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Pesquisa : D12.644.400.500 [Categoria DeCS]
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  1 / 9771 MEDLINE  
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[PMID]:28465077
[Au] Autor:Malet M; Leiguarda C; Gastón G; McCarthy C; Brumovsky P
[Ad] Endereço:Instituto de Investigaciones en Medicina Traslacional (IIMT), Consejo Nacional de Investigaciones Cientiíficas y Técnicas (CONICET) - Austral University, Avenida Juan D. Perón 1500, B1629AHJ, Pilar, Buenos Aires, Argentina.
[Ti] Título:Spinal activation of the NPY Y1 receptor reduces mechanical and cold allodynia in rats with chronic constriction injury.
[So] Source:Peptides;92:38-45, 2017 Jun.
[Is] ISSN:1873-5169
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neuropeptide tyrosine (NPY) and its associated receptors Y1R and Y2R have been previously implicated in the spinal modulation of neuropathic pain induced by total or partial sectioning of the sciatic nerve. However, their role in chronic constrictive injuries of the sciatic nerve has not yet been described. In the present study, we analyzed the consequences of pharmacological activation of spinal Y1R, by using the specific Y1R agonist Leu Pro -NPY, in rats with chronic constriction injury (CCI). CCI and sham-injury rats were implanted with a permanent intrathecal catheter (at day 7 after injury), and their response to the administration of different doses (2.5, 5, 7, 10 or 20µg) of Leu Pro -NPY (at a volume of 10µl) through the implanted catheter, recorded 14days after injury. Mechanical allodynia was tested by means of the up-and-down method, using von Frey filaments. Cold allodynia was tested by application of an acetone drop to the affected hindpaw. Intrathecal Leu Pro -NPY induced an increase of mechanical thresholds in rats with CCI, starting at doses of 5µg and becoming stronger with higher doses. Intrathecal Leu Pro also resulted in reductions in the frequency of withdrawal to cold stimuli, although the effect was somewhat more moderate and mostly observed for doses of 7µg and higher. We thus show that spinal activation of the Y1R is able to reduce neuropathic pain due to a chronic constrictive injury and, together with other studies, support the use of a spinal Y1R agonist as a therapeutic agent against chronic pain induced by peripheral neuropathy.
[Mh] Termos MeSH primário: Hiperalgesia/metabolismo
Neuropeptídeo Y/metabolismo
Receptores de Neuropeptídeo Y/metabolismo
Nervo Isquiático/lesões
Neuropatia Ciática/metabolismo
Medula Espinal/metabolismo
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Dor Crônica/metabolismo
Temperatura Baixa
Constrição Patológica/complicações
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Hiperalgesia/etiologia
Injeções Espinhais
Masculino
Neuralgia/metabolismo
Medição da Dor
Limiar da Dor
Ratos
Ratos Sprague-Dawley
Receptores de Neuropeptídeo Y/agonistas
Neuropatia Ciática/etiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neuropeptide Y); 0 (Receptors, Neuropeptide Y)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  2 / 9771 MEDLINE  
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[PMID]:29017851
[Au] Autor:Priyadarshini; Lal B
[Ad] Endereço:Department of Zoology, Institute of Science, Banaras Hindu University, Varanasi 221 005, India.
[Ti] Título:Seasonal ovarian immunolocalization of neuropeptide Y and its role in steriodogenesis in Asian catfish, Clarias batrachus.
[So] Source:Gen Comp Endocrinol;255:32-39, 2018 Jan 01.
[Is] ISSN:1095-6840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The present study was undertaken to examine the cellular localization and potential steroidogenic role of neuropeptide Y (NPY) in the ovary of the freshwater catfish, Clarias batrachus. NPY-immunoreaction was observed in the follicular cells (granulosa and thecal cells) in the growing ovarian follicles, and the intensity of staining increased steadily from the initiation of follicular development until follicles were fully grown. Thereafter as follicles matured the stain intensity decreased. Positive correlations were found between NPY expression and the ovarian levels of 17ß-estradiol, testosterone, and activities of 3ß-hydroxysteroid dehydrogenase (3ß-HSD) and 17ß-hydroxysteroid dehydrogenase (17ß-HSD) in the ovary. In vitro NPY treatment stimulated the production of the two steroids and the activities of two enzymes. This is the first report of NPY immunoreactivity at the cellular level in the fish ovary and implicates this orexigenic peptide in the modulation of ovarian steroidogenesis.
