristina Lisboa Laboratory of Secretion Cell Biology, Department of Physiological Sciences, Department of Physiological Sciences, Department of Cell Biology and Genetics, State University of Maringá, Block H67, Room 19, Colombo Avenue 5970, 87020-900 Maringá, Paraná, Brazil

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Egberto Gaspar de Moura Laboratory of Secretion Cell Biology, Department of Physiological Sciences, Department of Physiological Sciences, Department of Cell Biology and Genetics, State University of Maringá, Block H67, Room 19, Colombo Avenue 5970, 87020-900 Maringá, Paraná, Brazil

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Luiz Felipe Barella
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Rosiane Aparecida Miranda
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Ananda Malta
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Claudinéia Conationi da Silva Franco
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Tatiane Aparecida da Silva Ribeiro
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Rosana Torrezan Laboratory of Secretion Cell Biology, Department of Physiological Sciences, Department of Physiological Sciences, Department of Cell Biology and Genetics, State University of Maringá, Block H67, Room 19, Colombo Avenue 5970, 87020-900 Maringá, Paraná, Brazil

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Clarice Gravena
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Paulo Cezar de Freitas Mathias
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metabolic programming or metabolic imprinting. There are strong associations between metabolic programming and functional and structural changes in the brain. Hypothalamic neuron dense areas related to body weight (BW) control are changed in adult rats that

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Simon Lecoutre Univ. Lille, EA4489, Équipe Malnutrition Maternelle et Programmation des Maladies Métaboliques, F59000 Lille, France

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Barbara Deracinois Univ. Lille, EA4489, Équipe Malnutrition Maternelle et Programmation des Maladies Métaboliques, F59000 Lille, France

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Christine Laborie Univ. Lille, EA4489, Équipe Malnutrition Maternelle et Programmation des Maladies Métaboliques, F59000 Lille, France

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Delphine Eberlé Univ. Lille, EA4489, Équipe Malnutrition Maternelle et Programmation des Maladies Métaboliques, F59000 Lille, France

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Céline Guinez Univ. Lille, EA4489, Équipe Malnutrition Maternelle et Programmation des Maladies Métaboliques, F59000 Lille, France

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Polina E Panchenko INRA, UMR1198 Biologie du Développement et Reproduction, F-78350 Jouy-en-Josas, France

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Jean Lesage Univ. Lille, EA4489, Équipe Malnutrition Maternelle et Programmation des Maladies Métaboliques, F59000 Lille, France

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Didier Vieau Univ. Lille, EA4489, Équipe Malnutrition Maternelle et Programmation des Maladies Métaboliques, F59000 Lille, France

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Claudine Junien INRA, UMR1198 Biologie du Développement et Reproduction, F-78350 Jouy-en-Josas, France
UVSQ, Université Versailles-Saint-Quentin-en-Yvelines, Versailles, France

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Anne Gabory INRA, UMR1198 Biologie du Développement et Reproduction, F-78350 Jouy-en-Josas, France

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Christophe Breton Univ. Lille, EA4489, Équipe Malnutrition Maternelle et Programmation des Maladies Métaboliques, F59000 Lille, France

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sensitize offspring to obesity ( Leddy et al. 2008 ). Thus, WAT may represent a prime target of metabolic programming induced by maternal obesity. Perturbations to the perinatal nutrient supply may affect adipocyte development, leading to persistent

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Ralf Baumeister
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Elke Schaffitzel
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Maren Hertweck
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Modulation of insulin/IGF signaling in the nematode Caenorhabditis elegans is the central determinant of the endocrine control of stress response, diapause, and aging. Mutations in many genes that interfere with, or are controlled by, insulin signaling have been identified in the last decade by genetic analyses in the worm. Most of these genes have orthologs in vertebrate genomes, and their functional characterization has provided multiple hints about conserved mechanisms for the genetic influence on aging. The emerging picture is that insulin-like molecules, through the activity of the DAF-2/insulin/ IGF-I-like receptor, and the DAF-16/FKHRL1/FOXO transcription factor, control the ability of the organism to deal with oxidative stress, and interfere with metabolic programs that help to determine lifespan.

