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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 entermine have been individually approved as anorectic agents by the Food and Drug Administration (FD
27 y, work in other laboratories indicates that anorectic agents consistently increase FLI in BNST and C
28  of these compounds are equipotent to CCK as anorectic agents in rats following intraperitoneal admin
29 re prominently activated by other classes of anorectic agents.
30  cores were designed and tested as potential anorectic agents.
31 ndimetrazine (PDM) is a clinically available anorectic and a candidate pharmacotherapy for cocaine ad
32                   The recent publications of anorectic and antiobesity effects of the first two selec
33                                The increased anorectic and anxiogenic-like behavior most likely is ca
34  inhibition of NTS astrocytes attenuates the anorectic and body weight-suppressive effects of intra-N
35                   Detailed information about anorectic and bulimic behaviors was assessed through per
36                                    The acute anorectic and glucose tolerance effects of peripherally
37  the role of each component in mediating the anorectic and metabolic effects of leptin, and in regula
38 e that nutrient partitioning, as well as the anorectic and metabolic responses to leptin, are depende
39 opioid control of feeding by comparing rats' anorectic and orexigenic responses to naloxone and butor
40 blockade of hypothalamic ERK1/2 reverses the anorectic and weight-reducing effects of leptin.
41 renal failure patients with malnutrition are anorectic, and dietary counseling has had limited succes
42 or type 1 (CB1) have been demonstrated to be anorectic antiobesity drug candidates.
43 enic (appetite-stimulating: MCH and NPY) and anorectic (appetite-suppressing: alpha-MSH, neurotensin,
44 tic agent mazindol and the amphetamine-based anorectic compounds diethylpropion, fenfluramine, and ph
45 ostmeal satiety and a reduced sensitivity to anorectic CRF(2) agonist stimulation.
46 ly inhibit the expression of proinflammatory anorectic cytokines such as IL-1beta, IL-6, and TNF-alph
47                         In addition to being anorectic, cytokines also contribute to lipolysis, muscl
48 to quantitate the brain concentration of the anorectic drug dexfenfluramine (DF) in human subjects re
49                              Ciclazindol, an anorectic drug, was shown to inhibit ATP-sensitive K+ (K
50 ) receptor antagonist metitepine as a potent anorectic drug.
51 suggests JNK2 or JNK3 mediates aspect of the anorectic effect by pan-JNK inhibition.
52 II into brain parenchyma is required for the anorectic effect following intravenous (IV) administrati
53 specific 5-HT receptors that account for its anorectic effect have yet to be elucidated.
54 K2 has a role in appetite regulation and its anorectic effect is mediated partly via the melanocortin
55 V at a dose of 1 nmol completely blocked the anorectic effect of 1 nmol alpha-MSH.
56                             Furthermore, the anorectic effect of a high dose of AM251 was further enh
57 onse to lipid feeding and contributes to the anorectic effect of a lipid meal.
58                             In contrast, the anorectic effect of amylin seems to be due principally t
59 ia following administration of DFEN, but the anorectic effect of amylin was completely eliminated.
60 tion of 5-HT1B receptors is required for the anorectic effect of fenfluramine, we assessed food intak
61 rk1/2 signaling in the DVC negated the acute anorectic effect of insulin in healthy rats, while DVC i
62    In addition, the GLP-1r dependence of the anorectic effect of intracerebroventricular Ex4 was asse
63                                          The anorectic effect of intracerebroventricular glucose and
64 r, GLP-1r antagonists completely blocked the anorectic effect of intraperitoneal Ex4.
65  Decreasing triglycerides may potentiate the anorectic effect of leptin by enhancing leptin transport
66                                Moreover, the anorectic effect of MTII was evaluated at 1, 2, and 24 h
67                                          The anorectic effect of oleic acid was independent of leptin
68 oth wild-type and 5-HT1B knock-out mice, the anorectic effect of the drug was absent in only the knoc
69 ot in Y2r-null mice, which suggests that the anorectic effect requires the Y2R.
70 DIO mice, JNK inhibition sensitized leptin's anorectic effect, and enhanced leptin-induced STAT3 acti
71 of 11 with the SSRI sertraline increased the anorectic effect.
72 inhibition of mTOR signaling blunts leptin's anorectic effect.
73 lic response that cannot be explained by its anorectic effects alone.
74 ary, our results demonstrate that BNP exerts anorectic effects and reduces ghrelin concentrations in
75 isoform-selective inhibitor, exerted similar anorectic effects as SR3306, which suggests JNK2 or JNK3
76 logical blockade of OX-1R by SB334867 caused anorectic effects by reducing food intake and body weigh
77  the unconditioned expression of estradiol's anorectic effects during the time of CTA assessment.
78 identified as a site-of-action mediating the anorectic effects of amylin.
79  neurobiological substrates that mediate the anorectic effects of both endogenous glucagon-like pepti
80  (1 nmol) administered ICV did not block the anorectic effects of CART (55-102) (1 h food intake, 0.2
81               We examined to what extent the anorectic effects of cocaine- and amphetamine-regulated
82  microstructure and are sensitive to central anorectic effects of corticotropin-releasing factor type
83 -pairing sucrose consumption even though the anorectic effects of estradiol had subsided.
