ライフサイエンスコーパス: anorexigenic

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 New evidence suggests that leptin and other anorexigenic agents reduce appetite by inactivating hypo

6 y distributed neurons activated by different anorexigenic agents.

7 is modulated by the opposing effects of the anorexigenic agonist alpha-melanocyte-stimulating hormon

8 The regulated release of anorexigenic alpha-melanocyte stimulating hormone (alpha

9 Notably, the density of anorexigenic alpha-melanocyte-stimulating hormone axons

10 We conclude that YO produces anorexigenic and aversive effects that correlate with ac

11 eficiency does not affect sensitivity to the anorexigenic and body weight-lowering actions of leptin.

12 Uremic metabolites, some of which are anorexigenic and many of which are products of protein m

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.

16 rtin receptor agonists have been found to be anorexigenic and to stimulate erectile activity.

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

20 hypothalamus and activates an MC4R-dependent anorexigenic (appetite-suppressing) pathway.

21 ects of leptin and insulin are integrated by anorexigenic but not by orexigenic neurons.

22 Here we show that interleukin 18, an anorexigenic cytokine, can act on neurons of the bed nuc

23 independent mechanism that includes a marked anorexigenic effect and an additional (likely metabolic)

24 This anorexigenic effect is masked by stress inhibition of ap

25 cal obesity model measuring food intake, the anorexigenic effect of a pyrrolo[2,3-c]pyridine GPR103 a

26 Feeding experiments indicate that the anorexigenic effect of central administration of glucose

27 the midbrain raphe nuclei at a time when the anorexigenic effect of estradiol is apparent.

28 -1 and 5-HTT mRNA plays a causal role in the anorexigenic effect of estradiol.

29 ockout mice exhibit an impaired hypothalamic anorexigenic effect of insulin that is associated with e

30 nt widely used in stress tests, had a strong anorexigenic effect.

31 e proinflammatory cytokine IL-18 has central anorexigenic effects and was proposed to contribute to l

32 n, neuronal subtypes that mediate estrogen's anorexigenic effects have not been identified.

33 HT) content in the synaptic cleft and exerts anorexigenic effects in animals and humans.

34 t to suppress appetite and necessary for the anorexigenic effects of appetite-suppressing substances

35 The anorexigenic effects of centrally injected glucose or OD

36 downstream target of POMC neurons, abolished anorexigenic effects of D-Fen.

37 Previous studies demonstrate that the anorexigenic effects of GLP-1 can be mediated through hy

38 cts of insulin release predominated over the anorexigenic effects of GLP-1 release after administrati

39 However, the mechanisms underlying the anorexigenic effects of oxytocin in humans are unknown a

40 ntagonist agouti-related peptide blocked the anorexigenic effects of PK2.

41 at leads to obesity, and is resistant to the anorexigenic effects of the hormone leptin.

42 owever, the neural circuits underlying their anorexigenic effects remain largely unknown.

43 These anorexigenic effects were restored in mice with 5-HT(2C)

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

47 Here, we show that CTRP13 is a novel anorexigenic factor in the mouse brain.

48 e secreted by astroglia, and ODN is a potent anorexigenic factor.

49 Neuropeptides mediating leptin anorexigenic function do not affect bone formation.

50 tosis, Interleukin 1 beta encoding gene with anorexigenic function, IL1B was downregulated.

51 eurons are essential mediators of estrogen's anorexigenic function.

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

57 ad libitum energy intake via stimulation of anorexigenic gut hormone secretion.

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

60 Persistent activity was reversed by the anorexigenic hormone leptin, and optogenetic photostimul

61 Levels of the anorexigenic hormone PYY(3-36) are low in overweight vol

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

64 neurons less responsive to signals evoked by anorexigenic hormones.

65 octurnal feeding and increased expression of anorexigenic hypothalamic peptides.

66 tified, it is not yet clear whether distinct anorexigenic influences are processed in a convergent or

67 nctionally less responsive to its endogenous anorexigenic ligand, alpha-MSH.

68 Leptin is an anorexigenic mediator that reduces food intake by acting

69 tory by pre- and postsynaptic mechanisms; an anorexigenic melanocortin agonist had no effect.

70 ion of orexigenic (neuropeptide Y [NPY]) and anorexigenic (melanocortin) signals, that NPY and melano

71 Anorexigenic melanocortins decrease food intake by activ

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

75 Collectively, our results identify an anorexigenic neural circuit originating from vHPC to LS

76 ctions in the density of both orexigenic and anorexigenic neural projections to the paraventricular n

77 The anorexigenic neuromodulator alpha-melanocyte-stimulating

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

86 neuropeptides and an abnormal expression of anorexigenic neuropeptides in response to fasting.

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

93 ltering the expression of key orexigenic and anorexigenic neuropeptides.

94 Central serotonin (5-HT) is an anorexigenic neurotransmitter in the brain.

95 lanocyte-stimulating hormone (alpha-MSH) and anorexigenic neurotransmitter serotonin.

96 potential neurobiological mechanism for the anorexigenic oxytocin effects in humans.

97 ling and consequent activation of downstream anorexigenic pathways.

98 tite suppression and to decrease activity in anorexigenic PBN CGRP neurons, thereby increasing food i

99 The Pomc gene encodes both the anorexigenic peptide alpha-melanocyte-stimulating hormon

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

103 Unlike many anorexigenic peptides, there is no increased sensitivity

104 cells and their regulation by orexigenic and anorexigenic peptides.

105 es the frequency of action potentials in the anorexigenic POMC neurons by two mechanisms: depolarizat

106 The inhibition of anorexigenic POMC neurons may be one mechanism underlyin

107 nic actions, at least in part, by inhibiting anorexigenic POMC neurons remains unclear.

108 onal activity and the inhibitory tone on the anorexigenic POMC neurons, as measured by the number of

109 P neurons and decreasing the activity of the anorexigenic POMC neurons.

110 expression of orexigenic (NPY and AgRP) and anorexigenic (POMC and CART) neuropeptide messages in th

111 s they occurred in the opposite direction in anorexigenic pro-opiomelanocortin (POMC) neurons.

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

118 -immunoreactive boutons terminate on or near anorexigenic proopiomelanocortin (POMC) cells.

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

126 We have characterized NDN as a potent anorexigenic signal acting through an uncharacterized en

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

130 How such anorexigenic signals inhibit feeding at the neural circu

131 ctions of ghrelin with respect to overcoming anorexigenic signals that act via the vagal afferent pat

132 node that mediates the influence of multiple anorexigenic signals.

133 tivated protein kinase (AMPK), indicating an anorexigenic state.

134 s sufficient to induce CTA in the absence of anorexigenic substances, whereas genetically induced sil

135 somedial hypothalamus, and 4) suppression of anorexigenic systems POMC and CART.

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