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1 d obesity and showed attenuated responses to anorexigenic 5-HT drugs.
2 uclei in wild-type mice, suggesting that its anorexigenic actions involve short-term mechanisms.
3              Together, these data argue that anorexigenic actions of PYY(3-36) are mediated more like
4 etite and body weight, and leptin exerts its anorexigenic actions partly by increasing hypothalamic p
5 ng that MRAP2 has the potential to alter the anorexigenic activity of PK2 in vivo.
6  New evidence suggests that leptin and other anorexigenic agents reduce appetite by inactivating hypo
7 system in regulating the response to various anorexigenic agents.
8 y distributed neurons activated by different anorexigenic agents.
9  is modulated by the opposing effects of the anorexigenic agonist alpha-melanocyte-stimulating hormon
10                     The regulated release of anorexigenic alpha-melanocyte stimulating hormone (alpha
11                      Notably, the density of anorexigenic alpha-melanocyte-stimulating hormone axons
12          LCN2 was previously suggested as an anorexigenic and anti-obesity agent.
13                 We conclude that YO produces anorexigenic and aversive effects that correlate with ac
14 c AgRP and POMC neurons and are activated by anorexigenic and aversive stimuli.
15 dministration of OT-12 exhibited more potent anorexigenic and body weight reducing effects than carbe
16 eficiency does not affect sensitivity to the anorexigenic and body weight-lowering actions of leptin.
17        Uremic metabolites, some of which are anorexigenic and many of which are products of protein m
18 sted potential sensitivity of the IGL/VLG to anorexigenic and orexigenic peptides, such as cholecysto
19 functional interactions of BDNF with central anorexigenic and orexigenic signaling pathways and evide
20 itical role in hormonal and nutrient-derived anorexigenic and orexigenic signals and in energy balanc
21 y estrogen (E2) replacement, reflecting both anorexigenic and potentially metabolic actions of E2.
22 rtin receptor agonists have been found to be anorexigenic and to stimulate erectile activity.
23 resting energy expenditure (243 kJ/d) and an anorexigenic appetite-sensation profile.Protein suppleme
24 eostasis, orexigenic (appetite-inducing) and anorexigenic (appetite suppressing) brain systems functi
25 sis, down-regulation of genes in the central anorexigenic (appetite-suppressing) pathway, peripheral
26 hypothalamus and activates an MC4R-dependent anorexigenic (appetite-suppressing) pathway.
27 ects of leptin and insulin are integrated by anorexigenic but not by orexigenic neurons.
28 one of these two groups of cells responds to anorexigenic (cholecystokinin, glucagon-like peptide 1 a
29 tanding of how energy balance influences the anorexigenic circuitry of the hypothalamus, and aid in u
30         Here we show that interleukin 18, an anorexigenic cytokine, can act on neurons of the bed nuc
31          Moreover, more neurons responded to anorexigenic drugs at night, while a high-fat diet affec
32 independent mechanism that includes a marked anorexigenic effect and an additional (likely metabolic)
33                                         This anorexigenic effect is masked by stress inhibition of ap
34 cal obesity model measuring food intake, the anorexigenic effect of a pyrrolo[2,3-c]pyridine GPR103 a
35        Feeding experiments indicate that the anorexigenic effect of central administration of glucose
36 the midbrain raphe nuclei at a time when the anorexigenic effect of estradiol is apparent.
37 -1 and 5-HTT mRNA plays a causal role in the anorexigenic effect of estradiol.
38               Contrasting with the predicted anorexigenic effect of increasing brain serotonin signal
39 ockout mice exhibit an impaired hypothalamic anorexigenic effect of insulin that is associated with e
40 elative contribution of PKR1 and PKR2 to the anorexigenic effect of PK2 and their site of action in t
41 nipulation of PKR2 neurons, we show that the anorexigenic effect of PK2 is mediated by PKR2 in the am
42 nt widely used in stress tests, had a strong anorexigenic effect.
43 cological activators of the MC4R to exert an anorexigenic effect.
44 e proinflammatory cytokine IL-18 has central anorexigenic effects and was proposed to contribute to l
45 n, neuronal subtypes that mediate estrogen's anorexigenic effects have not been identified.
46 HT) content in the synaptic cleft and exerts anorexigenic effects in animals and humans.
47  in muscle and also plays a role in leptin's anorexigenic effects in the hypothalamus.
48  inhibition of POMC(ARH) neurons blocked the anorexigenic effects of 27HC.
