ライフサイエンスコーパス: anorectic

1 ultimately contributed to the reduced use of anorectics.

2 enefit come under greater scrutiny than with anorectics.

3 ession are responsible for the impaired E2's anorectic action in obese females.

4 ese results demonstrate a previously unknown anorectic action of central TTR in the control of energy

5 n of S6K1 (S6K1(-/-)) did not respond to the anorectic action of either leptin or CNTF(Ax15), implyin

6 2.5-250 microg/kg) pretreatment reversed the anorectic action of FEN (1.25 mg/kg) and FLU (5 mg/kg) b

7 lly in the NTS significantly diminished E2's anorectic action, leading to increased food intake and b

8 Although VSG slightly improved leptin's anorectic action, the response was comparable to that ob

9 t not i3vt or IP glucose potentiated GLP-1's anorectic action.

10 have reported that nicotine exerts a marked anorectic action.

11 mice does not prevent their response to the anorectic actions of ciliary neurotrophic factor (CNTF),

12 ding behavior that temporarily abrogates the anorectic actions of leptin despite normalized circulati

13 d, diet-induced obese and fasted mice to the anorectic actions of leptin were examined.

14 ficient (Mc4r-/-) mice do not respond to the anorectic actions of MTII, an MSH-like agonist, suggesti

15 that is regulated by nutritional status and anorectic actions, as the endogenous ligand for the guan

16 A steroidal glycoside with anorectic activity in animals, termed P57AS3 (P57), was

17 ood intake in rats but failed to demonstrate anorectic activity in rodent natural feeding models.

18 Anorectic activity of peptide YY(3-36) has been confirme

19 Compound 6 produces potent anorectic activity via the CCK-A receptor system.

20 these results suggest that GNTI is a potent anorectic agent and opioid antagonist in rats.

21 In contrast, the structurally related anorectic agent mazindol and the amphetamine-based anore

22 y of fenfluramine as a serotonin neurotoxin, anorectic agent or discrimination stimulus.

23 Phendimetrazine (PDM) is a schedule III anorectic agent that functions as both a low-potency mon

24 the expression of anorexia to two classes of anorectic agent.

25 ed transcript (CART) has emerged as a potent anorectic agent.

26 e precise behavioural changes caused by each anorectic agent.

27 entermine have been individually approved as anorectic agents by the Food and Drug Administration (FD

28 y, work in other laboratories indicates that anorectic agents consistently increase FLI in BNST and C

29 of these compounds are equipotent to CCK as anorectic agents in rats following intraperitoneal admin

30 e changes in feeding behaviour evoked by the anorectic agents investigated do not mimic the behaviour

31 n demonstrated that increased sensitivity to anorectic agents was a generalized result of MC3R antago

32 tolerability issues that typically accompany anorectic agents, leveraging this approach to induce sus

33 re prominently activated by other classes of anorectic agents.

34 cores were designed and tested as potential anorectic agents.

35 n decreases insulin secretion and has potent anorectic, analgesic, anxiolytic and antidepressive-like

36 ndimetrazine (PDM) is a clinically available anorectic and a candidate pharmacotherapy for cocaine ad

37 GLP-1 exerts anorectic and antimotility actions that protect the body

38 The recent publications of anorectic and antiobesity effects of the first two selec

39 The increased anorectic and anxiogenic-like behavior most likely is ca

40 inhibition of NTS astrocytes attenuates the anorectic and body weight-suppressive effects of intra-N

41 Detailed information about anorectic and bulimic behaviors was assessed through per

42 The acute anorectic and glucose tolerance effects of peripherally

43 the role of each component in mediating the anorectic and metabolic effects of leptin, and in regula

44 e that nutrient partitioning, as well as the anorectic and metabolic responses to leptin, are depende

45 s involved in mediating associations between anorectic and noxious/stressful stimuli.

46 opioid control of feeding by comparing rats' anorectic and orexigenic responses to naloxone and butor

47 owth differentiation factor 15 (GDF15) is an anorectic and weight loss-inducing hormone that responds

48 blockade of hypothalamic ERK1/2 reverses the anorectic and weight-reducing effects of leptin.

