PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33427385-4 2020 In particular, NPY neurones in the arcuate nucleus of the hypothalamus are critical control centres for insulin"s central action on control energy homeostasis, as well as glucose homeostasis regulation. Glucose 171-178 neuropeptide Y Homo sapiens 15-18 3070587-4 1988 Since the immunocytochemical study showed that NPY was localized in brain structures known to alter food intake and the compound is a member of the pancreatic polypeptide family, a second study was designed to determine if the neuropeptide altered plasma concentrations of insulin, glucagon and glucose following intracerebroventricular administration. Glucose 295-302 neuropeptide Y Homo sapiens 47-50 33427385-7 2020 We will also look at the peripheral interaction of the NPY system with insulin release, thereby closing the loop between these two energy and glucose homeostasis controlling systems and highlighting the critical interaction points that may be dysregulated in conditions of obesity and diabetes. Glucose 142-149 neuropeptide Y Homo sapiens 55-58 32436432-6 2020 Multiple stepwise linear regression analysis showed that NPY, alpha-MSH, and AgRP levels were closely associated with blood pressure and glucose control. Glucose 137-144 neuropeptide Y Homo sapiens 57-60 30827863-2 2019 Here, we demonstrate that the clock transcription pathway maximizes eating during wakefulness and glucose production during sleep through autonomous circadian regulation of NPY/AgRP neurons. Glucose 98-105 neuropeptide Y Homo sapiens 173-176 28940946-8 2018 NPY receptor activation functionally protected islets by restoring glucose responsiveness following chemically induced injury in both species. Glucose 67-74 neuropeptide Y Homo sapiens 0-3 29208684-6 2017 Furthermore, central NPY decreased plasma glucose and triacylglycerol under CT and HT and kept plasma corticosterone and epinephrine lower under HT NPY increased plasma taurine and anserine concentrations. Glucose 42-49 neuropeptide Y Homo sapiens 21-24 29208684-8 2017 The NPY-mediated reduction in plasma glucose and stress hormone levels and the increase in free amino acids in plasma further suggest that NPY might potentially play a role in minimizing heat stress in fasted chicks. Glucose 37-44 neuropeptide Y Homo sapiens 4-7 28606559-0 2017 Adiponectin at physiological level glucose-independently enhances inhibitory postsynaptic current onto NPY neurons in the hypothalamic arcuate nucleus. Glucose 35-42 neuropeptide Y Homo sapiens 103-106 28606559-10 2017 These results demonstrate that adiponectin enhances IPSC onto NPY neurons to attenuate action potential firing in NPY neurons in a glucose-independent manner, being contrasted to its glucose-dependent effect on POMC neurons. Glucose 131-138 neuropeptide Y Homo sapiens 62-65 28606559-10 2017 These results demonstrate that adiponectin enhances IPSC onto NPY neurons to attenuate action potential firing in NPY neurons in a glucose-independent manner, being contrasted to its glucose-dependent effect on POMC neurons. Glucose 131-138 neuropeptide Y Homo sapiens 114-117 27979380-10 2017 Plasma glucose and triacylglycerol were increased by NPY in fed chicks, but triacylglycerol declined in fasted NPY-injected chicks. Glucose 7-14 neuropeptide Y Homo sapiens 53-56 23390522-10 2013 First functional investigations for one of the most prominent ERG rearrangement-associated genes - neuropeptide Y (NPY) - revealed increased glucose uptake in vitro indicating the potential role of NPY in regulating cellular metabolism. Glucose 141-148 neuropeptide Y Homo sapiens 99-113 25383463-7 2014 The