Base de dados : MEDLINE
Pesquisa : C18.654.726 [Categoria DeCS]
Referências encontradas : 397 [refinar]
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[PMID]:28958692
[Au] Autor:Granado M; Amor S; Fernández N; Carreño-Tarragona G; Iglesias-Cruz MC; Martín-Carro B; Monge L; García-Villalón AL
[Ad] Endereço:Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma de Madrid, Madrid, Spain; CIBER Fisiopatologia de la Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid, Spain. Electronic address: miriam.granado@uam.es.
[Ti] Título:Effects of early overnutrition on the renal response to Ang II and expression of RAAS components in rat renal tissue.
[So] Source:Nutr Metab Cardiovasc Dis;27(10):930-937, 2017 Oct.
[Is] ISSN:1590-3729
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIMS: The aim of this study was to analyze the effects of early overnutrition (EON) on the expression of the renin angiotensin aldosterone system (RAAS) components in renal cortex, renal arteries and renal perivascular adipose tissue (PVAT), as well as the vascular response of renal arteries to Angiotensin II (Ang II). METHODS AND RESULTS: On birth day litters were adjusted to twelve (L12-control) or three (L3-overfed) pups per mother. Half of the animals were sacrificed at weaning (21 days old) and the other half at 5 months of age. Ang II-induced vasoconstriction of renal artery segments increased in young overfed rats and decreased in adult overfed rats. EON decreased the gene expression of angiotensinogen (Agt), Ang II receptors AT1 and AT2 and eNOS in renal arteries of young rats, while it increased the mRNA levels of AT-2 and ET-1 in adult rats. In renal PVAT EON up-regulated the gene expression of COX-2 and TNF-α in young rats and the mRNA levels of renin receptor both in young and in adult rats. On the contrary, Ang II receptors mRNA levels were downregulated at both ages. Renal cortex of overfed rats showed increased gene expression of Agt in adult rats and of AT1 in young rats. However the mRNA levels of AT1 were decreased in the renal cortex of overfed adult rats. CONCLUSION: EON is associated with alterations in the vascular response of renal arteries to Ang II and changes in the gene expression of RAAS components in renal tissue.
[Mh] Termos MeSH primário: Angiotensina II/farmacologia
Rim/irrigação sanguínea
Hipernutrição/metabolismo
Artéria Renal/efeitos dos fármacos
Sistema Renina-Angiotensina/efeitos dos fármacos
Vasoconstrição/efeitos dos fármacos
Vasoconstritores/farmacologia
[Mh] Termos MeSH secundário: Tecido Adiposo/efeitos dos fármacos
Tecido Adiposo/metabolismo
Tecido Adiposo/fisiopatologia
Fatores Etários
Fenômenos Fisiológicos da Nutrição Animal
Animais
Ciclo-Oxigenase 2/genética
Ciclo-Oxigenase 2/metabolismo
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Regulação da Expressão Gênica
Óxido Nítrico Sintase Tipo III/genética
Óxido Nítrico Sintase Tipo III/metabolismo
Estado Nutricional
Hipernutrição/genética
Hipernutrição/fisiopatologia
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos Sprague-Dawley
Receptor Tipo 1 de Angiotensina/genética
Receptor Tipo 1 de Angiotensina/metabolismo
Receptor Tipo 2 de Angiotensina/genética
Receptor Tipo 2 de Angiotensina/metabolismo
Artéria Renal/metabolismo
Artéria Renal/fisiopatologia
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (Receptor, Angiotensin, Type 1); 0 (Receptor, Angiotensin, Type 2); 0 (Tumor Necrosis Factor-alpha); 0 (Vasoconstrictor Agents); 11128-99-7 (Angiotensin II); EC 1.14.13.39 (Nitric Oxide Synthase Type III); EC 1.14.13.39 (Nos3 protein, rat); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (Ptgs2 protein, rat)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170930
[St] Status:MEDLINE