49 t to suppress appetite and necessary for the anorexigenic effects of appetite-suppressing substances
50                                          The anorexigenic effects of centrally injected glucose or OD
51 downstream target of POMC neurons, abolished anorexigenic effects of D-Fen.
52 it reduced sensitivity to the orexigenic and anorexigenic effects of ghrelin and leptin, respectively
53        Previous studies demonstrate that the anorexigenic effects of GLP-1 can be mediated through hy
54 cts of insulin release predominated over the anorexigenic effects of GLP-1 release after administrati
55       However, the mechanisms underlying the anorexigenic effects of oxytocin in humans are unknown a
56 ntagonist agouti-related peptide blocked the anorexigenic effects of PK2.
57                                          The anorexigenic effects of QKT are driven by ammoniagenesis
58 at leads to obesity, and is resistant to the anorexigenic effects of the hormone leptin.
59 owever, the neural circuits underlying their anorexigenic effects remain largely unknown.
60                                        These anorexigenic effects were restored in mice with 5-HT(2C)
61 tokines are recognized as mediators of these anorexigenic effects, their mechanism and sites of actio
62  (ERalpha) is the key mediator of estrogen's anorexigenic effects, we find that expression of ERalpha
63   Since central CRH is also thought to be an anorexigenic factor and GLP-1 neurons contain leptin rec
64         Here, we show that CTRP13 is a novel anorexigenic factor in the mouse brain.
65 e secreted by astroglia, and ODN is a potent anorexigenic factor.
66               Neuropeptides mediating leptin anorexigenic function do not affect bone formation.
67 tosis, Interleukin 1 beta encoding gene with anorexigenic function, IL1B was downregulated.
68 eurons are essential mediators of estrogen's anorexigenic function.
69 mass and show that leptin antiosteogenic and anorexigenic functions are affected by similar amounts o
70 ic RT-PCR showed that mRNA expression of the anorexigenic genes POMC and CART was up-regulated by 1,
71 duction of orexigenic genes, upregulation of anorexigenic genes, and transcriptional decrease of gene
72 n and up-regulation of larval orexigenic and anorexigenic genes, respectively, an up-regulation of ge
73 that lack retrieval determinants such as the anorexigenic GPCR NPY2R undergo signal-dependent ectocyt
74 efined flours in a white bread stimulates an anorexigenic gut hormone response and has potential to i
75  ad libitum energy intake via stimulation of anorexigenic gut hormone secretion.
76 as associated with average reductions in the anorexigenic hormone leptin (decrease, 18%; P = 0.04), e
77 nd paraventricular hypothalamus (PVH) by the anorexigenic hormone leptin, and in multiple hypothalami
78      Persistent activity was reversed by the anorexigenic hormone leptin, and optogenetic photostimul
79                                Levels of the anorexigenic hormone PYY(3-36) are low in overweight vol
80 cotreating mice with Flx and lipocalin 2, an anorexigenic hormone signaling through this receptor, no
81 eal and in response to administration of the anorexigenic hormones amylin, cholecystokinin (CCK), and
82 ntly elevated and sustained release of these anorexigenic hormones and tended to increase fullness (t
83 BN CGRP neurons become active in response to anorexigenic hormones released following a meal, includi
84 mpanied by a skewed production of orexigenic/anorexigenic hormones, resulting in elevated food intake
85 hrelin reduces the sensory signals evoked by anorexigenic hormones, which act via the vagus nerve to
86 pheral tissues, which secrete orexigenic and anorexigenic hormones.
87 neurons less responsive to signals evoked by anorexigenic hormones.
88 octurnal feeding and increased expression of anorexigenic hypothalamic peptides.
89 tified, it is not yet clear whether distinct anorexigenic influences are processed in a convergent or
90 nctionally less responsive to its endogenous anorexigenic ligand, alpha-MSH.
91                                 Leptin is an anorexigenic mediator that reduces food intake by acting
92 tory by pre- and postsynaptic mechanisms; an anorexigenic melanocortin agonist had no effect.