[Mh] Termos MeSH primário: Peixes-Gato/metabolismo
Neuropeptídeo Y/metabolismo
Ovário/metabolismo
Estações do Ano
Esteroides/biossíntese
[Mh] Termos MeSH secundário: 17-Hidroxiesteroide Desidrogenases/metabolismo
3-Hidroxiesteroide Desidrogenases/metabolismo
Animais
Peixes-Gato/sangue
Estradiol/sangue
Estradiol/metabolismo
Feminino
Imuno-Histoquímica
Ovário/anatomia & histologia
Reprodução
Testosterona/sangue
Testosterona/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neuropeptide Y); 0 (Steroids); 3XMK78S47O (Testosterone); 4TI98Z838E (Estradiol); EC 1.1.- (17-Hydroxysteroid Dehydrogenases); EC 1.1.- (3-Hydroxysteroid Dehydrogenases); EC 1.1.1.51 (3 (or 17)-beta-hydroxysteroid dehydrogenase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171012
[St] Status:MEDLINE


  3 / 9771 MEDLINE  
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[PMID]:27773938
[Au] Autor:Dalvi PS; Chalmers JA; Luo V; Han DY; Wellhauser L; Liu Y; Tran DQ; Castel J; Luquet S; Wheeler MB; Belsham DD
[Ad] Endereço:Department of Physiology, University of Toronto, Toronto, Ontario, Canada.
[Ti] Título:High fat induces acute and chronic inflammation in the hypothalamus: effect of high-fat diet, palmitate and TNF-α on appetite-regulating NPY neurons.
[So] Source:Int J Obes (Lond);41(1):149-158, 2017 Jan.
[Is] ISSN:1476-5497
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Consumption of dietary fat is one of the key factors leading to obesity. High-fat diet (HFD)-induced obesity is characterized by induction of inflammation in the hypothalamus; however, the temporal regulation of proinflammatory markers and their impact on hypothalamic appetite-regulating neuropeptide Y/agouti-related peptide (NPY/AgRP) neurons remains undefined. METHODS: Mice were injected with an acute lipid infusion for 24 h or fed a HFD over 8-20 weeks. Characterized mouse NPY/AgRP hypothalamic cell lines were used for in vitro experimentation. Immunohistochemistry in brain slices or quantitative real-time PCR in cell lines, was performed to determine changes in the expression of key inflammatory markers and neuropeptides. RESULTS: Hypothalamic inflammation, indicated by tumor necrosis factor (TNF)-α expression and astrocytosis in the arcuate nucleus, was evident following acute lipid infusion. HFD for 8 weeks suppressed TNF-α, while significantly increasing heat-shock protein 70 and ciliary neurotrophic factor, both neuroprotective components. HFD for 20 weeks induced TNF-α expression in NPY/AgRP neurons, suggesting a detrimental temporal regulatory mechanism. Using NPY/AgRP hypothalamic cell lines, we found that palmitate provoked a mixed inflammatory response on a panel of inflammatory and endoplasmic reticulum (ER) stress genes, whereas TNF-α significantly upregulated IκBα, nuclear factor (NF)-κB and interleukin-6 mRNA levels. Palmitate and TNF-α exposure predominantly induced NPY mRNA levels. Utilizing an I kappa B kinase ß (IKKß) inhibitor, we demonstrated that these effects potentially occur via the inflammatory IKKß/NF-κB pathway. CONCLUSIONS: These findings indicate that acute lipid and chronic HFD feeding in vivo, as well as acute palmitate and TNF-α exposure in vitro, induce markers of inflammation or ER stress in the hypothalamic appetite-stimulating NPY/AgRP neurons over time, which may contribute to a dramatic alteration in NPY/AgRP content or expression. Acute and chronic HFD feeding in vivo temporally regulates arcuate TNF-α expression with reactive astrocytosis, which suggests a time-dependent neurotrophic or neurotoxic role of lipids.