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[PMID]:28859076
[Au] Autor:Schreiner F; Ackermann M; Michalik M; Hucklenbruch-Rother E; Bilkei-Gorzo A; Racz I; Bindila L; Lutz B; Dötsch J; Zimmer A; Woelfle J
[Ad] Endereço:Pediatric Endocrinology Division, Children's Hospital, University of Bonn, Bonn, Germany.
[Ti] Título:Developmental programming of somatic growth, behavior and endocannabinoid metabolism by variation of early postnatal nutrition in a cross-fostering mouse model.
[So] Source:PLoS One;12(8):e0182754, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Nutrient deprivation during early development has been associated with the predisposition to metabolic disorders in adulthood. Considering its interaction with metabolism, appetite and behavior, the endocannabinoid (eCB) system represents a promising target of developmental programming. METHODS: By cross-fostering and variation of litter size, early postnatal nutrition of CB6F1-hybrid mice was controlled during the lactation period (3, 6, or 10 pups/mother). After weaning and redistribution at P21, all pups received standard chow ad libitum. Gene expression analyses (liver, visceral fat, hypothalamus) were performed at P50, eCB concentrations were determined in liver and visceral fat. Locomotor activity and social behavior were analyzed by means of computer-assisted videotracking. RESULTS: Body growth was permanently altered, with differences for length, weight, body mass index and fat mass persisting beyond P100 (all 3>6>10,p<0.01). This was paralleled by differences in hepatic IGF-I expression (p<0.01). Distinct gene expression patterns for key enzymes of the eCB system were observed in fat (eCB-synthesis: 3>6>10 (DAGLα p<0.05; NAPE-PLD p = 0.05)) and liver (eCB-degradation: 3>6>10 (FAAH p<0.05; MGL p<0.01)). Concentrations of endocannabinoids AEA and 2-AG in liver and visceral fat were largely comparable, except for a borderline significance for higher AEA (liver, p = 0.049) in formerly overfed mice and, vice versa, tendencies (p<0.1) towards lower AEA (fat) and 2-AG (liver) in formerly underfed animals. In the arcuate nucleus, formerly underfed mice tended to express more eCB-receptor transcripts (CB1R p<0.05; CB2R p = 0.08) than their overfed fellows. Open-field social behavior testing revealed significant group differences, with formerly underfed mice turning out to be the most sociable animals (p<0.01). Locomotor activity did not differ. CONCLUSION: Our data indicate a developmental plasticity of somatic growth, behavior and parameters of the eCB system, with long-lasting impact of early postnatal nutrition. Developmental programming of the eCB system in metabolically active tissues, as shown here for liver and fat, may play a role in the formation of the adult cardiometabolic risk profile following perinatal malnutrition in humans.
[Mh] Termos MeSH primário: Endocanabinoides/metabolismo
Fator de Crescimento Insulin-Like I/genética
Estado Nutricional
Hipernutrição/genética
[Mh] Termos MeSH secundário: Animais
Peso Corporal
Modelos Animais de Doenças
Feminino
Expressão Gênica/genética
Seres Humanos
Hipotálamo/metabolismo
Gordura Intra-Abdominal/metabolismo
Fígado/metabolismo
Camundongos
Hipernutrição/metabolismo
Hipernutrição/patologia
Gravidez
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endocannabinoids); 67763-96-6 (Insulin-Like Growth Factor I)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182754


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[PMID]:28799554
[Au] Autor:Reilly SM; Saltiel AR
[Ad] Endereço:Department of Medicine, University of California, San Diego School of Medicine, 9500 Gilman Drive, La Jolla, California 92093, USA.
[Ti] Título:Adapting to obesity with adipose tissue inflammation.
[So] Source:Nat Rev Endocrinol;13(11):633-643, 2017 Nov.
[Is] ISSN:1759-5037
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Adipose tissue not only has an important role in the storage of excess nutrients but also senses nutrient status and regulates energy mobilization. An overall positive energy balance is associated with overnutrition and leads to excessive accumulation of fat in adipocytes. These cells respond by initiating an inflammatory response that, although maladaptive in the long run, might initially be a physiological response to the stresses obesity places on adipose tissue. In this Review, we characterize adipose tissue inflammation and review the current knowledge of what triggers obesity-associated inflammation in adipose tissue. We examine the connection between adipose tissue inflammation and the development of insulin resistance and catecholamine resistance and discuss the ensuing state of metabolic inflexibility. Finally, we review the current and potential new anti-inflammatory treatments for obesity-associated metabolic disease.
[Mh] Termos MeSH primário: Tecido Adiposo/imunologia
Metabolismo Energético/imunologia
Inflamação/imunologia
Resistência à Insulina/imunologia
Obesidade/imunologia
Hipernutrição/imunologia
[Mh] Termos MeSH secundário: Adaptação Fisiológica
Adipócitos/imunologia
Tecido Adiposo/metabolismo
Catecolaminas/metabolismo
Metabolismo Energético/fisiologia
Homeostase
Seres Humanos
Imunidade Inata/imunologia
Inflamação/metabolismo
Resistência à Insulina/fisiologia
Obesidade/metabolismo
Hipernutrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Catecholamines)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170812
[St] Status:MEDLINE
[do] DOI:10.1038/nrendo.2017.90


