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[PMID]:29300858
[Au] Autor:Fernandez G; Cabral A; Andreoli MF; Labarthe A; M'Kadmi C; Ramos JG; Marie J; Fehrentz JA; Epelbaum J; Tolle V; Perello M
[Ad] Endereço:Laboratory of Neurophysiology of the Multidisciplinary Institute of Cell Biology (Argentine Research Council, Scientific Research Commission of the Province of Buenos Aires and National University of La Plata), La Plata, Buenos Aires, Argentina.
[Ti] Título:Evidence Supporting a Role for Constitutive Ghrelin Receptor Signaling in Fasting-Induced Hyperphagia in Male Mice.
[So] Source:Endocrinology;159(2):1021-1034, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ghrelin is a potent orexigenic peptide hormone that acts through the growth hormone secretagogue receptor (GHSR), a G protein-coupled receptor highly expressed in the hypothalamus. In vitro studies have shown that GHSR displays a high constitutive activity, whose physiological relevance is uncertain. As GHSR gene expression in the hypothalamus is known to increase in fasting conditions, we tested the hypothesis that constitutive GHSR activity at the hypothalamic level drives the fasting-induced hyperphagia. We found that refed wild-type (WT) mice displayed a robust hyperphagia that continued for 5 days after refeeding and changed their food intake daily pattern. Fasted WT mice showed an increase in plasma ghrelin levels, as well as in GHSR expression levels and ghrelin binding sites in the hypothalamic arcuate nucleus. When fasting-refeeding responses were evaluated in ghrelin- or GHSR-deficient mice, only the latter displayed an ∼15% smaller hyperphagia, compared with WT mice. Finally, fasting-induced hyperphagia of WT mice was significantly smaller in mice centrally treated with the GHSR inverse agonist K-(D-1-Nal)-FwLL-NH2, compared with mice treated with vehicle, whereas it was unaffected in mice centrally treated with the GHSR antagonists D-Lys3-growth hormone-releasing peptide 6 or JMV2959. Taken together, genetic models and pharmacological results support the notion that constitutive GHSR activity modulates the magnitude of the compensatory hyperphagia triggered by fasting. Thus, the hypothalamic GHSR signaling system could affect the set point of daily food intake, independently of plasma ghrelin levels, in situations of negative energy balance.
[Mh] Termos MeSH primário: Jejum/fisiologia
Grelina/fisiologia
Hiperfagia/etiologia
Receptores de Grelina/fisiologia
[Mh] Termos MeSH secundário: Animais
Ingestão de Alimentos/fisiologia
Grelina/metabolismo
Hiperfagia/genética
Hiperfagia/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptores de Grelina/genética
Receptores de Grelina/metabolismo
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ghrelin); 0 (Receptors, Ghrelin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180105
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-03101


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[PMID]:29320575
[Au] Autor:Allas S; Caixàs A; Poitou C; Coupaye M; Thuilleaux D; Lorenzini F; Diene G; Crinò A; Illouz F; Grugni G; Potvin D; Bocchini S; Delale T; Abribat T; Tauber M
[Ad] Endereço:Alizé Pharma, Ecully, France.
[Ti] Título:AZP-531, an unacylated ghrelin analog, improves food-related behavior in patients with Prader-Willi syndrome: A randomized placebo-controlled trial.