49 cium and membrane potential, and blunted the anorectic and weight-reducing responses evoked by the 5-

50 renal failure patients with malnutrition are anorectic, and dietary counseling has had limited succes

51 or type 1 (CB1) have been demonstrated to be anorectic antiobesity drug candidates.

52 enic (appetite-stimulating: MCH and NPY) and anorectic (appetite-suppressing: alpha-MSH, neurotensin,

53 tic agent mazindol and the amphetamine-based anorectic compounds diethylpropion, fenfluramine, and ph

54 ostmeal satiety and a reduced sensitivity to anorectic CRF(2) agonist stimulation.

55 ly inhibit the expression of proinflammatory anorectic cytokines such as IL-1beta, IL-6, and TNF-alph

56 In addition to being anorectic, cytokines also contribute to lipolysis, muscl

57 ng upper gut emptying can be as effective as anorectic drug administration.

58 to quantitate the brain concentration of the anorectic drug dexfenfluramine (DF) in human subjects re

59 Ciclazindol, an anorectic drug, was shown to inhibit ATP-sensitive K+ (K

60 ) receptor antagonist metitepine as a potent anorectic drug.

61 suggests JNK2 or JNK3 mediates aspect of the anorectic effect by pan-JNK inhibition.

62 II into brain parenchyma is required for the anorectic effect following intravenous (IV) administrati

63 specific 5-HT receptors that account for its anorectic effect have yet to be elucidated.

64 K2 has a role in appetite regulation and its anorectic effect is mediated partly via the melanocortin

65 V at a dose of 1 nmol completely blocked the anorectic effect of 1 nmol alpha-MSH.

66 Furthermore, the anorectic effect of a high dose of AM251 was further enh

67 onse to lipid feeding and contributes to the anorectic effect of a lipid meal.

68 In contrast, the anorectic effect of amylin seems to be due principally t

69 ia following administration of DFEN, but the anorectic effect of amylin was completely eliminated.

70 tion of 5-HT1B receptors is required for the anorectic effect of fenfluramine, we assessed food intak

71 rk1/2 signaling in the DVC negated the acute anorectic effect of insulin in healthy rats, while DVC i

72 In addition, the GLP-1r dependence of the anorectic effect of intracerebroventricular Ex4 was asse

73 The anorectic effect of intracerebroventricular glucose and

74 r, GLP-1r antagonists completely blocked the anorectic effect of intraperitoneal Ex4.

75 Decreasing triglycerides may potentiate the anorectic effect of leptin by enhancing leptin transport

76 Moreover, the anorectic effect of MTII was evaluated at 1, 2, and 24 h

77 The anorectic effect of NTS GIPR agonist remained intact in

78 The anorectic effect of oleic acid was independent of leptin

79 oth wild-type and 5-HT1B knock-out mice, the anorectic effect of the drug was absent in only the knoc

80 ot in Y2r-null mice, which suggests that the anorectic effect requires the Y2R.

81 DIO mice, JNK inhibition sensitized leptin's anorectic effect, and enhanced leptin-induced STAT3 acti

82 of 11 with the SSRI sertraline increased the anorectic effect.

83 C receptors in the ARC diminished the leptin anorectic effect.

84 e (Gfral) in the area postrema negates lipid anorectic effect.

85 inhibition of mTOR signaling blunts leptin's anorectic effect.

86 vation through hM(3)Dq caused a strong acute anorectic effect.

87 lic response that cannot be explained by its anorectic effects alone.

88 ary, our results demonstrate that BNP exerts anorectic effects and reduces ghrelin concentrations in

89 isoform-selective inhibitor, exerted similar anorectic effects as SR3306, which suggests JNK2 or JNK3

90 logical blockade of OX-1R by SB334867 caused anorectic effects by reducing food intake and body weigh

91 the unconditioned expression of estradiol's anorectic effects during the time of CTA assessment.

92 identified as a site-of-action mediating the anorectic effects of amylin.