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[PMID]:28722707
[Au] Autor:Zitvogel L; Pietrocola F; Kroemer G
[Ad] Endereço:Gustave Roussy Cancer Campus, Villejuif, France.
[Ti] Título:Nutrition, inflammation and cancer.
[So] Source:Nat Immunol;18(8):843-850, 2017 Jul 19.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Quantitative and qualitative aspects of nutrition have a profound effect on leukocytes and thereby affect proinflammatory carcinogenic effects or anticancer immune responses. As a result, nutrition affects the incidence, natural progression and therapeutic response of malignant diseases, both in humans and in preclinical animal models. Here we discuss the molecular mechanisms through which alimentary cues modulate metabolic, microbial and neuroendocrine circuitries and thus affect the probability of developing premalignant lesions that progress to clinically manifested disease and the response to therapeutic intervention. We examine each of the connections that compose the triangle of nutrition, immunological and inflammatory reactions and cancer while focusing on the mechanistic aspects of these relationships.
[Mh] Termos MeSH primário: Inflamação/imunologia
Síndrome Metabólica/imunologia
Microbiota/imunologia
Neoplasias/imunologia
Obesidade/imunologia
[Mh] Termos MeSH secundário: Dieta
Dieta Ocidental
Seres Humanos
Hipernutrição/imunologia
Fatores de Risco
Vitaminas
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Vitamins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170720
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3754


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[PMID]:28677122
[Au] Autor:Caputo T; Gilardi F; Desvergne B
[Ad] Endereço:Center for Integrative Genomics, Lausanne Faculty of Biology and Medicine, University of Lausanne, Switzerland.
[Ti] Título:From chronic overnutrition to metaflammation and insulin resistance: adipose tissue and liver contributions.
[So] Source:FEBS Lett;591(19):3061-3088, 2017 Oct.
[Is] ISSN:1873-3468
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The close association of obesity with an increased risk of metabolic diseases, such as insulin resistance, type 2 diabetes, and nonalcoholic fatty liver disease, is now well established. In this review, we aim first to describe the inflammatory process activated in response to overnutrition, especially in the liver and the adipose tissue. We then discuss the systemic effects of low-grade inflammation on the onset of insulin resistance. Particular attention is given to a series of very recent reports that identify not only processes but also molecules (lipids and metabolites) that interfere with the normal insulin signaling. Finally, special notes concerning the roles of peroxisome proliferator-activated receptors in the various processes will be made.
[Mh] Termos MeSH primário: Tecido Adiposo/patologia
Inflamação/patologia
Resistência à Insulina
Fígado/patologia
Hipernutrição/patologia
[Mh] Termos MeSH secundário: Animais
Doença Crônica
Seres Humanos
Modelos Biológicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170706
[St] Status:MEDLINE
[do] DOI:10.1002/1873-3468.12742


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[PMID]:28445448
[Au] Autor:Gould J
[Ti] Título:Nutrition: A world of insecurity.
[So] Source:Nature;544(7651):S6-S7, 2017 04 26.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Abastecimento de Alimentos/estatística & dados numéricos
[Mh] Termos MeSH secundário: Américas
Ásia
Região do Caribe
Produção Agrícola/estatística & dados numéricos
Cucurbitaceae
Grãos Comestíveis/provisão & distribuição
Europa (Continente)
Seres Humanos
Desnutrição/epidemiologia
Oceania
Hipernutrição/epidemiologia
Verduras/provisão & distribuição
Gerenciamento de Resíduos/estatística & dados numéricos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1038/544S6a