[So] Source:PLoS One;13(1):e0190849, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CONTEXT AND OBJECTIVE: Prader-Willi syndrome (PWS) is characterized by early-onset hyperphagia and increased circulating levels of the orexigenic Acylated Ghrelin (AG) hormone with a relative deficit of Unacylated Ghrelin (UAG). AZP-531, a first-in-class UAG analog, was shown to inhibit the orexigenic effect of AG in animals, to improve glycemic control and decrease body weight in humans. We aimed to investigate the safety and efficacy of AZP-531 in patients with PWS for whom no approved treatment for hyperphagia is currently available. METHODS AND DESIGN: Multi-center, randomized, double-blind, placebo-controlled trial. Forty-seven patients with genetically confirmed PWS and evidence of hyperphagia received daily subcutaneous injections of AZP-531 (3 and 4 mg for 50-70 kg and >70 kg body weight, respectively) or matching placebo for 14 days. Assessments included adverse events, vital signs, safety laboratory tests, the Hyperphagia Questionnaire (HQ), patient-reported appetite, body composition and glycemic measures. RESULTS: AZP-531 was well tolerated. There was a significant improvement with AZP-531 versus placebo in the mean total score, the 9-item score and the severity domain score of the HQ (p < .05). The highest reduction in the total and 9-item scores was observed in AZP-531 subjects with the highest hyperphagia score at baseline. Findings were supported by a reduction in appetite scores observed with AZP-531 only. Body weight did not change in both groups while a significant reduction in waist circumference and fat mass was observed only with AZP-531. AZP-531 significantly decreased post-prandial glucose levels in a baseline glucose dependent fashion. CONCLUSIONS: AZP-531 may constitute a new treatment strategy to improve hyperphagia and metabolic issues in patients with PWS. These findings support further investigation in longer-term clinical trials.
[Mh] Termos MeSH primário: Comportamento Alimentar/efeitos dos fármacos
Grelina/uso terapêutico
Hiperfagia/tratamento farmacológico
Hipoglicemiantes/uso terapêutico
Fragmentos de Peptídeos/uso terapêutico
Peptídeos Cíclicos/uso terapêutico
Síndrome de Prader-Willi/tratamento farmacológico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Fármacos Antiobesidade/efeitos adversos
Fármacos Antiobesidade/uso terapêutico
Apetite/efeitos dos fármacos
Apetite/fisiologia
Glicemia/efeitos dos fármacos
Composição Corporal/efeitos dos fármacos
Peso Corporal/efeitos dos fármacos
Método Duplo-Cego
Comportamento Alimentar/fisiologia
Feminino
Seguimentos
Grelina/efeitos adversos
Seres Humanos
Hiperfagia/sangue
Hiperfagia/genética
Hipoglicemiantes/efeitos adversos
Masculino
Meia-Idade
Fragmentos de Peptídeos/efeitos adversos
Peptídeos Cíclicos/efeitos adversos
Síndrome de Prader-Willi/sangue
Síndrome de Prader-Willi/genética
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Obesity Agents); 0 (Blood Glucose); 0 (Ghrelin); 0 (Hypoglycemic Agents); 0 (Peptide Fragments); 0 (Peptides, Cyclic); 0 (cyclic des-acyl ghrelin (6-13))
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190849


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[PMID]:29190687
[Au] Autor:da Silva AA; Hall JE; do Carmo JM
[Ad] Endereço:Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, Mississippi, United States of America.
[Ti] Título:Leptin reverses hyperglycemia and hyperphagia in insulin deficient diabetic rats by pituitary-independent central nervous system actions.
[So] Source:PLoS One;12(11):e0184805, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The hypothalamic-pituitary-adrenal (HPA) axis has been postulated to play a major role in mediating the antidiabetic effects of leptin. We tested if the pituitary is essential for the chronic central nervous system mediated actions of leptin on metabolic and cardiovascular function in insulin-dependent diabetic and non-diabetic rats. Male 12-week-old hypophysectomized Sprague-Dawley rats (Hypo, n = 5) were instrumented with telemetry probes for determination of mean arterial pressure (MAP) and heart rate (HR) 24-hrs/day and an intracerebroventricular (ICV) cannula was placed into the brain lateral ventricle for continuous leptin infusion. In additional groups of Hypo and control rats (n = 5/group), diabetes was induced by single injection of streptozotocin (50 mg/kg, IP). Hypo rats were lighter, had lower MAP and HR (83±4 and 317±2 vs 105±4 mmHg and 339±4 bpm), with similar caloric intake per kilogram of body weight and fasting plasma glucose levels (84±4 vs 80±4 mg/dl) compared to controls. Chronic ICV leptin infusion (7 days, 0.62 µg/hr) in non-diabetic rats reduced caloric intake and body weight (-10%) in Hypo and control rats and markedly increased HR in control rats (~25 bpm) while causing only modest HR increases in Hypo rats (8 bpm). In diabetic Hypo and control rats, leptin infusion reduced caloric intake, body weight and glucose levels (323±74 to 99±20 and 374±27 to 108±10 mg/dl), respectively; however, the effects of leptin on HR were abolished in Hypo rats. These results indicate that hypophysectomy attenuates leptin's effect on HR regulation without altering leptin's ability to suppress appetite or normalize glucose levels in diabetes.
