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4 etite and body weight, and leptin exerts its anorexigenic actions partly by increasing hypothalamic p
5 New evidence suggests that leptin and other anorexigenic agents reduce appetite by inactivating hypo
7 is modulated by the opposing effects of the anorexigenic agonist alpha-melanocyte-stimulating hormon
11 eficiency does not affect sensitivity to the anorexigenic and body weight-lowering actions of leptin.
13 functional interactions of BDNF with central anorexigenic and orexigenic signaling pathways and evide
14 itical role in hormonal and nutrient-derived anorexigenic and orexigenic signals and in energy balanc
15 y estrogen (E2) replacement, reflecting both anorexigenic and potentially metabolic actions of E2.
17 resting energy expenditure (243 kJ/d) and an anorexigenic appetite-sensation profile.Protein suppleme
18 eostasis, orexigenic (appetite-inducing) and anorexigenic (appetite suppressing) brain systems functi
19 sis, down-regulation of genes in the central anorexigenic (appetite-suppressing) pathway, peripheral
23 independent mechanism that includes a marked anorexigenic effect and an additional (likely metabolic)
25 cal obesity model measuring food intake, the anorexigenic effect of a pyrrolo[2,3-c]pyridine GPR103 a
29 ockout mice exhibit an impaired hypothalamic anorexigenic effect of insulin that is associated with e
31 e proinflammatory cytokine IL-18 has central anorexigenic effects and was proposed to contribute to l
34 t to suppress appetite and necessary for the anorexigenic effects of appetite-suppressing substances
38 cts of insulin release predominated over the anorexigenic effects of GLP-1 release after administrati
44 tokines are recognized as mediators of these anorexigenic effects, their mechanism and sites of actio
45 (ERalpha) is the key mediator of estrogen's anorexigenic effects, we find that expression of ERalpha
46 Since central CRH is also thought to be an anorexigenic factor and GLP-1 neurons contain leptin rec
52 mass and show that leptin antiosteogenic and anorexigenic functions are affected by similar amounts o
53 ic RT-PCR showed that mRNA expression of the anorexigenic genes POMC and CART was up-regulated by 1,
54 duction of orexigenic genes, upregulation of anorexigenic genes, and transcriptional decrease of gene
55 n and up-regulation of larval orexigenic and anorexigenic genes, respectively, an up-regulation of ge
56 that lack retrieval determinants such as the anorexigenic GPCR NPY2R undergo signal-dependent ectocyt
58 as associated with average reductions in the anorexigenic hormone leptin (decrease, 18%; P = 0.04), e
59 nd paraventricular hypothalamus (PVH) by the anorexigenic hormone leptin, and in multiple hypothalami
62 BN CGRP neurons become active in response to anorexigenic hormones released following a meal, includi
63 hrelin reduces the sensory signals evoked by anorexigenic hormones, which act via the vagus nerve to
66 tified, it is not yet clear whether distinct anorexigenic influences are processed in a convergent or
70 ion of orexigenic (neuropeptide Y [NPY]) and anorexigenic (melanocortin) signals, that NPY and melano
72 ues, overcomes the satiety signals evoked by anorexigenic molecules, such as cholecystokinin (CCK) an
73 elin overcomes the satiety signals evoked by anorexigenic molecules, such as cholecystokinin (CCK) an
74 thalamic leptin-dependent antiosteogenic and anorexigenic networks differ, and that the peripheral me
76 ctions in the density of both orexigenic and anorexigenic neural projections to the paraventricular n
78 leus (VMH), a known satiety center, activate anorexigenic neuronal pathways in the ARC by projecting
79 ments indicate that RIP(HER) neurons inhibit anorexigenic neurons in the PVN, revealing a basic orexi
80 ted peptide and neuropeptide Y but inhibited anorexigenic neurons that synthesize POMC, as determined
81 gRP and NPY for specifying AgRP-neurons, the anorexigenic neuropeptide alphaMSH for POMC-neurons, and
82 uced" changes of hypothalamic orexigenic and anorexigenic neuropeptide mRNAs, repeated administration
83 d by aberrant expression of the hypothalamic anorexigenic neuropeptide proopiomelanocortin (POMC).