  7 / 397 MEDLINE  
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[PMID]:28428362
[Au] Autor:Geisler CE; Renquist BJ
[Ad] Endereço:School of Animal and Comparative Biomedical SciencesUniversity of Arizona, Tucson, Arizona, USA.
[Ti] Título:Hepatic lipid accumulation: cause and consequence of dysregulated glucoregulatory hormones.
[So] Source:J Endocrinol;234(1):R1-R21, 2017 Jul.
[Is] ISSN:1479-6805
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Fatty liver can be diet, endocrine, drug, virus or genetically induced. Independent of cause, hepatic lipid accumulation promotes systemic metabolic dysfunction. By acting as peroxisome proliferator-activated receptor (PPAR) ligands, hepatic non-esterified fatty acids upregulate expression of gluconeogenic, beta-oxidative, lipogenic and ketogenic genes, promoting hyperglycemia, hyperlipidemia and ketosis. The typical hormonal environment in fatty liver disease consists of hyperinsulinemia, hyperglucagonemia, hypercortisolemia, growth hormone deficiency and elevated sympathetic tone. These endocrine and metabolic changes further encourage hepatic steatosis by regulating adipose tissue lipolysis, liver lipid uptake, lipogenesis (DNL), beta-oxidation, ketogenesis and lipid export. Hepatic lipid accumulation may be induced by 4 separate mechanisms: (1) increased hepatic uptake of circulating fatty acids, (2) increased hepatic fatty acid synthesis, (3) decreased hepatic beta-oxidation and (4) decreased hepatic lipid export. This review will discuss the hormonal regulation of each mechanism comparing multiple physiological models of hepatic lipid accumulation. Nonalcoholic fatty liver disease (NAFLD) is typified by increased hepatic lipid uptake, synthesis, oxidation and export. Chronic hepatic lipid signaling through PPARgamma results in gene expression changes that allow concurrent activity of DNL and beta-oxidation. The importance of hepatic steatosis in driving systemic metabolic dysfunction is highlighted by the common endocrine and metabolic disturbances across many conditions that result in fatty liver. Understanding the mechanisms underlying the metabolic dysfunction that develops as a consequence of hepatic lipid accumulation is critical to identifying points of intervention in this increasingly prevalent disease state.
[Mh] Termos MeSH primário: Homeostase/fisiologia
Hormônios/fisiologia
Metabolismo dos Lipídeos/fisiologia
Fígado/metabolismo
[Mh] Termos MeSH secundário: Tecido Adiposo/metabolismo
Animais
Dieta
Doenças do Sistema Endócrino
Fígado Gorduroso/epidemiologia
Fígado Gorduroso/metabolismo
Glucagon/sangue
Gluconeogênese
Glucose/metabolismo
Seres Humanos
Hidrocortisona/sangue
Hiperinsulinismo
Lipídeos/fisiologia
Lipogênese
Lipólise
Hepatopatia Gordurosa não Alcoólica/etiologia
Hepatopatia Gordurosa não Alcoólica/metabolismo
Obesidade/metabolismo
Hipernutrição
Oxirredução
Transdução de Sinais
Viroses
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Hormones); 0 (Lipids); 9007-92-5 (Glucagon); IY9XDZ35W2 (Glucose); WI4X0X7BPJ (Hydrocortisone)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170422
[St] Status:MEDLINE
[do] DOI:10.1530/JOE-16-0513


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[PMID]:28414763
[Au] Autor:Wankhade UD; Zhong Y; Kang P; Alfaro M; Chintapalli SV; Thakali KM; Shankar K
[Ad] Endereço:Arkansas Children's Nutrition Center, Little Rock, Arkansas, United States of America.
[Ti] Título:Enhanced offspring predisposition to steatohepatitis with maternal high-fat diet is associated with epigenetic and microbiome alterations.
[So] Source:PLoS One;12(4):e0175675, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Non-alcoholic fatty liver disease (NAFLD) is an important co-morbidity associated with obesity and a precursor to steatohepatitis. However, the contributions of gestational and early life influences on development of NAFLD and NASH remain poorly appreciated. METHODS: Two independent studies were performed to examine whether maternal over-nutrition via exposure to high fat diet (HFD) leads to exacerbated hepatic responses to post-natal HFD and methionine choline deficient (MCD) diets in the offspring. Offspring of both control diet- and HFD-fed dams were weaned onto control and HFD, creating four groups. RESULTS: When compared to their control diet-fed littermates, offspring of HF-dams weaned onto HFD gained greater body weight; had increased relative liver weight and showed hepatic steatosis and inflammation. Similarly, this group revealed significantly greater immune response and pro-fibrogenic gene expression via RNA-seq. In parallel, 7-8 week old offspring were challenged with either control or MCD diets for 3 weeks. Responses to MCD diets were also exacerbated due to maternal HFD as seen by gene expression of classical pro-fibrogenic genes. Quantitative genome-scale DNA methylation analysis of over 1 million CpGs showed persistent epigenetic changes in key genes in tissue development and metabolism (Fgf21, Ppargc1ß) with maternal HFD and in cell adhesion and communication (VWF, Ephb2) in the combination of maternal HFD and offspring MCD diets. Maternal HFD also influenced gut microbiome profiles in offspring leading to a decrease in α-diversity. Linear regression analysis revealed association between serum ALT levels and Coprococcus, Coriobacteriacae, Helicobacterioceae and Allobaculum. CONCLUSION: Our findings indicate that maternal HFD detrimentally alters epigenetic and gut microbiome pathways to favor development of fatty liver disease and its progressive sequelae.
[Mh] Termos MeSH primário: Dieta Hiperlipídica/efeitos adversos
Hepatopatia Gordurosa não Alcoólica/etiologia
Efeitos Tardios da Exposição Pré-Natal/etiologia
[Mh] Termos MeSH secundário: Animais
Colina/administração & dosagem
Deficiência de Colina/complicações
Metilação de DNA
Modelos Animais de Doenças
Epigênese Genética
Feminino
Microbioma Gastrointestinal/genética
Perfilação da Expressão Gênica
Fígado/metabolismo
Masculino
Fenômenos Fisiológicos da Nutrição Materna
Metionina/administração & dosagem
Metionina/deficiência
Camundongos
Camundongos Endogâmicos C57BL
Hepatopatia Gordurosa não Alcoólica/genética
Hepatopatia Gordurosa não Alcoólica/microbiologia
Hipernutrição/complicações
Gravidez
Efeitos Tardios da Exposição Pré-Natal/genética
Efeitos Tardios da Exposição Pré-Natal/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
AE28F7PNPL (Methionine); N91BDP6H0X (Choline)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170509
[Lr] Data última revisão:
170509
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170418
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0175675