[Mh] Termos MeSH primário: Sistema Nervoso Central/fisiopatologia
Diabetes Mellitus Experimental/complicações
Hiperglicemia/tratamento farmacológico
Hiperfagia/tratamento farmacológico
Leptina/uso terapêutico
Hipófise/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Glicemia/metabolismo
Pressão Sanguínea
Bradicardia/tratamento farmacológico
Bradicardia/etiologia
Ingestão de Energia
Frequência Cardíaca
Hiperglicemia/complicações
Hiperfagia/complicações
Hipofisectomia
Infusões Intraventriculares
Insulina/sangue
Leptina/administração & dosagem
Masculino
Hipófise/cirurgia
Ratos
Ratos Sprague-Dawley
Estreptozocina
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insulin); 0 (Leptin); 5W494URQ81 (Streptozocin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180130
[Lr] Data última revisão:
180130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184805


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[PMID]:28957383
[Au] Autor:Vargas VE; Gurung S; Grant B; Hyatt K; Singleton K; Myers SM; Saunders D; Njoku C; Towner R; Myers DA
[Ad] Endereço:Departments of Obstetrics and Gynecology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
[Ti] Título:Gestational hypoxia disrupts the neonatal leptin surge and programs hyperphagia and obesity in male offspring in the Sprague-Dawley rat.
[So] Source:PLoS One;12(9):e0185272, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The effect of gestational hypoxia on the neonatal leptin surge, development of hypothalamic arcuate nuclei (ARH) projections and appetite that could contribute to the programming of offspring obesity is lacking. We examined the effect of 12% O2 from gestational days 15-19 in the Sprague-Dawley rat on post-weaning appetite, fat deposition by MRI, adipose tissue cytokine expression, the neonatal leptin surge, ARH response to exogenous leptin, and αMSH projections to the paraventricular nucleus (PVN) in response to a high fat (HFD) or control diet (CD) in male offspring. Normoxia (NMX) and Hypoxia (HPX) offspring exhibited increased food intake when fed a HFD from 5-8 weeks post-birth; HPX offspring on the CD had increased food intake from weeks 5-7 vs. NMX offspring on a CD. HPX offspring on a HFD remained hyperphagic through 23 weeks. Body weight were the same between offspring from HPX vs. NMX dams from 4-12 weeks of age fed a CD or HFD. By 14-23 weeks of age, HPX offspring fed the CD or HFD as well as male NMX offspring fed the HFD were heavier vs. NMX offspring fed the CD. HPX offspring fed a CD exhibited increased abdominal adiposity (MRI) that was amplified by a HFD. HPX offspring fed a HFD exhibited the highest abdominal fat cytokine expression. HPX male offspring had higher plasma leptin from postnatal day (PN) 6 through 14 vs. NMX pups. HPX offspring exhibited increased basal c-Fos labeled cells in the ARH vs. NMX pups on PN16. Leptin increased c-Fos staining in the ARH in NMX but not HPX offspring at PN16. HPX offspring had fewer αMSH fibers in the PVN vs. NMX offspring on PN16. In conclusion, gestational hypoxia impacts the developing ARH resulting in hyperphagia contributing to adult obesity on a control diet and exacerbated by a HFD.