93 neurobiological substrates that mediate the anorectic effects of both endogenous glucagon-like pepti

94 (1 nmol) administered ICV did not block the anorectic effects of CART (55-102) (1 h food intake, 0.2

95 SP led to an even greater attenuation of the anorectic effects of cisplatin compared to either agent

96 We examined to what extent the anorectic effects of cocaine- and amphetamine-regulated

97 microstructure and are sensitive to central anorectic effects of corticotropin-releasing factor type

98 -pairing sucrose consumption even though the anorectic effects of estradiol had subsided.

99 e the dissociability of the conditioning and anorectic effects of estradiol, providing evidence again

100 Despite the anorectic effects of exogenous peptide YY(3-36) followin

101 Agrp (83-132) also did not block the anorectic effects of GLP-1 or CRF (1 h food intake, 0.3

102 , but the cellular mechanisms underlying the anorectic effects of GLP-1 require further investigation

103 As the anorectic effects of glucagon-like peptide-1 receptor (G

104 In the present studies, the anorectic effects of GNTI, a newly synthesized antagonis

105 RESEARCH DESIGN AND In this study, the anorectic effects of intracerebroventricular GLP-1 and E

106 , preobese Bbs4 mutant mice responded to the anorectic effects of leptin and did not display other ph

107 ning period increases the sensitivity to the anorectic effects of leptin and protects obesity-prone o

108 that neuronal GLP1Rs mediate body weight and anorectic effects of liraglutide, but are not required f

109 re more sensitive than wild-type mice to the anorectic effects of MTII.

110 t leptin and its receptor play a role in the anorectic effects of nicotine on food intake and body we

111 current study was to investigate whether the anorectic effects of PYY(3-36) and oxyntomodulin can be

112 The anorectic effects of PYY(3-36) and oxyntomodulin can be

113 e revealed that the Y2-receptor mediates the anorectic effects of PYY3-36 whilst mechanistic studies

114 ding virtually obliterated the metabolic and anorectic effects of the central administration of oleic

115 t not 5-HT2C receptors, are required for the anorectic effects of the interoceptive stressor LiCl, su

116 lesions of the medial or lateral PBN on the anorectic effects of two systemically administered drug

117 This compound demonstrated potent anorectic effects similar to the CB1 antagonist rimonaba

118 demonstrate that PACAP in the CeA exerts its anorectic effects via local melanocortin and the TrKB sy

119 n energy balance control and exerting strong anorectic effects via the central melanocortin system.

120 ; although mice became resistant to leptin's anorectic effects, the ability to increase renal sympath

121 eletal muscle can be largely ascribed to its anorectic effects.

122 ctive ligands, many of which have observable anorectic effects.

123 makes an important contribution to leptin's anorectic effects.

124 ols demonstrating a lack of tolerance to its anorectic effects.

125 ause central CRF(2) stimulation retains full anorectic efficacy at higher doses in the DIO model, man

126 tration of a 5-HT1BR agonist potentiates the anorectic efficacy of 5-HT2CR compounds by increasing th

127 idemic must continue, investigation into the anorectic functions of potential molecules we present he

128 tin receptor (LepRb) and is activated by the anorectic hormone leptin (Nts(LepRb) neurons).

129 The adipocyte-derived, anorectic hormone leptin was recently shown to owe part

130 e the suppression of appetite induced by the anorectic hormones amylin and cholecystokinin, as well a

131 hormone (a-MSH), triggers the release of the anorectic hormones Glucagon-like peptide-1 (GLP-1) and p

132 Aged mice were anorectic longer and lost more weight than adults after

133 eptin resistance may have evolved as an anti-anorectic mechanism during starvation.

134 OEA is an anorectic N-acylethanolamine produced from dietary fats

135 e of leptin, are electrically excited by the anorectic neuromodulator cholecystokinin, and inhibited

136 on is mediated by a number of orexigenic and anorectic neuronal systems in the hypothalamus.

137 both a rapid and a slower role in acting as anorectic neurons in CNS control of food intake and ener

138 40% of them expressed the mRNA encoding the anorectic neuropeptide cholecystokinin.

139 In contrast, IHT administration of the anorectic neuropeptide, pituitary adenylate cyclase acti

140 eased food intake, suggesting that PK2 is an anorectic neuropeptide.

