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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
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
14 f the central IL-1 and IL-6 in mediating the anorexic and body weight loss effects of GLP-1 receptor
19 n situ hybridization and hormone analyses of anorexic and paired food-restricted rats revealed two di
20 verexpression, which reduces body weight via anorexic and thermogenic actions, induces triglyceride d
22 of whom 62 (46%) were bulimic, 30 (22%) were anorexic, and 43 (32%) met criteria for an eating disord
28 cology of ghrelin, ghrelin-null mice are not anorexic dwarfs; their size, growth rate, food intake, b
30 tered intracerebroventricularly reverses the anorexic effect of C75, suggesting that C75 acts upstrea
32 yet was entirely effective in preventing the anorexic effect of exogenously administered leptin (2 mg
33 e aversion to saccharin, suggesting that the anorexic effect of NAc core GLP-1 is not caused by malai
37 rsely, cold TA caused resistance to leptin's anorexic effects but amplified its effects to raise BP a
39 lamic arcuate nucleus (ARH) in mediating the anorexic effects of a systemic interleukin-1 (IL-1) chal
42 ypothalamic melanocortin system mediates the anorexic effects of central insulin, as well as of lepti
43 y physiological responses that attenuate the anorexic effects of exogenous melanocortin agonists.
44 To investigate whether leptin enhances the anorexic effects of GLP-1, rats received either saline o
46 These results demonstrate that the chronic anorexic effects of leptin are enhanced at TNZ, while it
47 he neurobiological mechanisms underlying the anorexic effects of smoking would facilitate the develop
51 ence of manifest QT prolongation, adolescent anorexic females have impaired repolarization reserve in
55 small intestine, it causes the formation of anorexic lipid mediators, such as oleoylethanolamide, wh
58 bulimic probands compared with relatives of anorexic probands, and familial aggregation was independ
59 isorder was elevated only among relatives of anorexic probands, and there was evidence that these 2 d
61 ts maintained on a high-fat (HF)-diet had no anorexic response to intracerebroventricular leptin.
64 esioned to determine their role in mediating anorexic responses to gastric stimulation and in conveyi
65 ce, which, although reliably inducing strong anorexic responses, does not cause aversive reactions.
69 MCF-7IL-1 alpha cell-derived tumors were not anorexic suggesting only peripheral action of tumor-deri
70 symptoms alone groups together patients with anorexic symptoms who are high functioning and self-crit
71 tic choriomeningitis virus (LCMV) results in anorexic weight loss, mediated by T cells and gamma inte
73 % of the non-hyperphagic cases (n = 23) were anorexic, with a low body-mass index and normal growth-h
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