ライフサイエンスコーパス: hypophagia

1 sions of the lateral hypothalamus (LH) cause hypophagia.

2 CNS with an H3 receptor antagonist-increased hypophagia.

3 hether histamine participates in OEA-induced hypophagia.

4 levated in obesity, but paradoxically causes hypophagia.

5 Chow/Palatable rats, without affecting chow hypophagia.

6 actus solitarii abolished rimonabant-induced hypophagia.

7 metabolic rate, causing weight gain despite hypophagia.

8 cally than NTX, abolishing anticipatory chow hypophagia.

9 ies in Ox signaling lead to hypoactivity and hypophagia.

10 d along with the blockade of leptin-mediated hypophagia.

11 y a rapid loss of body weight resulting from hypophagia.

12 yperphagia during the first 2 h, followed by hypophagia.

13 testinal satiety signaling and contribute to hypophagia.

14 y nonresponsive (tolerant) to S-O-PG-induced hypophagia.

15 regained full responsiveness to LPS-mediated hypophagia.

16 ving four regions: post-treatment hours 1-6 (hypophagia), 7-12 (normal intake), 13-27 (hypophagia), a

17 butyric acid receptor signaling mediates the hypophagia after LDTg amylin receptor activation.

18 Inhibition of weight gain is due to hypophagia after mice are fed a highly palatable diet ri

19 2 microg/g) but manifest normal AMPH-induced hypophagia after restoration of DA signaling in the caud

20 ay contribute to a decrease in adiposity and hypophagia and an enhancement of energy expenditure acco

21 B agonist RU24969 was able to mimic both the hypophagia and c-fos induction elicited by fenfluramine

22 Mc3r KO rats displayed hypophagia and decreased body weight, while Mc4r KO and

23 The observations suggest that the hypophagia and hypoactivity of mutants result not only b

24 1R stimulation in DR is sufficient to induce hypophagia and increase the electrical activity of the D

25 Leanness was characterized by hypophagia and increased energy expenditure.

26 e ciliary neurotrophic factor (CNTF) induces hypophagia and increases signal transduction activator o

27 uced mutations of the MCH gene in mice cause hypophagia and leanness.

28 Because genetic MCH deficiency induces hypophagia and loss of body fat, we hypothesized that MC

29 pression of GDF15 leads to a lean phenotype, hypophagia and other improvements in metabolic parameter

30 uated in short day (SD) animals that display hypophagia and reduced adiposity.

31 selective loss of the orexin neurons develop hypophagia and severe obesity in addition to the narcole

32 the dorsal striatum is sufficient to induce hypophagia and suggest that regulated release of dopamin

33 atal DA is the primary cause of AMPH-induced hypophagia and that regulated striatal dopaminergic sign

34 The mechanisms may involve the sustained hypophagia and the augmentation of thermogenesis in BAT.

35 ), display a remarkable anorexia with severe hypophagia and weight loss.

36 6 (hypophagia), 7-12 (normal intake), 13-27 (hypophagia), and 28 and beyond (normal intake).

37 excessive intake of the palatable diet, chow hypophagia, and anxiety-like behavior.

38 -like effect in the Porsolt, novelty induced hypophagia, and learned helplessness tests in rats witho

39 reduced latency to drink in novelty-induced hypophagia, and LiCl was not effective in VGF(+/-) mice,

40 LP-1 receptor antagonist blocked RES-induced hypophagia, and reduced the ability of RES to activate P

41 agia of palatable food and anticipatory chow hypophagia (anticipatory negative contrast).

42 ssion in NAcC DA mediates VTA amylin-induced hypophagia, as combined NAcC D1/D2 receptor agonists blo

43 achial nucleus (PBN) to systemic Ex4-induced hypophagia, as the PBN receives gustatory and visceral a

44 sulin/IGF signalling, as well as by maternal hypophagia depending on the timing and severity of the h

45 -fed experiment showed that adjuvant-induced hypophagia did not alter corticosterone levels.

46 From day 16 onward, the mice developed hypophagia, exhibited severe weight loss, lost triglycer

47 least two mechanisms of tolerance to S-O-PG hypophagia exist: an early tolerance which is nonspecifi

48 an eating disorder characterized by extreme hypophagia, hyperactivity, and fear of weight gain.

49 1a (BMPR1A) in the OLIG1 lineage resulted in hypophagia, hypoglycemia, and weight loss after the seco

50 nversely, intra-BlA R121919 reduced the chow hypophagia in Chow/Palatable rats, without affecting exc

51 2 diabetes mellitus, is well known to induce hypophagia in human and animal models.

52 e, we assessed the efficacy of D-Fen-induced hypophagia in mouse models with manipulations of several

53 By contrast, AMPH-induced hypophagia in response to the same dose of AMPH is not b

54 control rats attenuated CART hypothermia and hypophagia, indicating that GLP-1R activation contribute

55 essential for sustained feeding suppression (hypophagia) induced by Ucn.

56 pport the view that tolerance to amphetamine hypophagia involves a behavioral adaptation to the motor

57 f feeding, and (b) tolerance to drug-induced hypophagia involves learning to suppress such movements,

58 gy transfer rate from the human fat store in hypophagia is deduced from experimental data of underfed

59 esting metabolic rate of subjects undergoing hypophagia is shown to decrease linearly as a function o

60 Thus the attenuation of the hypophagia may have been caused by this IL-1ra-induced i

61 r antagonist-reversible behaviors, including hypophagia, motivational deficits to obtain less palatab

62 xiety-like phenotypes in the novelty-induced hypophagia (NIH) paradigm.

63 chronic AD treatment in the novelty-induced hypophagia (NIH) test may rely on neurogenesis.

64 s, chronic forced swim test, novelty-induced hypophagia (NIH), novelty-suppressed feeding (NSF), soci

65 This complete reversal of regulatory hypophagia not only maintained but actually increased th

66 ist, caffeine (5-25 mgkg i.p.), reversed the hypophagia of mutant mice and induced hyperactivity in b

67 ich include excessive palatable food intake, hypophagia of regular chow, and anxiety-like behavior.

68 antidepressant response, the novelty-induced hypophagia procedure, hippocampal CREB deletion, did not

69 Although the hypophagia promoted expression of the orexigenic neurope

70 After recovery from 6-OHDA-induced hypophagia, rats were sacrificed to assess neostriatal D

71 have reduced body weight and leanness due to hypophagia (reduced feeding) and an inappropriately incr

72 We also show that serotonin-induced hypophagia requires downstream activation of melanocorti

73 ic MANF protein levels causes hyperphagia or hypophagia, respectively.

74 lopram administration in the novelty induced hypophagia test (NIH) and fail to exhibit enhanced proli

75 ed anxiety levels, using the Novelty-Induced Hypophagia test, and cognition, using a contextual fear

76 iety-related behavior in the novelty-induced hypophagia test.

77 r behavioral response in the novelty-induced hypophagia test.

78 anxiety-like behavior in the Novelty-Induced Hypophagia test.

79 ow tolerance develops to amphetamine-induced hypophagia, the authors recorded real-time licking respo

80 phagia, whereas lactoferrin caused prolonged hypophagia; the hypophagia was likely due to decreased p

81 elopment of tolerance to amphetamine-induced hypophagia was assessed by recording changes in lick par

82 CB1 receptor antagonist-induced hypophagia was fully abolished by peripheral blockade of

83 lactoferrin caused prolonged hypophagia; the hypophagia was likely due to decreased preference.

84 Whey and lactalbumin produced transient hypophagia, whereas lactoferrin caused prolonged hypopha