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1 rons), which precipitates hyperglycaemia and hypophagia.
2 ons, providing a mechanism for threat-evoked hypophagia.
3 perience seasonal periods of hyperphagia and hypophagia.
4 responsible for the loss of ADCP activity in hypophagia.
5 sions of the lateral hypothalamus (LH) cause hypophagia.
6 CNS with an H3 receptor antagonist-increased hypophagia.
7 hether histamine participates in OEA-induced hypophagia.
8 levated in obesity, but paradoxically causes hypophagia.
9  Chow/Palatable rats, without affecting chow hypophagia.
10 actus solitarii abolished rimonabant-induced hypophagia.
11  metabolic rate, causing weight gain despite hypophagia.
12 cally than NTX, abolishing anticipatory chow hypophagia.
13 ies in Ox signaling lead to hypoactivity and hypophagia.
14 ced acoustic startle and less stress-induced hypophagia.
15 d along with the blockade of leptin-mediated hypophagia.
16 intake after fast and blocked stress-induced hypophagia.
17 y a rapid loss of body weight resulting from hypophagia.
18 yperphagia during the first 2 h, followed by hypophagia.
19 testinal satiety signaling and contribute to hypophagia.
20 od-odor related stimuli, and potently drives hypophagia.
21 y nonresponsive (tolerant) to S-O-PG-induced hypophagia.
22 regained full responsiveness to LPS-mediated hypophagia.
23 lencing, attenuated intra-VTA amylin-induced hypophagia.
24 central mechanism in methylphenidate-induced hypophagia.
25 ving four regions: post-treatment hours 1-6 (hypophagia), 7-12 (normal intake), 13-27 (hypophagia), a
26 butyric acid receptor signaling mediates the hypophagia after LDTg amylin receptor activation.
27          Inhibition of weight gain is due to hypophagia after mice are fed a highly palatable diet ri
28 2 microg/g) but manifest normal AMPH-induced hypophagia after restoration of DA signaling in the caud
29 ay contribute to a decrease in adiposity and hypophagia and an enhancement of energy expenditure acco
30 B agonist RU24969 was able to mimic both the hypophagia and c-fos induction elicited by fenfluramine
31  disruption of PVN 2-AG synthesis results in hypophagia and death.
32                       Mc3r KO rats displayed hypophagia and decreased body weight, while Mc4r KO and
33            The observations suggest that the hypophagia and hypoactivity of mutants result not only b
34 1R stimulation in DR is sufficient to induce hypophagia and increase the electrical activity of the D
35                Leanness was characterized by hypophagia and increased energy expenditure.
36 e ciliary neurotrophic factor (CNTF) induces hypophagia and increases signal transduction activator o
37 uced mutations of the MCH gene in mice cause hypophagia and leanness.
38       Because genetic MCH deficiency induces hypophagia and loss of body fat, we hypothesized that MC
39 pression of GDF15 leads to a lean phenotype, hypophagia and other improvements in metabolic parameter
40 uated in short day (SD) animals that display hypophagia and reduced adiposity.
41 selective loss of the orexin neurons develop hypophagia and severe obesity in addition to the narcole
42  the dorsal striatum is sufficient to induce hypophagia and suggest that regulated release of dopamin
43 atal DA is the primary cause of AMPH-induced hypophagia and that regulated striatal dopaminergic sign
44     The mechanisms may involve the sustained hypophagia and the augmentation of thermogenesis in BAT.
45             The central MCH knockdown causes hypophagia and weight loss in diet-induced obese wild-ty
46 ), display a remarkable anorexia with severe hypophagia and weight loss.
47 6 (hypophagia), 7-12 (normal intake), 13-27 (hypophagia), and 28 and beyond (normal intake).
48 excessive intake of the palatable diet, chow hypophagia, and anxiety-like behavior.
49 exia (ABA), which refers to the weight loss, hypophagia, and hyperactivity exhibited by rodents expos
50 t is characterized by a low body-mass index, hypophagia, and hyperactivity.
51 -like effect in the Porsolt, novelty induced hypophagia, and learned helplessness tests in rats witho
52  reduced latency to drink in novelty-induced hypophagia, and LiCl was not effective in VGF(+/-) mice,
53  accompanied by hypolocomotion, hypothermia, hypophagia, and nausea.
54 LP-1 receptor antagonist blocked RES-induced hypophagia, and reduced the ability of RES to activate P
55 agia of palatable food and anticipatory chow hypophagia (anticipatory negative contrast).
56 ssion in NAcC DA mediates VTA amylin-induced hypophagia, as combined NAcC D1/D2 receptor agonists blo
57 achial nucleus (PBN) to systemic Ex4-induced hypophagia, as the PBN receives gustatory and visceral a
58 sulin/IGF signalling, as well as by maternal hypophagia depending on the timing and severity of the h
59 -fed experiment showed that adjuvant-induced hypophagia did not alter corticosterone levels.