93 ion of orexigenic (neuropeptide Y [NPY]) and anorexigenic (melanocortin) signals, that NPY and melano
94                                              Anorexigenic melanocortins decrease food intake by activ
95 ues, overcomes the satiety signals evoked by anorexigenic molecules, such as cholecystokinin (CCK) an
96 elin overcomes the satiety signals evoked by anorexigenic molecules, such as cholecystokinin (CCK) an
97 thalamic leptin-dependent antiosteogenic and anorexigenic networks differ, and that the peripheral me
98        Collectively, our results identify an anorexigenic neural circuit originating from vHPC to LS
99  mPFC-LH circuit as a novel stress-sensitive anorexigenic neural pathway involved in the cortical con
100 ctions in the density of both orexigenic and anorexigenic neural projections to the paraventricular n
101 gy balance by inhibiting the excitability of anorexigenic neural substrates, an effect that is dimini
102                                          The anorexigenic neuromodulator alpha-melanocyte-stimulating
103  establish a critical role for Prdm12 in the anorexigenic neuron identity and suggest that it acts de
104 eviously unrecognized role for Prdm12 in the anorexigenic neuron identity and suggest that it acts de
105 leus (VMH), a known satiety center, activate anorexigenic neuronal pathways in the ARC by projecting
106  appetite due to its connectivity with other anorexigenic neuronal populations and because these neur
107 ments indicate that RIP(HER) neurons inhibit anorexigenic neurons in the PVN, revealing a basic orexi
108 ted peptide and neuropeptide Y but inhibited anorexigenic neurons that synthesize POMC, as determined
109 gRP and NPY for specifying AgRP-neurons, the anorexigenic neuropeptide alphaMSH for POMC-neurons, and
110 uced" changes of hypothalamic orexigenic and anorexigenic neuropeptide mRNAs, repeated administration
111 d by aberrant expression of the hypothalamic anorexigenic neuropeptide proopiomelanocortin (POMC).
112  protein (AgRP)] and activates expression of anorexigenic neuropeptides [proopiomelanocortin (POMC) a
113 ed comparable upregulation of orexigenic and anorexigenic neuropeptides in rats that were fed on a hi
114  neuropeptides and an abnormal expression of anorexigenic neuropeptides in response to fasting.
115 xigenic neuropeptides and down-regulation of anorexigenic neuropeptides in the hypothalami of mice.
116 protein and down-regulation of expression of anorexigenic neuropeptides pro-opiomelanocortinalpha-mel
117 amic neurons that express the orexigenic and anorexigenic neuropeptides that regulate food intake and
118  basal levels of hypothalamic orexigenic and anorexigenic neuropeptides, and no impairment of reflexi
119 POMC-encoded melanocortins, which are potent anorexigenic neuropeptides, and their absence from mice
120 ells and subsequent release of orexigenic or anorexigenic neuropeptides, is a crucial process that re
121 ltering the expression of key orexigenic and anorexigenic neuropeptides.
122               Central serotonin (5-HT) is an anorexigenic neurotransmitter in the brain.
123 lanocyte-stimulating hormone (alpha-MSH) and anorexigenic neurotransmitter serotonin.
124  (Agrp)-containing neurons, thus priming net anorexigenic output.
125  potential neurobiological mechanism for the anorexigenic oxytocin effects in humans.
126 ling and consequent activation of downstream anorexigenic pathways.
127 tite suppression and to decrease activity in anorexigenic PBN CGRP neurons, thereby increasing food i
128               The Pomc gene encodes both the anorexigenic peptide alpha-melanocyte-stimulating hormon
129 agal complex of the hindbrain synthesize the anorexigenic peptide octadecaneuropeptide (ODN), the inf
130 nocyte stimulating hormone (alpha-MSH) is an anorexigenic peptide.
131                                          The anorexigenic peptides nucleobindin-2 (NUCB2)/nesfatin-1
132 ic peptides such as neuropeptide Y (NPY) and anorexigenic peptides such as alpha-melanocyte-stimulati
133 fic to amylin treatment, compared with other anorexigenic peptides, and dissociable from amylin's eff
134  while the spring increase in genes encoding anorexigenic peptides, POMC, and somatostatin may accoun
135                                  Unlike many anorexigenic peptides, there is no increased sensitivity
136 cells and their regulation by orexigenic and anorexigenic peptides.
137 es the frequency of action potentials in the anorexigenic POMC neurons by two mechanisms: depolarizat
138                            The inhibition of anorexigenic POMC neurons may be one mechanism underlyin
139 nic actions, at least in part, by inhibiting anorexigenic POMC neurons remains unclear.
140 onal activity and the inhibitory tone on the anorexigenic POMC neurons, as measured by the number of
141 n that kisspeptin neurons also interact with anorexigenic POMC neurons, which are affected by obesity
142 ating orexigenic AgRP neurons and inhibiting anorexigenic POMC neurons.
143 P neurons and decreasing the activity of the anorexigenic POMC neurons.
144  provide inhibitory synaptic input to nearby anorexigenic POMC neurons.