moderate increase in [Ca]i with 5 mM glucose was suppressed by NPY, but further increased by alpha-MSH in the PVN neurons that were shown to be immunoreactive to nesfatin-1/NUCB2. Glucose 41-48 neuropeptide Y Homo sapiens 67-70 23390522-10 2013 First functional investigations for one of the most prominent ERG rearrangement-associated genes - neuropeptide Y (NPY) - revealed increased glucose uptake in vitro indicating the potential role of NPY in regulating cellular metabolism. Glucose 141-148 neuropeptide Y Homo sapiens 115-118 23390522-10 2013 First functional investigations for one of the most prominent ERG rearrangement-associated genes - neuropeptide Y (NPY) - revealed increased glucose uptake in vitro indicating the potential role of NPY in regulating cellular metabolism. Glucose 141-148 neuropeptide Y Homo sapiens 198-201 23107365-8 2012 Lowering glucose concentration activates 40% of NPY neurons. Glucose 9-16 neuropeptide Y Homo sapiens 48-51 20203197-5 2010 Approximately 80% of VMN neurons expressing leptin receptors were sensitive to the actions of NPY, whereas 75% of NPY-sensitive neurons in VMN also responded to glucose by being uniformly inhibited by elevations in glucose. Glucose 161-168 neuropeptide Y Homo sapiens 114-117 21801810-2 2012 Although NPY impacts on glucose utilization in vivo, the underlying cellular mechanism is yet to be fully elucidated. Glucose 24-31 neuropeptide Y Homo sapiens 9-12 21801810-6 2012 Our data suggest that in 3T3-L1 adipocytes NPY inhibits insulin-stimulated glucose uptake in a GLUT4-dependent manner. Glucose 75-82 neuropeptide Y Homo sapiens 43-46 22808091-8 2012 These results suggest an activation of NPY producing neurons in the arcuate nucleus, which, according to animal experimental studies, is related to a catabolic state and might be the basis for increased hepatic glucose production in type-2 diabetes. Glucose 211-218 neuropeptide Y Homo sapiens 39-42 21907249-5 2011 In contrast, the NPY increase during ITT was completely abolished when the concomitant infusion of glucose prevented insulin-induced hypoglycemia. Glucose 99-106 neuropeptide Y Homo sapiens 17-20 21907249-7 2011 Furthermore, since glucose but not fructose crosses the blood-brain-barrier (BBB), the NPY increase during ITT appears to be generated by low glucose concentrations at the level of glucosensitive areas located inside the brain. Glucose 19-26 neuropeptide Y Homo sapiens 87-90 21907249-7 2011 Furthermore, since glucose but not fructose crosses the blood-brain-barrier (BBB), the NPY increase during ITT appears to be generated by low glucose concentrations at the level of glucosensitive areas located inside the brain. Glucose 142-149 neuropeptide Y Homo sapiens 87-90 20203197-5 2010 Approximately 80% of VMN neurons expressing leptin receptors were sensitive to the actions of NPY, whereas 75% of NPY-sensitive neurons in VMN also responded to glucose by being uniformly inhibited by elevations in glucose. Glucose 215-222 neuropeptide Y Homo sapiens 114-117 19211911-0 2009 Fasting enhances the response of arcuate neuropeptide Y-glucose-inhibited neurons to decreased extracellular glucose. Glucose 56-63 neuropeptide Y Homo sapiens 41-55 19211911-0 2009 Fasting enhances the response of arcuate neuropeptide Y-glucose-inhibited neurons to decreased extracellular glucose. Glucose 109-116 neuropeptide Y Homo sapiens 41-55 19211911-2 2009 A subpopulation of ARC-NPY neurons ( approximately 40%) are glucose-inhibited (GI)-type glucose-sensing neurons. Glucose 60-67 neuropeptide Y Homo sapiens 23-26 19211911-2 2009 A subpopulation of ARC-NPY neurons ( approximately 40%) are glucose-inhibited (GI)-type glucose-sensing neurons. Glucose 88-95 neuropeptide Y Homo sapiens 23-26 19211911-5 2009 This increased excitation in response to glucose decreases would increase NPY-GI neuronal excitability and enhance NPY neurotransmission. Glucose 41-48 neuropeptide Y Homo sapiens 74-77 19211911-6 2009 Using an in vitro hypothalamic explant system, we show that fasting enhances NPY release in response to decreased glucose concentration. Glucose 114-121 neuropeptide Y Homo sapiens 77-80 19211911-7 2009 By measuring relative changes in membrane potential using a membrane potential-sensitive dye, we demonstrate that during fasting, a smaller decrease in glucose depolarizes NPY-GI neurons. Glucose 152-159 neuropeptide Y Homo sapiens 172-175 19211911-9 2009 Fasting, leptin, and glucose-induced changes in NPY-GI neuron glucose sensing were mediated by 5"-AMP-activated protein kinase (AMPK). Glucose 21-28 neuropeptide Y Homo sapiens 48-51 19211911-9 2009 Fasting, leptin, and glucose-induced changes in NPY-GI neuron glucose sensing were mediated by 5"-AMP-activated protein kinase (AMPK). Glucose 62-69 neuropeptide Y Homo sapiens 48-51 19211911-10 2009 We conclude that during energy sufficiency, leptin reduces the ability of NPY-GI neurons to sense decreased glucose. Glucose 108-115 neuropeptide Y Homo sapiens 74-77 19211911-11 2009 However, after a fast, decreased leptin and glucose activate AMPK in NPY-GI neurons. Glucose 44-51 neuropeptide Y Homo sapiens 69-72 19211911-12 2009 As a result, NPY-GI neurons become depolarized in response to smaller glucose fluctuations. Glucose 70-77 neuropeptide Y Homo sapiens 13-16 18662858-7 2008 The NPY signal interacts with glucose- and fat-sensitive signals arriving in the hypothalamus and effects changes in anorexigenic pathways, such as those mediated by the melanocortins. Glucose 30-37 neuropeptide Y Homo sapiens 4-7 18983451-3 2009 In mammalian brains, two groups of glucose-inhibited neurones are best understood at present: neurones of the hypothalamic arcuate nucleus (ARC) that express peptide transmitters NPY and agouti-related peptide (AgRP) and neurones of the lateral hypothalamus (LH) that express peptide transmitters orexins/hypocretins. Glucose 35-42 neuropeptide Y Homo sapiens 179-182 18815063-10 2008 LL homocygotes in NPY had a greater reduction in glucose, triglycerides, and LDL cholesterol whereas in resistin carriers of the G allele had a greater reduction in weight and triglycerides. Glucose 49-56 neuropeptide Y Homo sapiens 18-21 18225446-6 2007 Glucose sensing can be modulated by other nutrients (particularly fatty acids) and also by hormones (insulin, leptin and ghrelin) and peptides (NPY). Glucose 0-7 neuropeptide Y Homo sapiens 144-147 17516289-13 2007 Also a statistically significant negative association of plasma NPY levels with plasma glucose levels was found in both genotypes. Glucose 87-94 neuropeptide Y Homo sapiens 64-67 16713643-4 2006 This idea was confirmed by subsequent experiments in which ICV injection of NPY significantly reduced plasma glucose and triacylglycerol concentrations but increased non-esterified fatty acid concentrations. Glucose 109-116 neuropeptide Y Homo sapiens 76-79 15931058-4 2005 Lowering glucose (1 mM) increased cytosolic Ca2+ concentration ([Ca2+]i) in isolated ARC neurons that were immunoreactive to NPY. Glucose 9-16 neuropeptide Y Homo sapiens 125-128 16210367-1 2006 The reductions in circulating levels of leptin, insulin, and glucose with fasting serve as important homeostasis signals to neurons of the hypothalamic arcuate nucleus that synthesize neuropeptide Y (NPY)/agouti-related protein (AGRP) and