84 e the dissociability of the conditioning and anorectic effects of estradiol, providing evidence again
85                                  Despite the anorectic effects of exogenous peptide YY(3-36) followin
86         Agrp (83-132) also did not block the anorectic effects of GLP-1 or CRF (1 h food intake, 0.3
87 , but the cellular mechanisms underlying the anorectic effects of GLP-1 require further investigation
88                                       As the anorectic effects of glucagon-like peptide-1 receptor (G
89                  In the present studies, the anorectic effects of GNTI, a newly synthesized antagonis
90       RESEARCH DESIGN AND In this study, the anorectic effects of intracerebroventricular GLP-1 and E
91 , preobese Bbs4 mutant mice responded to the anorectic effects of leptin and did not display other ph
92 ning period increases the sensitivity to the anorectic effects of leptin and protects obesity-prone o
93 that neuronal GLP1Rs mediate body weight and anorectic effects of liraglutide, but are not required f
94 re more sensitive than wild-type mice to the anorectic effects of MTII.
95 t leptin and its receptor play a role in the anorectic effects of nicotine on food intake and body we
96 current study was to investigate whether the anorectic effects of PYY(3-36) and oxyntomodulin can be
97                                          The anorectic effects of PYY(3-36) and oxyntomodulin can be
98 e revealed that the Y2-receptor mediates the anorectic effects of PYY3-36 whilst mechanistic studies
99 ding virtually obliterated the metabolic and anorectic effects of the central administration of oleic
100  lesions of the medial or lateral PBN on the anorectic effects of two systemically administered drug
101            This compound demonstrated potent anorectic effects similar to the CB1 antagonist rimonaba
102 demonstrate that PACAP in the CeA exerts its anorectic effects via local melanocortin and the TrKB sy
103 ; although mice became resistant to leptin's anorectic effects, the ability to increase renal sympath
104 ctive ligands, many of which have observable anorectic effects.
105  makes an important contribution to leptin's anorectic effects.
106 ols demonstrating a lack of tolerance to its anorectic effects.
107 eletal muscle can be largely ascribed to its anorectic effects.
108 ause central CRF(2) stimulation retains full anorectic efficacy at higher doses in the DIO model, man
109 tration of a 5-HT1BR agonist potentiates the anorectic efficacy of 5-HT2CR compounds by increasing th
110 idemic must continue, investigation into the anorectic functions of potential molecules we present he
111                       The adipocyte-derived, anorectic hormone leptin was recently shown to owe part
112 e the suppression of appetite induced by the anorectic hormones amylin and cholecystokinin, as well a
113                               Aged mice were anorectic longer and lost more weight than adults after
114 eptin resistance may have evolved as an anti-anorectic mechanism during starvation.
115 on is mediated by a number of orexigenic and anorectic neuronal systems in the hypothalamus.
116  40% of them expressed the mRNA encoding the anorectic neuropeptide cholecystokinin.
117       In contrast, IHT administration of the anorectic neuropeptide, pituitary adenylate cyclase acti
118 eased food intake, suggesting that PK2 is an anorectic neuropeptide.
119 uch as leptin and a number of orexigenic and anorectic neuropeptides.
120  however, the Fos response to other putative anorectics or weight reducing agents is not affected.
121     PRRSV piglets were febrile (p < 0.0001), anorectic (p < 0.0001), and weighed less at the end of t
122               Oleoyl-L-valinolamide enhances anorectic pathways and lead to decreased glucose levels,
123 cuate nucleus, and reduced expression of the anorectic peptide corticotropin-releasing hormone (CRH)
124 ed body weight in rats indicates that NT, an anorectic peptide, is involved in mediating leptin's act
125 Here we investigated whether 5-HT2CR agonist anorectic potency could be significantly enhanced by coa
126                           To investigate the anorectic potential of NPY5 receptor antagonists, we hav
127 lts lead to the suggestion that fluoxetine's anorectic properties could disrupt the female's normal e
128  anti-epileptic, analeptic, anti-ataxic, and anorectic properties.
129         The data imply that the enterostatin anorectic response may be modulated by 5-HT1B receptors
130 a circuit that is involved in the short term anorectic response to amino acid imbalanced diets.
131 nserin (10 nmol) into the PVN attenuated the anorectic response to amygdala enterostatin.
132 nd non-specific 5-HT antagonists blocked the anorectic response to icv enterostatin.
133 limiting amino acid into the APC, blocks the anorectic response to IMB.
134 et (HFD) has been related to the loss of the anorectic response to insulin injections into the centra
135 ow before AgRP neuron ablation abolished the anorectic response.
136       We suggest that glutamate mediates the anorectic responses to AA-deficient diets through recogn
137 in the hypothalamus mediates the febrile and anorectic responses to disease, but the mechanism by whi
138 hort hypothalamic cilia exhibited attenuated anorectic responses to leptin, insulin, and glucose, whi
139            Moreover, these mice did not show anorectic responses to serotonergic agents that suppress
140 s of hypothalamic ACC activation in leptin's anorectic signaling cascade.
141 ctive neurons were visualized in Control and anorectic TB rats in the preoptic region, the arcuate nu
142 ostaining in some hypothalamic nuclei of the anorectic TB rats, most prominently in the supraoptic nu
143 ression in sham operated Fischer Control and anorectic TB rats.
144                      Sibutramine, the latest anorectic to enter the market, is now the focus of a lan
145 ne gave rise to widespread, long-term use of anorectics to treat obesity.
146 ntrations and hypothalamic leptin binding in anorectic tumor-bearing and pair-fed control rats.
147  that ate the same amount of food as did the anorectic tumor-bearing rats exhibited a 50% decrease in
148 vels of triglycerides were increased only in anorectic tumor-bearing rats.
149 opeptide Y feeding systems may be minimal in anorectic tumor-bearing rats.

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