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Luba Sominsky School of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria, Australia

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Ilvana Ziko School of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria, Australia

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Thai-Xinh Nguyen School of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria, Australia

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Julie Quach School of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria, Australia

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Sarah J Spencer School of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria, Australia

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Early life diet influences metabolic programming, increasing the risk for long-lasting metabolic ill health. Neonatally overfed rats have an early increase in leptin that is maintained long term and is associated with a corresponding elevation in body weight. However, the immediate and long-term effects of neonatal overfeeding on hypothalamic anorexigenic pro-opiomelanocortin (POMC) and orexigenic agouti-related peptide (AgRP)/neuropeptide Y (NPY) circuitry, and if these are directly mediated by leptin, have not yet been examined. Here, we examined the effects of neonatal overfeeding on leptin-mediated development of hypothalamic POMC and AgRP/NPY neurons and whether these effects can be normalised by neonatal leptin antagonism in male Wistar rats. Neonatal overfeeding led to an acute (neonatal) resistance of hypothalamic neurons to exogenous leptin, but this leptin resistance was resolved by adulthood. While there were no effects of neonatal overfeeding on POMC immunoreactivity in neonates or adults, the neonatal overfeeding-induced early increase in arcuate nucleus (ARC) AgRP/NPY fibres was reversed by adulthood so that neonatally overfed adults had reduced NPY immunoreactivity in the ARC compared with controls, with no further differences in AgRP immunoreactivity. Short-term neonatal leptin antagonism did not reverse the excess body weight or hyperleptinaemia in the neonatally overfed, suggesting factors other than leptin may also contribute to the phenotype. Our findings show that changes in the availability of leptin during early life period influence the development of hypothalamic connectivity short term, but this is partly resolved by adulthood indicating an adaptation to the metabolic mal-programming effects of neonatal overfeeding.

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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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can also cause metabolic dysfunctions during adulthood ( de Oliveira et al . 2012 b ), leading us to conclude that the peripubertal phase could be another window for metabolic programing beyond perinatal development. It is important to note that

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Bo He Department of Pharmacology, Wuhan University School of Basic Medical Sciences, Wuhan, China
School of Pharmaceutical Sciences and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, Kunming, China

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Yinxian Wen Department of Orthopedic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China
Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan, China

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Shuwei Hu Department of Pharmacology, Wuhan University School of Basic Medical Sciences, Wuhan, China

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Guihua Wang Department of Pharmacology, Wuhan University School of Basic Medical Sciences, Wuhan, China

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Wen Hu Department of Pharmacology, Wuhan University School of Basic Medical Sciences, Wuhan, China

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Jacques Magdalou UMR 7561 CNRS-Université de Lorraine, Faculté de Médicine, Vandoeuvre-lès-Nancy, Nancy, France

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Liaobin Chen Department of Orthopedic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China
Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan, China

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Hui Wang Department of Pharmacology, Wuhan University School of Basic Medical Sciences, Wuhan, China
Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan, China

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have demonstrated that PCE can lead to fetal overexposure to maternal glucocorticoids and hypothalamic-pituitary-adrenal (HPA) axis-associated neuroendocrine metabolic programming alterations, resulting in the increased susceptibility of adult offspring

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Malathi Srinivasan
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Paul Mitrani
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Gigani Sadhanandan
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Catherine Dodds
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Suhad Shbeir-ElDika
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Shanthie Thamotharan Department of Biochemistry, Department of Pediatrics, Department of Medicine, Diabetes and Endocrinology Center of Western New York, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York at Buffalo, 140 Farber Hall, 3435 Main Street, Buffalo, New York 14214, USA

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Hussam Ghanim Department of Biochemistry, Department of Pediatrics, Department of Medicine, Diabetes and Endocrinology Center of Western New York, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York at Buffalo, 140 Farber Hall, 3435 Main Street, Buffalo, New York 14214, USA

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Paresh Dandona Department of Biochemistry, Department of Pediatrics, Department of Medicine, Diabetes and Endocrinology Center of Western New York, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York at Buffalo, 140 Farber Hall, 3435 Main Street, Buffalo, New York 14214, USA
Department of Biochemistry, Department of Pediatrics, Department of Medicine, Diabetes and Endocrinology Center of Western New York, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York at Buffalo, 140 Farber Hall, 3435 Main Street, Buffalo, New York 14214, USA

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Sherin U Devaskar Department of Biochemistry, Department of Pediatrics, Department of Medicine, Diabetes and Endocrinology Center of Western New York, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York at Buffalo, 140 Farber Hall, 3435 Main Street, Buffalo, New York 14214, USA

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Mulchand S Patel
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.05 compared with MF (Student's t -test) . Discussion The results from the present study indicate that the hypothalamus is vulnerable to metabolic programming effects of the high carbohydrate content of the milk formula received in the immediate postnatal life

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