[Mh] Termos MeSH primário: Apetite/efeitos dos fármacos
Dieta Hiperlipídica/efeitos adversos
Hipotálamo/patologia
Inflamação/induzido quimicamente
Neurônios/efeitos dos fármacos
Neuropeptídeo Y/metabolismo
Palmitatos/farmacologia
Fator de Necrose Tumoral alfa/farmacologia
[Mh] Termos MeSH secundário: Animais
Núcleo Arqueado do Hipotálamo/patologia
Modelos Animais de Doenças
Regulação da Expressão Gênica
Hipotálamo/efeitos dos fármacos
Inflamação/patologia
Interleucina-6/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Neurônios/metabolismo
Obesidade/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-6); 0 (Neuropeptide Y); 0 (Palmitates); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1038/ijo.2016.183


  4 / 9771 MEDLINE  
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[PMID]:29177493
[Au] Autor:Adorjan I; Ahmed B; Feher V; Torso M; Krug K; Esiri M; Chance SA; Szele FG
[Ad] Endereço:Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
[Ti] Título:Calretinin interneuron density in the caudate nucleus is lower in autism spectrum disorder.
[So] Source:Brain;140(7):2028-2040, 2017 Jul 01.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Autism spectrum disorder is a debilitating condition with possible neurodevelopmental origins but unknown neuroanatomical correlates. Whereas investigators have paid much attention to the cerebral cortex, few studies have detailed the basal ganglia in autism. The caudate nucleus may be involved in the repetitive movements and limbic changes of autism. We used immunohistochemistry for calretinin and neuropeptide Y in 24 age- and gender-matched patients with autism spectrum disorder and control subjects ranging in age from 13 to 69 years. Patients with autism had a 35% lower density of calretinin+ interneurons in the caudate that was driven by loss of small calretinin+ neurons. This was not caused by altered size of the caudate, as its cross-sectional surface areas were similar between diagnostic groups. Controls exhibited an age-dependent increase in the density of medium and large calretinin+ neurons, whereas subjects with autism did not. Diagnostic groups did not differ regarding ionized calcium-binding adapter molecule 1+ immunoreactivity for microglia, suggesting chronic inflammation did not cause the decreased calretinin+ density. There was no statistically significant difference in the density of neuropeptide Y+ neurons between subjects with autism and controls. The decreased calretinin+ density may disrupt the excitation/inhibition balance in the caudate leading to dysfunctional corticostriatal circuits. The description of such changes in autism spectrum disorder may clarify pathomechanisms and thereby help identify targets for drug intervention and novel therapeutic strategies.
[Mh] Termos MeSH primário: Transtorno do Espectro Autista/patologia
Calbindina 2/metabolismo
Núcleo Caudado/patologia
Interneurônios/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Transtorno do Espectro Autista/diagnóstico por imagem
Estudos de Casos e Controles
Núcleo Caudado/diagnóstico por imagem
Córtex Cerebral/patologia
Proteínas de Ligação a DNA/metabolismo
Feminino
Seres Humanos
Masculino
Microglia/patologia
Meia-Idade
Neuropeptídeo Y/metabolismo
Estatísticas não Paramétricas
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AIF1 protein, human); 0 (Calbindin 2); 0 (DNA-Binding Proteins); 0 (Neuropeptide Y)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171130
[Lr] Data última revisão:
171130
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awx131


  5 / 9771 MEDLINE  
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[PMID]:28977590
[Au] Autor:Foradori CD; Whitlock BK; Daniel JA; Zimmerman AD; Jones MA; Read CC; Steele BP; Smith JT; Clarke IJ; Elsasser TH; Keisler DH; Sartin JL
[Ad] Endereço:Department of Anatomy, Physiology & Pharmacology, Auburn University, Auburn, Alabama 36849.