[Mh] Termos MeSH primário: Hiperfagia/sangue
Hiperfagia/complicações
Hipóxia/sangue
Hipóxia/complicações
Leptina/sangue
Obesidade/sangue
Obesidade/complicações
[Mh] Termos MeSH secundário: Tecido Adiposo/metabolismo
Animais
Animais Recém-Nascidos
Ansiedade/sangue
Ansiedade/complicações
Núcleo Arqueado do Hipotálamo/metabolismo
Comportamento Animal
Dieta
Medo
Comportamento Alimentar
Feminino
Peso Fetal
Interleucina-1beta/genética
Interleucina-1beta/metabolismo
Interleucina-6/genética
Interleucina-6/metabolismo
Imagem por Ressonância Magnética
Masculino
Fenômenos Fisiológicos da Nutrição Materna
Aprendizagem em Labirinto
Atividade Motora
Gravidez
Ratos Sprague-Dawley
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
Água
Desmame
alfa-MSH/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Leptin); 0 (Tumor Necrosis Factor-alpha); 059QF0KO0R (Water); 581-05-5 (alpha-MSH)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170929
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185272


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[PMID]:28814400
[Au] Autor:de Lauzon-Guillain B; Clifton EA; Day FR; Clément K; Brage S; Forouhi NG; Griffin SJ; Koudou YA; Pelloux V; Wareham NJ; Charles MA; Heude B; Ong KK
[Ad] Endereço:Early Origin of Child Health and Development (ORCHAD) Team 6, Center of Research in Epidemiology and UMR 1153 Statistics Sorbonne Paris Cité (CRESS), National Institute of Health and Medical Research (INSERM), Paris, France.
[Ti] Título:Mediation and modification of genetic susceptibility to obesity by eating behaviors.
[So] Source:Am J Clin Nutr;106(4):996-1004, 2017 Oct.
[Is] ISSN:1938-3207
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Many genetic variants show highly robust associations with body mass index (BMI). However, the mechanisms through which genetic susceptibility to obesity operates are not well understood. Potentially modifiable mechanisms, including eating behaviors, are of particular interest to public health. Here we explore whether eating behaviors mediate or modify genetic susceptibility to obesity. Genetic risk scores for BMI (BMI-GRSs) were calculated for 3515 and 2154 adults in the Fenland and EDEN (Etude des déterminants pré et postnatals de la santé et du développement de l'enfant) population-based cohort studies, respectively. The eating behaviors-emotional eating, uncontrolled eating, and cognitive restraint-were measured through the use of a validated questionnaire. The mediating effect of each eating behavior on the association between the BMI-GRS and measured BMI was assessed by using the Sobel test. In addition, we tested for interactions between each eating behavior and the BMI-GRS on BMI. The association between the BMI-GRS and BMI was mediated by both emotional eating (EDEN: Sobel = 0.01; Fenland: Sobel = 0.02) and uncontrolled eating (EDEN: Sobel = 0.04; Fenland: -Sobel = 0.0006) in both sexes combined. Cognitive restraint did not mediate this association ( -Sobel > 0.10), except among EDEN women ( -Sobel = 0.0009). Cognitive restraint modified the relation between the BMI-GRS and BMI among men (EDEN: -interaction = 0.0001; Fenland: -interaction = 0.04) and Fenland women ( -interaction = 0.0004). By tertiles of cognitive restraint, the association between the BMI-GRS and BMI was strongest in the lowest tertile of cognitive restraint, and weakest in the highest tertile. Genetic susceptibility to obesity was partially mediated by the "appetitive" eating behavior traits (uncontrolled and emotional eating) and, in 3 of the 4 population groups studied, was modified by cognitive restraint. High levels of cognitive control over eating appear to attenuate the genetic susceptibility to obesity. Future research into interventions designed to support restraint may help to protect genetically susceptible individuals from weight gain.
[Mh] Termos MeSH primário: Cognição
Ingestão de Alimentos/psicologia
Emoções
Comportamento Alimentar
Interação Gene-Ambiente
Obesidade/etiologia
Autocontrole
[Mh] Termos MeSH secundário: Adulto
Apetite
Índice de Massa Corporal
Comportamento Alimentar/psicologia
Feminino
Predisposição Genética para Doença
Seres Humanos
Hiperfagia/complicações
Hiperfagia/psicologia
Masculino
Meia-Idade
Obesidade/genética
Obesidade/psicologia
Fatores de Risco
Fatores Sexuais
Inquéritos e Questionários
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE
[do] DOI:10.3945/ajcn.117.157396


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[PMID]:28805659
[Au] Autor:Lord CC; Wyler SC; Wan R; Castorena CM; Ahmed N; Mathew D; Lee S; Liu C; Elmquist JK
[Ad] Endereço:Division of Hypothalamic Research, Department of Internal Medicine, and.