84 protein (AgRP)] and activates expression of anorexigenic neuropeptides [proopiomelanocortin (POMC) a
85 ed comparable upregulation of orexigenic and anorexigenic neuropeptides in rats that were fed on a hi
87 xigenic neuropeptides and down-regulation of anorexigenic neuropeptides in the hypothalami of mice.
88 protein and down-regulation of expression of anorexigenic neuropeptides pro-opiomelanocortinalpha-mel
89 amic neurons that express the orexigenic and anorexigenic neuropeptides that regulate food intake and
90 basal levels of hypothalamic orexigenic and anorexigenic neuropeptides, and no impairment of reflexi
91 POMC-encoded melanocortins, which are potent anorexigenic neuropeptides, and their absence from mice
92 ells and subsequent release of orexigenic or anorexigenic neuropeptides, is a crucial process that re
98 tite suppression and to decrease activity in anorexigenic PBN CGRP neurons, thereby increasing food i
100 ic peptides such as neuropeptide Y (NPY) and anorexigenic peptides such as alpha-melanocyte-stimulati
101 fic to amylin treatment, compared with other anorexigenic peptides, and dissociable from amylin's eff
102 while the spring increase in genes encoding anorexigenic peptides, POMC, and somatostatin may accoun
105 es the frequency of action potentials in the anorexigenic POMC neurons by two mechanisms: depolarizat
108 onal activity and the inhibitory tone on the anorexigenic POMC neurons, as measured by the number of
110 expression of orexigenic (NPY and AgRP) and anorexigenic (POMC and CART) neuropeptide messages in th
112 orexigenic agouti-related peptide (AgRP) and anorexigenic pro-opiomelanocortin (POMC) neuropeptides.
113 uropeptide Y and agouti-related protein) and anorexigenic (pro-opiomelanocortinalpha-melanocyte-stimu
114 gRP), and melanin-concentrating hormone] and anorexigenic [pro-opiomelanocortin (POMC) and cocaine-am
115 of the hypothalamus (ARH) satiety signaling (anorexigenic) pro-opiomelanocortin (POMC)-expressing and
116 as the number and neuropeptide expression of anorexigenic proopiomelanocortin (POMC) and orexigenic a
117 trong kisspeptin innervation of hypothalamic anorexigenic proopiomelanocortin (POMC) cells, coupled w
119 Second, specific deletion of Pcdh-gammas in anorexigenic proopiomelanocortin (POMC) expressing neuro
120 he postulated mechanism is the activation of anorexigenic proopiomelanocortin (POMC) neurons of the h
121 postsynaptic neuronal system, including the anorexigenic proopiomelanocortin (POMC)-expressing cells
122 ignaling results in inhibition of downstream anorexigenic proopiomelanocortin (POMC)-positive neurons
123 the contribution of the loss of CEACAM1 from anorexigenic proopiomelanocortin neurons in the arcuate
124 f hypothalamic orexigenic (NPY and AgRP) and anorexigenic (proopiomelanocortin) neuropeptide mRNAs.
125 ession of other receptors for orexigenic and anorexigenic regulatory peptides at the level of vagal a
127 st that the neuropeptide oxytocin acts as an anorexigenic signal in the central nervous control of fo
128 ch between states that promote orexigenic or anorexigenic signalling through mechanisms mediated, at
129 +) neurons in mice were activated by diverse anorexigenic signals in vivo, were required for the inhi
131 ctions of ghrelin with respect to overcoming anorexigenic signals that act via the vagal afferent pat
134 s sufficient to induce CTA in the absence of anorexigenic substances, whereas genetically induced sil
136 hypothalamic arcuate nucleus, increasing the anorexigenic tone due to activated pro-opiomelanocortin
137 together with the finding that BIBP3226, an anorexigenic Y1 receptor ligand, also binds to NPFF1 sug
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