[Ti] Título:Kisspeptin Stimulates Growth Hormone Release by Utilizing Neuropeptide Y Pathways and Is Dependent on the Presence of Ghrelin in the Ewe.
[So] Source:Endocrinology;158(10):3526-3539, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although kisspeptin is the primary stimulator of gonadotropin-releasing hormone secretion and therefore the hypothalamic-pituitary-gonadal axis, recent findings suggest kisspeptin can also regulate additional neuroendocrine processes including release of growth hormone (GH). Here we show that central delivery of kisspeptin causes a robust rise in plasma GH in fasted but not fed sheep. Kisspeptin-induced GH secretion was similar in animals fasted for 24 hours and those fasted for 72 hours, suggesting that the factors involved in kisspeptin-induced GH secretion are responsive to loss of food availability and not the result of severe negative energy balance. Pretreatment with the neuropeptide Y (NPY) Y1 receptor antagonist, BIBO 3304, blocked the effects of kisspeptin-induced GH release, implicating NPY as an intermediary. Kisspeptin treatment induced c-Fos in NPY and GH-releasing hormone (GHRH) cells of the arcuate nucleus. The same kisspeptin treatment resulted in a reduction in c-Fos in somatostatin (SS) cells in the periventricular nucleus. Finally, blockade of systemic ghrelin release or antagonism of the ghrelin receptor eliminated or reduced the ability of kisspeptin to induce GH release, suggesting the presence of ghrelin is required for kisspeptin-induced GH release in fasted animals. Our findings support the hypothesis that during short-term fasting, systemic ghrelin concentrations and NPY expression in the arcuate nucleus rise. This permits kisspeptin activation of NPY cells. In turn, NPY stimulates GHRH cells and inhibits SS cells, resulting in GH release. We propose a mechanism by which kisspeptin conveys reproductive and hormone status onto the somatotropic axis, resulting in alterations in GH release.
[Mh] Termos MeSH primário: Grelina/metabolismo
Hormônio do Crescimento/efeitos dos fármacos
Kisspeptinas/farmacologia
Neuropeptídeo Y/metabolismo
Células Secretoras de Somatostatina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Núcleo Arqueado do Hipotálamo/efeitos dos fármacos
Núcleo Arqueado do Hipotálamo/metabolismo
Arginina/análogos & derivados
Arginina/farmacologia
Atropina/farmacologia
Jejum/metabolismo
Feminino
Imunofluorescência
Hormônio do Crescimento/secreção
Hormônio Liberador de Hormônio do Crescimento
Antagonistas Muscarínicos/farmacologia
Oligopeptídeos/farmacologia
Proteínas Proto-Oncogênicas c-fos/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-fos/metabolismo
Receptores de Grelina/antagonistas & inibidores
Receptores de Neuropeptídeo Y/antagonistas & inibidores
Ovinos
Carneiro Doméstico
Células Secretoras de Somatostatina/secreção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GHRP-6, Lys(3)-); 0 (Ghrelin); 0 (Kisspeptins); 0 (Muscarinic Antagonists); 0 (Neuropeptide Y); 0 (Oligopeptides); 0 (Proto-Oncogene Proteins c-fos); 0 (Receptors, Ghrelin); 0 (Receptors, Neuropeptide Y); 7C0697DR9I (Atropine); 9002-72-6 (Growth Hormone); 9034-39-3 (Growth Hormone-Releasing Hormone); 94ZLA3W45F (Arginine); O35HK034KO (BIBO 3304)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00303


  6 / 9771 MEDLINE  
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[PMID]:28877214
[Au] Autor:Hashiguchi H; Sheng Z; Routh V; Gerzanich V; Simard JM; Bryan J
[Ad] Endereço:Department of Diabetes and Endocrinology, Kagoshima University Graduate School of Medicine and Dental Science, Kagoshima, Kagoshima, Japan.
[Ti] Título:Direct versus indirect actions of ghrelin on hypothalamic NPY neurons.