[Ti] Título:The atypical antipsychotic olanzapine causes weight gain by targeting serotonin receptor 2C.
[So] Source:J Clin Invest;127(9):3402-3406, 2017 Sep 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Atypical antipsychotics such as olanzapine often induce excessive weight gain and type 2 diabetes. However, the mechanisms underlying these drug-induced metabolic perturbations remain poorly understood. Here, we used an experimental model that reproduces olanzapine-induced hyperphagia and obesity in female C57BL/6 mice. We found that olanzapine treatment acutely increased food intake, impaired glucose tolerance, and altered physical activity and energy expenditure in mice. Furthermore, olanzapine-induced hyperphagia and weight gain were blunted in mice lacking the serotonin 2C receptor (HTR2C). Finally, we showed that treatment with the HTR2C-specific agonist lorcaserin suppressed olanzapine-induced hyperphagia and weight gain. Lorcaserin treatment also improved glucose tolerance in olanzapine-fed mice. Collectively, our studies suggest that olanzapine exerts some of its untoward metabolic effects via antagonism of HTR2C.
[Mh] Termos MeSH primário: Antipsicóticos/farmacologia
Benzodiazepinas/farmacologia
Diabetes Mellitus Tipo 2/tratamento farmacológico
Antagonistas da Serotonina/farmacologia
Ganho de Peso/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antipsicóticos/efeitos adversos
Benzodiazepinas/efeitos adversos
Composição Corporal
Peso Corporal
Feminino
Glucose/química
Teste de Tolerância a Glucose
Hiperfagia/induzido quimicamente
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Receptor 5-HT2C de Serotonina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antipsychotic Agents); 0 (Receptor, Serotonin, 5-HT2C); 0 (Serotonin Antagonists); 12794-10-4 (Benzodiazepines); IY9XDZ35W2 (Glucose); N7U69T4SZR (olanzapine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170815
[St] Status:MEDLINE


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[PMID]:28585195
[Au] Autor:Engin A
[Ad] Endereço:Faculty of Medicine, Department of General Surgery, Gazi University, Besevler, Ankara, Turkey. dr.aengin@gmail.com.
[Ti] Título:Eat and Death: Chronic Over-Eating.
[So] Source:Adv Exp Med Biol;960:53-80, 2017.
[Is] ISSN:0065-2598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Obesity-related co-morbidities decrease life quality, reduce working ability and lead to early death. The total amount of dietary fat consumption may be the most potent food-related risk factor for weight gain. In this respect, dietary intake of high-caloric, high-fat diets due to chronic over-eating and sedentary lifestyle lead to increased storage of triglycerides not only in adipose tissue but also ectopically in other tissues . Increased plasma concentrations of non-esterified free fatty acids and lipid-overloaded hypertrophic adipocytes may cause insulin resistance in an inflammation-independent manner. Even in the absence of metabolic disorders, mismatch between fatty acid uptake and utilization leads to the accumulation of toxic lipid species resulting in organ dysfunction. Lipid-induced apoptosis, ceramide accumulation, reactive oxygen species overproduction, endoplasmic reticulum stress, and mitochondrial dysfunction may play role in the pathogenesis of lipotoxicity. The hypothalamus senses availability of circulating levels of glucose, lipids and amino acids, thereby modifies feeding according to the levels of those molecules. However, the hypothalamus is also similarly vulnerable to lipotoxicity as the other ectopic lipid accumulated tissues. Chronic overnutrition most likely provides repetitive and persistent signals that up-regulate inhibitor of nuclear factor kappa B kinase beta subunit/nuclear factor kappa B (IKKß/NF-κB) in the hypothalamus before the onset of obesity. However, the mechanisms by which high-fat diet induced peripheral signals affect the hypothalamic arcuate nucleus remain largely unknown. In this chapter, besides lipids and leptin, the role of glucose and insulin on specialized fuel-sensing neurons of hypothalamic neuronal circuits has been debated.