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[PMID]:28400363
[Au] Autor:Aguayo VM; Paintal K
[Ad] Endereço:United Nations Children's Fund (Unicef), New York vaguayo@unicef.org.
[Ti] Título:Nutrition in adolescent girls in South Asia.
[So] Source:BMJ;357:j1309, 2017 04 11.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Desnutrição/epidemiologia
Desnutrição/prevenção & controle
Estado Nutricional
Hipernutrição/epidemiologia
Hipernutrição/prevenção & controle
[Mh] Termos MeSH secundário: Adolescente
Ásia/epidemiologia
Feminino
Seres Humanos
Serviços Preventivos de Saúde
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170721
[Lr] Data última revisão:
170721
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170413
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.j1309


  10 / 397 MEDLINE  
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[PMID]:28081146
[Au] Autor:Robles M; Gautier C; Mendoza L; Peugnet P; Dubois C; Dahirel M; Lejeune JP; Caudron I; Guenon I; Camous S; Tarrade A; Wimel L; Serteyn D; Bouraima-Lelong H; Chavatte-Palmer P
[Ad] Endereço:UMR BDR, INRA, ENVA, Université Paris Saclay, Jouy en Josas, France.
[Ti] Título:Maternal Nutrition during Pregnancy Affects Testicular and Bone Development, Glucose Metabolism and Response to Overnutrition in Weaned Horses Up to Two Years.
[So] Source:PLoS One;12(1):e0169295, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Pregnant mares and post-weaning foals are often fed concentrates rich in soluble carbohydrates, together with forage. Recent studies suggest that the use of concentrates is linked to alterations of metabolism and the development of osteochondrosis in foals. The aim of this study was to determine if broodmare diet during gestation affects metabolism, osteoarticular status and growth of yearlings overfed from 20 to 24 months of age and/or sexual maturity in prepubertal colts. MATERIAL AND METHODS: Twenty-four saddlebred mares were fed forage only (n = 12, group F) or cracked barley and forage (n = 12, group B) from mid-gestation until foaling. Colts were gelded at 12 months of age. Between 20 and 24 months of age, all yearlings were overfed (+140% of requirements) using an automatic concentrate feeder. Offspring were monitored for growth between 6 and 24 months of age, glucose homeostasis was evaluated via modified frequently sampled intra veinous glucose tolerance test (FSIGT) at 19 and 24 months of age and osteoarticular status was investigated using radiographic examinations at 24 months of age. The structure and function of testicles from prepubertal colts were analyzed using stereology and RT-qPCR. RESULTS: Post-weaning weight growth was not different between groups. Testicular maturation was delayed in F colts compared to B colts at 12 months of age. From 19 months of age, the cannon bone was wider in B vs F yearlings. F yearlings were more insulin resistant at 19 months compared to B yearlings but B yearlings were affected more severely by overnutrition with reduced insulin sensitivity. The osteoarticular status at 24 months of age was not different between groups. CONCLUSION: In conclusion, nutritional management of the pregnant broodmare and the growing foal may affect sexual maturity of colts and the metabolism of foals until 24 months of age. These effects may be deleterious for reproductive and sportive performances in older horses.
[Mh] Termos MeSH primário: Desenvolvimento Ósseo
Exposição Materna/efeitos adversos
Hipernutrição
Testículo/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: Animais
Feminino
Cavalos
Masculino
Gravidez
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170803
[Lr] Data última revisão:
170803
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170113
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0169295



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