[So] Source:PLoS One;12(9):e0184261, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Assess direct versus indirect action(s) of ghrelin on hypothalamic NPY neurons. MATERIALS AND METHODS: Electrophysiology was used to measure ion channel activity in NPY-GFP neurons in slice preparations. Ca2+ imaging was used to monitor ghrelin activation of isolated NPY GFP-labeled neurons. Immunohistochemistry was used to localize Trpm4, SUR1 and Kir6.2 in the hypothalamus. RESULTS: Acylated ghrelin depolarized the membrane potential (MP) of NPY-GFP neurons in brain slices. Depolarization resulted from a decreased input resistance (IR) in ~70% of neurons (15/22) or an increased IR in the remainder (7/22), consistent with the opening or closing of ion channels, respectively. Although tetrodotoxin (TTX) blockade of presynaptic action potentials reduced ghrelin-induced changes in MP and IR, ghrelin still significantly depolarized the MP and decreased IR in TTX-treated neurons, suggesting that ghrelin directly opens cation channel(s) in NPY neurons. In isolated NPY-GFP neurons, ghrelin produced a sustained rise of [Ca2+]c, with an EC50 ~110 pM. Pharmacologic studies confirmed that the direct action of ghrelin was through occupation of the growth hormone secretagogue receptor, GHS-R, and demonstrated the importance of the adenylate cyclase/cAMP/protein kinase A (PKA) and phospholipase C/inositol triphosphate (PLC/IP3) pathways as activators of 5' AMP-activated protein kinase (AMPK). Activation of isolated neurons was not affected by CNQX or TTX, but reducing [Na+]o suppressed activation, suggesting a role for Na+-permeable cation channels. SUR1 and two channel partners, Kir6.2 and Trpm4, were identified immunologically in NPY-GFP neurons in situ. The actions of SUR1 and Trpm4 modulators were informative: like ghrelin, diazoxide, a SUR1 agonist, elevated [Ca2+]c and glibenclamide, a SUR1 antagonist, partially suppressed ghrelin action, while 9-phenanthrol and flufenamic acid, selective Trpm4 antagonists, blocked ghrelin actions on isolated neurons. Ghrelin activation was unaffected by nifedipine and ω-conotoxin, inhibitors of L- and N-type Ca2+ channels, respectively, while Ni2+, mibefradil, and TTA-P2 completely or partially inhibited ghrelin action, implicating T-type Ca2+ channels. Activation was also sensitive to a spider toxin, SNX-482, at concentrations selective for R-type Ca2+ channels. Nanomolar concentrations of GABA markedly inhibited ghrelin-activation of isolated NPY-GFP neurons, consistent with chronic suppression of ghrelin action in vivo. CONCLUSIONS: NPY neurons express all the molecular machinery needed to respond directly to ghrelin. Consistent with recent studies, ghrelin stimulates presynaptic inputs that activate NPY-GFP neurons in situ. Ghrelin can also directly activate a depolarizing conductance. Results with isolated NPY-GFP neurons suggest the ghrelin-activated, depolarizing current is a Na+ conductance with the pharmacologic properties of SUR1/Trpm4 non-selective cation channels. In the isolated neuron model, the opening of SUR1/Trpm4 channels activates T- and SNX482-sensitive R-type voltage dependent Ca2+ channels, which could contribute to NPY neuronal activity in situ.
[Mh] Termos MeSH primário: Grelina/fisiologia
Hipotálamo Médio/fisiologia
Neurônios/fisiologia
Neuropeptídeo Y/fisiologia
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Imunofluorescência
Hipotálamo Médio/citologia
Masculino
Potenciais da Membrana/fisiologia
Camundongos
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ghrelin); 0 (Neuropeptide Y); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170907
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184261


  7 / 9771 MEDLINE  
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[PMID]:28864114
[Au] Autor:Ding X; Kou X; Zhang Y; Zhang X; Cheng G; Jia T
[Ad] Endereço:Department of internal neurology, Henan women and children health Hospital, Affiliated hospital of Zhengzhou University, Zhengzhou 450000, PR China.