60       From day 16 onward, the mice developed hypophagia, exhibited severe weight loss, lost triglycer
61  least two mechanisms of tolerance to S-O-PG hypophagia exist: an early tolerance which is nonspecifi
62 CK-1 receptor blockade partly attenuated the hypophagia from RS-4.
63                                 Importantly, hypophagia had no effect on Ab-independent phagocytosis
64  an eating disorder characterized by extreme hypophagia, hyperactivity, and fear of weight gain.
65 1a (BMPR1A) in the OLIG1 lineage resulted in hypophagia, hypoglycemia, and weight loss after the seco
66 ment with 13 led to significant weight loss, hypophagia, improved glucose utilization, reduced liver
67 nversely, intra-BlA R121919 reduced the chow hypophagia in Chow/Palatable rats, without affecting exc
68 2 diabetes mellitus, is well known to induce hypophagia in human and animal models.
69 e, we assessed the efficacy of D-Fen-induced hypophagia in mouse models with manipulations of several
70                    By contrast, AMPH-induced hypophagia in response to the same dose of AMPH is not b
71 control rats attenuated CART hypothermia and hypophagia, indicating that GLP-1R activation contribute
72 d intake in normal conditions but attenuates hypophagia induced by stress and anxiety.
73                            Behaviorally, the hypophagia induced by the pharmacological activation of
74  interoceptive stressor LiCl, suggesting the hypophagia induced by these 5-HT receptors may be driven
75 essential for sustained feeding suppression (hypophagia) induced by Ucn.
76 pport the view that tolerance to amphetamine hypophagia involves a behavioral adaptation to the motor
77 f feeding, and (b) tolerance to drug-induced hypophagia involves learning to suppress such movements,
78                           These data suggest hypophagia is a critical limiting step in macrophage-med
79 gy transfer rate from the human fat store in hypophagia is deduced from experimental data of underfed
80 esting metabolic rate of subjects undergoing hypophagia is shown to decrease linearly as a function o
81                  Thus the attenuation of the hypophagia may have been caused by this IL-1ra-induced i
82 oned taste avoidance (CTA) without affecting hypophagia mediated by a PYY analog.
83 r antagonist-reversible behaviors, including hypophagia, motivational deficits to obtain less palatab
84 xiety-like phenotypes in the novelty-induced hypophagia (NIH) paradigm.
85  chronic AD treatment in the novelty-induced hypophagia (NIH) test may rely on neurogenesis.
86 s, chronic forced swim test, novelty-induced hypophagia (NIH), novelty-suppressed feeding (NSF), soci
87         This complete reversal of regulatory hypophagia not only maintained but actually increased th
88 ist, caffeine (5-25 mgkg i.p.), reversed the hypophagia of mutant mice and induced hyperactivity in b
89 ich include excessive palatable food intake, hypophagia of regular chow, and anxiety-like behavior.
90 antidepressant response, the novelty-induced hypophagia procedure, hippocampal CREB deletion, did not
91                                 Although the hypophagia promoted expression of the orexigenic neurope
92           After recovery from 6-OHDA-induced hypophagia, rats were sacrificed to assess neostriatal D
93 have reduced body weight and leanness due to hypophagia (reduced feeding) and an inappropriately incr
94 r, the mechanisms by which olfaction induces hypophagia remain elusive.
95          We also show that serotonin-induced hypophagia requires downstream activation of melanocorti
96 ic MANF protein levels causes hyperphagia or hypophagia, respectively.
97                       In the novelty-induced hypophagia task, males with a history of ethanol consump
98 lopram administration in the novelty induced hypophagia test (NIH) and fail to exhibit enhanced proli
99 fective-like behavior in the novelty-induced hypophagia test following restraint stress-a phenotype t
100 ed anxiety levels, using the Novelty-Induced Hypophagia test, and cognition, using a contextual fear
101 anxiety-like behavior in the Novelty-Induced Hypophagia test.
102 iety-related behavior in the novelty-induced hypophagia test.
103 r behavioral response in the novelty-induced hypophagia test.
104 ow tolerance develops to amphetamine-induced hypophagia, the authors recorded real-time licking respo
105 phagia, whereas lactoferrin caused prolonged hypophagia; the hypophagia was likely due to decreased p
106 eding motivation to attenuate stress-induced hypophagia through exciting PVT neurons.
107 elopment of tolerance to amphetamine-induced hypophagia was assessed by recording changes in lick par
108              CB1 receptor antagonist-induced hypophagia was fully abolished by peripheral blockade of
109 lactoferrin caused prolonged hypophagia; the hypophagia was likely due to decreased preference.
110 iously unknown refractory period of ADCP, or hypophagia, was observed in all macrophage, mAb, and tar
111 us Maze, Marble Burying, and Novelty Induced Hypophagia) were assessed following a 2-week abstinence
112      Whey and lactalbumin produced transient hypophagia, whereas lactoferrin caused prolonged hypopha
113 creases social avoidance and novelty-induced hypophagia without impairing working memory, establishin

 
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