[Mh] Termos MeSH primário: Comportamento Alimentar/fisiologia
Hiperfagia/mortalidade
Hiperfagia/fisiopatologia
[Mh] Termos MeSH secundário: Morte
Glucose/metabolismo
Seres Humanos
Hiperfagia/metabolismo
Hipotálamo/fisiologia
Insulina/metabolismo
Leptina/metabolismo
Metabolismo dos Lipídeos/fisiologia
Obesidade/metabolismo
Obesidade/mortalidade
Obesidade/fisiopatologia
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Insulin); 0 (Leptin); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170607
[St] Status:MEDLINE
[do] DOI:10.1007/978-3-319-48382-5_3


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[PMID]:28549063
[Au] Autor:Finlayson G
[Ad] Endereço:School of Psychology, Faculty of Medicine &Health, Lifton Place, University of Leeds, Leeds LS2 9JT, West Yorkshire, UK.
[Ti] Título:Food addiction and obesity: unnecessary medicalization of hedonic overeating.
[So] Source:Nat Rev Endocrinol;13(8):493-498, 2017 Aug.
[Is] ISSN:1759-5037
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The concept of addiction is loaded with connotations and is often used for its political as much as its medical utility. The scientific case for 'food addiction' as a clinical phenotype currently rests on its association with generic diagnostic criteria for substance-related disorders being applied to everyday foods and eating-related problems. This has fused the concept of obesity with addiction regardless of whether it fits the definition. The hedonic, or reward, system can account for the ingestion of foods and drugs, confirming that they share neural substrates that differentiate liking and wanting. These are normal processes that are recruited for natural homeostatic behaviours and can explain the phenomenon of hedonic overeating as a consequence of human motivation pushed to extremes by an obesogenic environment. Food addiction constitutes a medicalization of common eating behaviours, taking on the properties of a disease. The use of this medical language has implications for the way in which society views overeating and obesity.
[Mh] Termos MeSH primário: Comportamento Aditivo/diagnóstico
Hiperfagia/diagnóstico
Medicalização/tendências
Obesidade/diagnóstico
Filosofia
[Mh] Termos MeSH secundário: Animais
Comportamento Aditivo/psicologia
Comportamento Aditivo/terapia
Comportamento Alimentar/psicologia
Seres Humanos
Hiperfagia/psicologia
Hiperfagia/terapia
Obesidade/psicologia
Obesidade/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[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:170527
[St] Status:MEDLINE
[do] DOI:10.1038/nrendo.2017.61


  9 / 2767 MEDLINE  
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[PMID]:28533422
[Au] Autor:Shi X; Li X; Hou Y; Cao X; Zhang Y; Wang H; Wang H; Peng C; Li J; Li Q; Wu C; Xiao X
[Ad] Endereço:Laboratory of Lipid & Glucose MetabolismThe First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
[Ti] Título:Paternal hyperglycemia in rats exacerbates the development of obesity in offspring.
[So] Source:J Endocrinol;234(2):175-186, 2017 Aug.