[Ti] Título:Leptin siRNA promotes ovarian granulosa cell apoptosis and affects steroidogenesis by increasing NPY2 receptor expression.
[So] Source:Gene;633:28-34, 2017 Oct 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Leptin has been found to be involved in the ovarian granulosa cell apoptosis and steroidogenesis. Loss of neuropeptide Y (NPY) can correct the obesity syndrome of mutant mice lacking of leptin (ob/ob). However, the association of NPY and leptin in ovarian granulosa cells and ovarian steroidogenesis has not been investigated. Here, C57BL/6J ob/ob mice and C57BL/6J (control) mice were intraperitoneally injected with PBS, leptin (0.4µg/g bodyweight) or BIIE0246 (NPY2 receptor [NPY2R] antagonist, 30µg/kg bodyweight) every day for 15days. We found that NPY2R mRNA expression in mouse ovary was suppressed by leptin treatment, but increased by leptin deficiency. Leptin or BIIE0246 treatment significantly increased E2, but notably decreased progesterone in both mice. A lower level of E2 and a higher level of progesterone was observed in ob/ob mice than in control mice. Further, we then knocked down leptin expression in human ovarian granulosa cells by siRNA transfection and treated the cells with DMSO or BIIE0246. In vitro experiments confirmed the findings in mice. siLeptin treatment decreased the secretion of E2, anti-Mullerian hormone (AMH), insulin-like growth factor (IGF)-1 and transforming growth factor (TGF)-ß, and the cell proliferation, but increased the secretion of progesterone and cell apoptosis. Western blotting analysis of PCNA, Bcl-2 and Bax confirmed the results of cell proliferation and apoptosis. Activation of JAK2 and STAT3 was also suppressed by knocking down leptin. All the effects of siLeptin on ovarian granulosa cells were partially reversed by BIIE0246. In conclusion, knockdown of leptin significantly affected ovarian steroidogenesis and ovarian function through NPY. siLeptin transfection impaired the activation of JAK2/STAT3 and contributed to ovarian granulosa cell apoptosis partially through up-regulating NPY2R expression.
[Mh] Termos MeSH primário: Apoptose/genética
Hormônios Esteroides Gonadais/genética
Células da Granulosa/fisiologia
Leptina/metabolismo
Neuropeptídeo Y/metabolismo
Progesterona/biossíntese
Receptores de Neuropeptídeo Y/biossíntese
[Mh] Termos MeSH secundário: Androstenodiona/genética
Animais
Apoptose/efeitos dos fármacos
Arginina/administração & dosagem
Arginina/análogos & derivados
Arginina/farmacologia
Benzazepinas/administração & dosagem
Benzazepinas/farmacologia
Proliferação Celular
Dinoprostona/genética
Feminino
Hormônio Foliculoestimulante/metabolismo
Técnicas de Silenciamento de Genes
Células da Granulosa/citologia
Células da Granulosa/efeitos dos fármacos
Seres Humanos
Janus Quinase 2/biossíntese
Janus Quinase 2/genética
Leptina/genética
Leptina/farmacologia
Camundongos
Camundongos Endogâmicos C57BL
Neuropeptídeo Y/antagonistas & inibidores
Progesterona/genética
RNA Interferente Pequeno/metabolismo
Receptores de Neuropeptídeo Y/antagonistas & inibidores
Receptores de Neuropeptídeo Y/genética
Fator de Transcrição STAT3/biossíntese
Fator de Transcrição STAT3/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzazepines); 0 (Gonadal Steroid Hormones); 0 (Leptin); 0 (Neuropeptide Y); 0 (RNA, Small Interfering); 0 (Receptors, Neuropeptide Y); 0 (STAT3 Transcription Factor); 0 (neuropeptide Y2 receptor); 409J2J96VR (Androstenedione); 4G7DS2Q64Y (Progesterone); 9002-68-0 (Follicle Stimulating Hormone); 94ZLA3W45F (Arginine); EC 2.7.10.2 (JAK2 protein, human); EC 2.7.10.2 (Janus Kinase 2); K7Q1JQR04M (Dinoprostone); N3Z657H81X (BIIE 0246)
[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:170903
[St] Status:MEDLINE


  8 / 9771 MEDLINE  
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[PMID]:28628036
[Au] Autor:Shi Z; Madden CJ; Brooks VL
[Ad] Endereço:Department of Physiology and Pharmacology and.