145  expression of orexigenic (NPY and AgRP) and anorexigenic (POMC and CART) neuropeptide messages in th
146 nal precursors subsequently adopt either the anorexigenic (POMC) or the orexigenic (NPY/AgRP) identit
147 tion of PSTN(Tac1) projections to individual anorexigenic populations reduces food consumption.
148 elated protein (AGRP) neurons and activating anorexigenic pro-opiomelanocortin (POMC) neurons(2).
149 s they occurred in the opposite direction in anorexigenic pro-opiomelanocortin (POMC) neurons.
150 orexigenic agouti-related peptide (AgRP) and anorexigenic pro-opiomelanocortin (POMC) neuropeptides.
151 uropeptide Y and agouti-related protein) and anorexigenic (pro-opiomelanocortinalpha-melanocyte-stimu
152 gRP), and melanin-concentrating hormone] and anorexigenic [pro-opiomelanocortin (POMC) and cocaine-am
153 of the hypothalamus (ARH) satiety signaling (anorexigenic) pro-opiomelanocortin (POMC)-expressing and
154 as the number and neuropeptide expression of anorexigenic proopiomelanocortin (POMC) and orexigenic a
155 trong kisspeptin innervation of hypothalamic anorexigenic proopiomelanocortin (POMC) cells, coupled w
156 -immunoreactive boutons terminate on or near anorexigenic proopiomelanocortin (POMC) cells.
157  Second, specific deletion of Pcdh-gammas in anorexigenic proopiomelanocortin (POMC) expressing neuro
158 energy balance, i.e. fasting, N/OFQ inhibits anorexigenic proopiomelanocortin (POMC) neurones to a gr
159 eurons also releases glutamate to excite the anorexigenic proopiomelanocortin (POMC) neurons and inhi
160 hat the control of energy homeostasis by the anorexigenic proopiomelanocortin (POMC) neurons and orex
161 he postulated mechanism is the activation of anorexigenic proopiomelanocortin (POMC) neurons of the h
162  postsynaptic neuronal system, including the anorexigenic proopiomelanocortin (POMC)-expressing cells
163 ignaling results in inhibition of downstream anorexigenic proopiomelanocortin (POMC)-positive neurons
164 the contribution of the loss of CEACAM1 from anorexigenic proopiomelanocortin neurons in the arcuate
165 ly increased excitatory synaptic activity in anorexigenic proopiomelanocortin neurons.
166 f hypothalamic orexigenic (NPY and AgRP) and anorexigenic (proopiomelanocortin) neuropeptide mRNAs.
167 tide Y/agouti-related protein; NPY/AgRP) and anorexigenic (proopiomelanocortin; POMC) neurons via an
168 d intestinal secretion of hormones GLP-1 and anorexigenic PYY, which is believed to contribute to the
169 the metalloprotease MT1-MMP from cleaving an anorexigenic receptor may be an anti-obesity strategy.
170 ession of other receptors for orexigenic and anorexigenic regulatory peptides at the level of vagal a
171 ncrease in colonic acetate synthesis, and an anorexigenic response characterized by an increased plas
172 amplifies orexigenic responses and decreases anorexigenic responses, providing a putative mechanism e
173  distinct PSTN cell types and demonstrate an anorexigenic role for PSTN(Tac1) neurons in the hormonal
174        We have characterized NDN as a potent anorexigenic signal acting through an uncharacterized en
175 f LCN2 as a satiety factor and indicator and anorexigenic signal in primates.
176 st that the neuropeptide oxytocin acts as an anorexigenic signal in the central nervous control of fo
177 ch between states that promote orexigenic or anorexigenic signalling through mechanisms mediated, at
178 +) neurons in mice were activated by diverse anorexigenic signals in vivo, were required for the inhi
179                                     How such anorexigenic signals inhibit feeding at the neural circu
180 ctions of ghrelin with respect to overcoming anorexigenic signals that act via the vagal afferent pat
181  regulate food intake in response to several anorexigenic signals.
182 node that mediates the influence of multiple anorexigenic signals.
183 tivated protein kinase (AMPK), indicating an anorexigenic state.
184 s sufficient to induce CTA in the absence of anorexigenic substances, whereas genetically induced sil
185 somedial hypothalamus, and 4) suppression of anorexigenic systems POMC and CART.
186 hypothalamic arcuate nucleus, increasing the anorexigenic tone due to activated pro-opiomelanocortin
187  together with the finding that BIBP3226, an anorexigenic Y1 receptor ligand, also binds to NPFF1 sug

 
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