alpha-MSH/cocaine and amphetamine-regulated transcript. Glucose 61-68 neuropeptide Y Homo sapiens 184-198 16210367-1 2006 The reductions in circulating levels of leptin, insulin, and glucose with fasting serve as important homeostasis signals to neurons of the hypothalamic arcuate nucleus that synthesize neuropeptide Y (NPY)/agouti-related protein (AGRP) and alpha-MSH/cocaine and amphetamine-regulated transcript. Glucose 61-68 neuropeptide Y Homo sapiens 200-203 16383005-2 2006 High or low abundance of NPY and cognate receptors dysregulates the homeostatic milieu engendering hyperphagia, decreased energy expenditure, obesity and attendant metabolic syndrome cluster of dyslipidemia, glucose intolerance, insulin resistance and hyperinsulinemia, risk factors for type II diabetes and cardiovascular diseases. Glucose 208-215 neuropeptide Y Homo sapiens 25-28 15931058-7 2005 These results indicate that GABA regulates ARC glucose-sensitive NPY neurons via GABAA and GABAB receptors, which could function to attenuate the orexigenic NPY pathway when it is not beneficial. Glucose 47-54 neuropeptide Y Homo sapiens 65-68 15931058-7 2005 These results indicate that GABA regulates ARC glucose-sensitive NPY neurons via GABAA and GABAB receptors, which could function to attenuate the orexigenic NPY pathway when it is not beneficial. Glucose 47-54 neuropeptide Y Homo sapiens 157-160 11330489-12 2000 The NPY-LI increase during the interview was related to higher fasting blood glucose before the interview (p<0.01) and a stronger increase in systolic blood pressure during the test (p<0.05). Glucose 77-84 neuropeptide Y Homo sapiens 4-7 8837218-6 1996 Mammalian NPY stimulated SS-25 release in a dose-related manner in the presence of low (1 mM) glucose; the efficacy of this effect decreased at higher glucose concentrations. Glucose 94-101 neuropeptide Y Homo sapiens 10-13 8837218-6 1996 Mammalian NPY stimulated SS-25 release in a dose-related manner in the presence of low (1 mM) glucose; the efficacy of this effect decreased at higher glucose concentrations. Glucose 151-158 neuropeptide Y Homo sapiens 10-13 8837218-7 1996 SS-14 release was inhibited by NPY in the presence of 10 mM glucose. Glucose 60-67 neuropeptide Y Homo sapiens 31-34 8964837-9 1996 Added NPY (100 nmol/L) decreased (P = 0.001) glucose-stimulated (8 mmol/L) insulin release from the human islets by 45% in a perfusion system. Glucose 45-52 neuropeptide Y Homo sapiens 6-9 8743287-1 1996 Neuropeptide Y (NPY) is a 36 aminoacid peptide known to inhibit glucose-stimulated insulin secretion. Glucose 64-71 neuropeptide Y Homo sapiens 0-14 8743287-1 1996 Neuropeptide Y (NPY) is a 36 aminoacid peptide known to inhibit glucose-stimulated insulin secretion. Glucose 64-71 neuropeptide Y Homo sapiens 16-19 1582134-8 1992 Plasma noradrenaline fell by 20% (P less than 0.02) and arterial glucose by 3% (P less than 0.005) during the NPY infusion. Glucose 65-72 neuropeptide Y Homo sapiens 110-113 8205750-8 1994 During the NPY infusion both splanchnic blood flow and arterial glucose fell (P < 0.05). Glucose 64-71 neuropeptide Y Homo sapiens 11-14 7479336-1 1995 Neuropeptide Y (NPY) is a 36 amino acid peptide known to inhibit glucose-stimulated insulin secretion. Glucose 65-72 neuropeptide Y Homo sapiens 0-14 7479336-1 1995 Neuropeptide Y (NPY) is a 36 amino acid peptide known to inhibit glucose-stimulated insulin secretion. Glucose 65-72 neuropeptide Y Homo sapiens 16-19 1582134-10 1992 The results also suggest that elevated plasma NPY-levels may be associated with changes in the turnover of noradrenaline and glucose. Glucose 125-132 neuropeptide Y Homo sapiens 46-49