[Ti] Título:Arcuate neuropeptide Y inhibits sympathetic nerve activity via multiple neuropathways.
[So] Source:J Clin Invest;127(7):2868-2880, 2017 Jun 30.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Obesity increases sympathetic nerve activity (SNA) via activation of proopiomelanocortin neurons in the arcuate nucleus (ArcN), and this action requires simultaneous withdrawal of tonic neuropeptide Y (NPY) sympathoinhibition. However, the sites and neurocircuitry by which NPY decreases SNA are unclear. Here, using designer receptors exclusively activated by designer drugs (DREADDs) to selectively activate or inhibit ArcN NPY neurons expressing agouti-related peptide (AgRP) in mice, we have demonstrated that this neuronal population tonically suppresses splanchnic SNA (SSNA), arterial pressure, and heart rate via projections to the paraventricular nucleus (PVN) and dorsomedial hypothalamus (DMH). First, we found that ArcN NPY/AgRP fibers closely appose PVN and DMH presympathetic neurons. Second, nanoinjections of NPY or an NPY receptor Y1 (NPY1R) antagonist into PVN or DMH decreased or increased SSNA, respectively. Third, blockade of DMH NPY1R reversed the sympathoinhibition elicited by selective, DREADD-mediated activation of ArcN NPY/AgRP neurons. Finally, stimulation of ArcN NPY/AgRP terminal fields in the PVN and DMH decreased SSNA. Considering that chronic obesity decreases ArcN NPY content, we propose that the ArcN NPY neuropathway to the PVN and DMH is pivotal in obesity-induced elevations in SNA.
[Mh] Termos MeSH primário: Núcleo Arqueado do Hipotálamo/metabolismo
Pressão Sanguínea
Neuropeptídeo Y/metabolismo
Sistema Nervoso Simpático/metabolismo
Sistema Nervoso Simpático/fisiopatologia
[Mh] Termos MeSH secundário: Proteína Relacionada com Agouti/biossíntese
Proteína Relacionada com Agouti/genética
Animais
Núcleo Arqueado do Hipotálamo/patologia
Núcleo Arqueado do Hipotálamo/fisiopatologia
Doença Crônica
Regulação da Expressão Gênica
Frequência Cardíaca
Camundongos
Camundongos Transgênicos
Neuropeptídeo Y/genética
Obesidade/genética
Obesidade/metabolismo
Obesidade/patologia
Obesidade/fisiopatologia
Núcleo Hipotalâmico Paraventricular/metabolismo
Núcleo Hipotalâmico Paraventricular/patologia
Núcleo Hipotalâmico Paraventricular/fisiopatologia
Receptores de Neuropeptídeo Y/genética
Receptores de Neuropeptídeo Y/metabolismo
Sistema Nervoso Simpático/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Agouti-Related Protein); 0 (Agrp protein, mouse); 0 (Neuropeptide Y); 0 (Npy1r protein, mouse); 0 (Receptors, Neuropeptide Y)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170930
[Lr] Data última revisão:
170930
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE


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[PMID]:28625910
[Au] Autor:Wang G; Williams CA; McConn BR; Cline MA; Gilbert ER
[Ad] Endereço:Department of Animal and Poultry Sciences, Virginia Polytechnic Institute and State University, Blacksburg, VA, USA.
[Ti] Título:A high fat diet enhances the sensitivity of chick adipose tissue to the effects of centrally injected neuropeptide Y on gene expression of adipogenesis-associated factors.
[So] Source:Comp Biochem Physiol A Mol Integr Physiol;211:49-55, 2017 Sep.
