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1 ese results suggest that PVN injection of an anorexic 500-pmol dose of CCK-8 does not increase plasma
2 araventricular nucleus (PVN) injection of an anorexic 500-pmol dose of cholecystokinin (CCK)-8 could
3 ere significantly more sensitive to leptin's anorexic action in the brain (i3vt), as well as signific
4   Discerning the neurobiology underlying the anorexic action of d-FEN may facilitate the development
5 ed phosphorylation of S6K1 and S6, and their anorexic action was reduced in rapamycin-treated rats an
6 provide a mechanistic explanation of d-FEN's anorexic actions and indicate that drugs targeting these
7 eurons containing serotonin (5-HT), a potent anorexic agent, come into contact with neuropeptide Y-er
8 ssociation of fenfluramine and certain other anorexic agents with serious side effects, such as cardi
9  the hypothesis that fenfluramine (and other anorexic agents) might increase the risk of PPH through
10             These observations indicate that anorexic agents, like hypoxia, can inhibit potassium cur
11 some patients taking other amphetamine-like, anorexic agents: fenfluramine and its d-isomer, dexfenfl
12  tonic, anti-inflammatory, antihypertensive, anorexic, analgesic, antibacterial and antidiabetic effe
13                         We conclude that the anorexic and antilipopenic actions of leptin decline wit
14 f the central IL-1 and IL-6 in mediating the anorexic and body weight loss effects of GLP-1 receptor
15                                 Relatives of anorexic and bulimic probands had increased risk of clin
16 ks were 11.3 and 12.3 in female relatives of anorexic and bulimic probands, respectively.
17 osa were 4.2 and 4.4 for female relatives of anorexic and bulimic probands, respectively.
18 rvosa aggregated in female relatives of both anorexic and bulimic probands.
19                       CART and NPY are major anorexic and orexic factors, respectively, but the intra
20  (CART) and neuropeptide Y (NPY) have potent anorexic and orexic functions, respectively, and show en
21 3R) impairs the behavioural response to both anorexic and orexigenic stimuli, with MC3R knockout mice
22 n situ hybridization and hormone analyses of anorexic and paired food-restricted rats revealed two di
23 verexpression, which reduces body weight via anorexic and thermogenic actions, induces triglyceride d
24 agouti obese mice, exhibit resistance to the anorexic and weight-reducing effects of leptin.
25 of whom 62 (46%) were bulimic, 30 (22%) were anorexic, and 43 (32%) met criteria for an eating disord
26          The second pattern occurred only in anorexic animals and had two components: (1) reduced cor
27                 Thus, opposing activities of anorexic CART and orexic NPY reconfigure circuit functio
28 allenges and increased weight loss following anorexic challenges (i.e. impaired energy rheostasis).
29 n MH in the acute response to orexigenic and anorexic challenges.
30              Dehydrated animals are strongly anorexic despite these attributes, showing that the outp
31                                              Anorexics die at a rate of 10-20% from complications of
32        Rats received injections of either an anorexic dose of CCK (8 nmol/kg, i.p.) or vehicle and we
33 at might account for the association between anorexic drugs and pulmonary hypertension.
34 cology of ghrelin, ghrelin-null mice are not anorexic dwarfs; their size, growth rate, food intake, b
35           Leptin infusion produced a greater anorexic effect in PTP1B knockout mice and a marked incr
36 tered intracerebroventricularly reverses the anorexic effect of C75, suggesting that C75 acts upstrea
37 pothesis that lPBN neurons contribute to the anorexic effect of central GLP-1R activation.
38 yet was entirely effective in preventing the anorexic effect of exogenously administered leptin (2 mg
39 e aversion to saccharin, suggesting that the anorexic effect of NAc core GLP-1 is not caused by malai
40                                         This anorexic effect of protein may contribute to the weight
41 subjects to control for the drug's potential anorexic effect.
42 not be established independent of the drug's anorexic effect.
43 rsely, cold TA caused resistance to leptin's anorexic effects but amplified its effects to raise BP a
44                      Cerebral insulin exerts anorexic effects in humans and animals.
45 lamic arcuate nucleus (ARH) in mediating the anorexic effects of a systemic interleukin-1 (IL-1) chal
46 cortin system is demonstrated to mediate the anorexic effects of both leptin and insulin.
47 ion of feeding behavior and in mediating the anorexic effects of C75.
48 ypothalamic melanocortin system mediates the anorexic effects of central insulin, as well as of lepti
49 y physiological responses that attenuate the anorexic effects of exogenous melanocortin agonists.
50   To investigate whether leptin enhances the anorexic effects of GLP-1, rats received either saline o
51       The arcuate nucleus (ARC) mediates the anorexic effects of leptin and expresses the long form (
52   These results demonstrate that the chronic anorexic effects of leptin are enhanced at TNZ, while it
53 wing high-fat diet feeding, and enhances the anorexic effects of semaglutide, in a sexually dimorphic
54 he neurobiological mechanisms underlying the anorexic effects of smoking would facilitate the develop
55 el anatomical substrate for their well known anorexic effects.
56  mice within a time window compatible to its anorexic effects.
57 nous formaldehyde, while also suppressing an anorexic endocrine signal.
58 n the women, healthy female adolescents, and anorexic female adolescents, respectively.
59 ence of manifest QT prolongation, adolescent anorexic females have impaired repolarization reserve in
60 ropeptide Y, was lower and expression of the anorexic gene, proopiomelanocortin, was higher.
61               Orexigenic hormone ghrelin and anorexic hormone obestatin are encoded by the same prepr
62 t this neural circuit may be disrupted in an anorexic-like condition.
63  small intestine, it causes the formation of anorexic lipid mediators, such as oleoylethanolamide, wh
64 s [PVN]), where it regulates the activity of anorexic neural circuits.
65                                              Anorexic patients experienced significant percentage inc
66 ither homosexual or bisexual, and 58% of the anorexic patients were identified as asexual.
67  bulimic probands compared with relatives of anorexic probands, and familial aggregation was independ
68 isorder was elevated only among relatives of anorexic probands, and there was evidence that these 2 d
69 oncology as activation of GFRAL mediates the anorexic response that is responsible for cancer anorexi
70           Conversely, fasting attenuated the anorexic response to GLP-1 or Ex4 treatment via a leptin
71 ts maintained on a high-fat (HF)-diet had no anorexic response to intracerebroventricular leptin.
72       However, fasted animals maintained the anorexic response to melanotan II, a melanocortin recept
73 d intake, consistent with an illness-induced anorexic response.
74 esioned to determine their role in mediating anorexic responses to gastric stimulation and in conveyi
75 ce, which, although reliably inducing strong anorexic responses, does not cause aversive reactions.
76 rphin and met-enkephalin, consistent with an anorexic role in energy homeostasis.
77 thalamic neurons respond to leptin to induce anorexic signaling.
78 the parabrachial nucleus (PBN) that transmit anorexic signals.
79 y in the BNST have also been associated with anorexic states in rodents.
80 eptin than WT animals and are insensitive to anorexic stimuli induced by leptin administration.
81 MCF-7IL-1 alpha cell-derived tumors were not anorexic suggesting only peripheral action of tumor-deri
82 symptoms alone groups together patients with anorexic symptoms who are high functioning and self-crit
83       Novel therapeutic approaches that help anorexics to better interpret or improve tolerance of af
84 tic choriomeningitis virus (LCMV) results in anorexic weight loss, mediated by T cells and gamma inte
85 S and infiltrating APC populations, and (iv) anorexic weight loss.
86 % of the non-hyperphagic cases (n = 23) were anorexic, with a low body-mass index and normal growth-h