[Is] ISSN:1479-6805
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Parental history with obesity or diabetes will increase the risk for developing metabolic diseases in offspring. However, literatures as to transgenerational inheritance of metabolic dysfunctions through male lineage are relatively scarce. In the current study, we aimed to evaluate influences of paternal hyperglycemia on metabolic phenotypes in offspring. Male SD rats were i.p. injected with streptozotocin (STZ) or citrate buffer (CB, as control). STZ-injected rats with glucose levels higher than 16.7 mM were selected to breed with normal female rats. Offspring from STZ or CB treated fathers (STZ-O and CB-O) were maintained in the identical condition. We monitored body weight and food intake, and tests of glucose and insulin tolerance (GTTs and ITTs), fasting-refeeding and cold exposure were performed. Expression of factors involved in hypothalamic feeding and brown adipose tissue (BAT) thermogenic activity was performed by real-time PCR and Western blot. Adult STZ-O were heavier than CB-O. Impairment of GTTs was observed in STZ-O compared with CB-O at 22 and 32 weeks of age; ITTs results showed decreased insulin sensitivity in STZ-O. Daily food intake and accumulated food intake during 12-h refeeding after fasting were significantly higher in STZ-O. UCP1 levels were downregulated in BAT from STZ-O at room temperature and cold exposure. Finally, STZ-O rats showed suppressed leptin signaling in the hypothalamus as evidenced by upregulated SOCS3, reduced phosphorylation of STAT3, impaired processing POMC and decreased α-MSH production. Our study revealed that paternal hyperglycemia predisposes offspring to developing obesity, which is possibly associated with impaired hypothalamic leptin signaling.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica/fisiologia
Hiperglicemia/complicações
Obesidade/etiologia
[Mh] Termos MeSH secundário: Tecido Adiposo Marrom/fisiologia
Tecido Adiposo Branco/fisiologia
Animais
Diabetes Mellitus Experimental
Epididimo
Feminino
Hiperfagia
Hipotálamo/fisiologia
Leptina/sangue
Leptina/metabolismo
Masculino
Ratos
Ratos Sprague-Dawley
Transdução de Sinais/fisiologia
alfa-MSH/sangue
alfa-MSH/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Leptin); 581-05-5 (alpha-MSH)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE
[do] DOI:10.1530/JOE-17-0082


  10 / 2767 MEDLINE  
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[PMID]:28446630
[Au] Autor:McCrickerd K; Lim CM; Leong C; Chia EM; Forde CG
[Ad] Endereço:Clinical Nutrition Research Centre, Singapore Institute for Clinical Sciences, Agency for Science, Technology, and Research, and National University Health System, Singapore, Singapore.
[Ti] Título:Texture-Based Differences in Eating Rate Reduce the Impact of Increased Energy Density and Large Portions on Meal Size in Adults.
[So] Source:J Nutr;147(6):1208-1217, 2017 Jun.
[Is] ISSN:1541-6100
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Large portions and high dietary energy density promote overconsumption at meal times. This could be reduced by eating slowly. Two studies investigated whether texture-based reductions in eating rate and oral processing moderate consumption at breakfast in combination with variations in energy density and portion size. Adults attended 4 breakfast sessions (2 × 2 repeated-measures design) to consume rice porridge, combining a 45% reduction in eating rate [thin porridge (140 g/min) compared with thick porridge (77 g/min)] with a 77% increase in energy density (0.57 compared with 1.01 kcal/g) in study 1 [ = 61; aged 21-48 y; body mass index (BMI; in kg/m ): 16-29] and a 50% increase in portion size (100% compared with 150%) in study 2 ( = 53; aged 21-42 y; BMI: 16-29). Oral processing behaviors were coded by using webcams. Porridge intake was measured alongside changes in rated appetite. Increases in energy density and portion size led to increases of 80% and 13% in energy intake at breakfast, respectively ( < 0.001), but only portion size increased the weight of food consumed (13%). The thicker porridges were consumed at a slower rate and led to 11-13% reductions in food weight and energy intake compared with the thin versions ( < 0.001). Combined, the least energy was consumed when the thick "slow" porridge was served with a lower energy density or smaller portion ( < 0.05). Although intake was reduced for the thick porridges, they were expected to be more filling than the thin versions and experienced as equally satiating postconsumption. Adults eat in response to external features of the food environment. An opportunity exists to use a combination of energy-density dilution, smaller portions, and natural variations in food texture to design meals that promote reductions in energy intake while maintaining satiety.
[Mh] Termos MeSH primário: Apetite
Desjejum
Ingestão de Alimentos
Ingestão de Energia
Comportamento Alimentar
Tamanho da Porção
Saciação
[Mh] Termos MeSH secundário: Adulto
Grãos Comestíveis
Feminino
Seres Humanos
Hiperfagia/prevenção & controle
Masculino
Meia-Idade
Obesidade/etiologia
Obesidade/prevenção & controle
Oryza
Viscosidade
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170705
[Lr] Data última revisão:
170705
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.3945/jn.116.244251



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