[Is] ISSN:1531-4332
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The purpose of this study was to determine how dietary macronutrient composition and exogenous neuropeptide Y (NPY) affect mRNA abundance of factors associated with lipid metabolism in chick adipose tissue. Chicks were fed one of three isocaloric (3000kcal metabolizable energy (ME)/kg) diets after hatch: high carbohydrate (HC; control), high fat (HF; 30% of ME from soybean oil) or high protein (HP; 25% crude protein). On day 4 post-hatch, vehicle or 0.2nmol of NPY was injected intracerebroventricularly and abdominal and subcutaneous fat depots collected 1h later. In abdominal fat, mRNA abundance of peroxisome proliferator-activated receptor γ (PPARγ) and fatty acid binding protein 4 (FABP4) increased after NPY injection in HF diet-fed chicks. NPY injection decreased expression of PPARγ and sterol regulatory element-binding transcription factor 1 (SREBP1) in the subcutaneous fat of HC diet-fed chicks, whereas SREBP1 expression was increased in the subcutaneous fat of HF diet-fed chicks after NPY injection. An acutely increased central concentration of NPY in chicks affects adipose tissue physiology in a depot- and diet-dependent manner. The chick may serve as a model to understand the relationship between diet and the brain-fat axis' role in maintaining whole body energy homeostasis, as well as to understand metabolic distinctions among fat depots.
[Mh] Termos MeSH primário: Adipogenia/genética
Tecido Adiposo/efeitos dos fármacos
Dieta Hiperlipídica
Expressão Gênica
Neuropeptídeo Y/farmacologia
[Mh] Termos MeSH secundário: Animais
Galinhas
Injeções Intraventriculares
Neuropeptídeo Y/administração & dosagem
PPAR gama/genética
RNA Mensageiro/genética
Proteína de Ligação a Elemento Regulador de Esterol 1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neuropeptide Y); 0 (PPAR gamma); 0 (RNA, Messenger); 0 (Sterol Regulatory Element Binding Protein 1)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE


  10 / 9771 MEDLINE  
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[PMID]:28598785
[Au] Autor:Iannuccelli C; Guzzo MP; Atzeni F; Mannocci F; Alessandri C; Gerardi MC; Valesini G; Di Franco M
[Ad] Endereço:Rheumatology Unit, Department of Internal Medicine and Medical Specialties, Sapienza University, Rome, Italy. cristina.iannuccelli@uniroma1.it.
[Ti] Título:Pain modulation in patients with fibromyalgia undergoing acupuncture treatment is associated with fluctuations in serum neuropeptide Y levels.
[So] Source:Clin Exp Rheumatol;35 Suppl 105(3):81-85, 2017 May-Jun.
[Is] ISSN:0392-856X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Neuropeptide Y (NPY) is a neurotransmitter released by sympathetic neurons, which is probably involved in pain modulation. Acupuncture is increasingly used as an alternative or complementary means of controlling pain in rheumatic diseases such as fibromyalgia (FM), a chronic widespread pain syndrome accompanied by allodynia and hyperalgesia. The aim of the present study was to assess the effects of an acupuncture cycle on serum NPY levels in patients with FM, and identify possible correlations between its serum levels and clinical and clinimetric parameters. METHODS: The study involved 30 FM patients who underwent clinical and clinimetric evaluations and blood sampling at baseline and at the end of the treatment, and 20 healthy subjects who underwent blood sampling. RESULTS: The baseline serum NPY levels of the patients were higher than those of the controls. They had significantly increased by the end of the treatment, when there was also a statistically significant reduction in pain, the number of tender points number, and the clinimetric scores. CONCLUSIONS: These findings confirm the analgesic properties of acupuncture as a complementary treatment in FM, and indicate that NPY could play a role in pain modulation.
[Mh] Termos MeSH primário: Terapia por Acupuntura
Fibromialgia/terapia
Neuropeptídeo Y/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Feminino
Fibromialgia/sangue
Seres Humanos
Meia-Idade
Medição da Dor
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neuropeptide Y)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170831
[Lr] Data última revisão:
170831
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE



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