141 uch as leptin and a number of orexigenic and anorectic neuropeptides.

142 however, the Fos response to other putative anorectics or weight reducing agents is not affected.

143 PRRSV piglets were febrile (p < 0.0001), anorectic (p < 0.0001), and weighed less at the end of t

144 Oleoyl-L-valinolamide enhances anorectic pathways and lead to decreased glucose levels,

145 energy homeostasis; they were excited by the anorectic peptide cholecystokinin, but inhibited by orex

146 cuate nucleus, and reduced expression of the anorectic peptide corticotropin-releasing hormone (CRH)

147 Hypothalamic neurons expressing the anorectic peptide Pro-opiomelanocortin (Pomc) regulate f

148 ed body weight in rats indicates that NT, an anorectic peptide, is involved in mediating leptin's act

149 Glucose supplementation during the anorectic period induced by bacterial inflammation suppr

150 tools that highlight possible predictors of anorectic phenotypes.

151 Here we investigated whether 5-HT2CR agonist anorectic potency could be significantly enhanced by coa

152 To investigate the anorectic potential of NPY5 receptor antagonists, we hav

153 lts lead to the suggestion that fluoxetine's anorectic properties could disrupt the female's normal e

154 anti-epileptic, analeptic, anti-ataxic, and anorectic properties.

155 The enhanced anorectic response in Mc3r-/- mice after administration

156 The data imply that the enterostatin anorectic response may be modulated by 5-HT1B receptors

157 ture of GIP involvement with an at best weak anorectic response profile being reported for GIP recept

158 a circuit that is involved in the short term anorectic response to amino acid imbalanced diets.

159 nserin (10 nmol) into the PVN attenuated the anorectic response to amygdala enterostatin.

160 locking central ODN signaling attenuated the anorectic response to GLP-1R agonists in rats.

161 nd non-specific 5-HT antagonists blocked the anorectic response to icv enterostatin.

162 limiting amino acid into the APC, blocks the anorectic response to IMB.

163 et (HFD) has been related to the loss of the anorectic response to insulin injections into the centra

164 An enhanced anorectic response to the acute satiety factors peptide

165 t or food intake of lean mice but induces an anorectic response when coadministered with exogenous le

166 ow before AgRP neuron ablation abolished the anorectic response.

167 We suggest that glutamate mediates the anorectic responses to AA-deficient diets through recogn

168 in the hypothalamus mediates the febrile and anorectic responses to disease, but the mechanism by whi

169 hort hypothalamic cilia exhibited attenuated anorectic responses to leptin, insulin, and glucose, whi

170 Moreover, these mice did not show anorectic responses to serotonergic agents that suppress

171 AAH knockdown in AgRP neurons blunted leptin anorectic responses.

172 ously appreciated, and play predominantly an anorectic role in energy metabolism.

173 so ADM2 and LDLR, genes that are involved in anorectic signaling and lipid homeostasis.

174 s of hypothalamic ACC activation in leptin's anorectic signaling cascade.

175 y volume contraction observed in response to anorectic states.

176 ctive neurons were visualized in Control and anorectic TB rats in the preoptic region, the arcuate nu

177 ostaining in some hypothalamic nuclei of the anorectic TB rats, most prominently in the supraoptic nu

178 ression in sham operated Fischer Control and anorectic TB rats.

179 Sibutramine, the latest anorectic to enter the market, is now the focus of a lan

180 ne gave rise to widespread, long-term use of anorectics to treat obesity.

181 foraging when food is abundant and that the anorectic TOL-1/PMK-1 pathway is attenuated during starv

182 ntrations and hypothalamic leptin binding in anorectic tumor-bearing and pair-fed control rats.

183 that ate the same amount of food as did the anorectic tumor-bearing rats exhibited a 50% decrease in

184 vels of triglycerides were increased only in anorectic tumor-bearing rats.

185 opeptide Y feeding systems may be minimal in anorectic tumor-bearing rats.

186 yne syndrome as well as chemotherapy-induced anorectic weight loss.