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1 hepatic steatosis yet are not hyperactive or hypophagic.
2                             Reduction in the hypophagic action of 5-HT, possibly acting at 5-HT(1A),
3 type-1 (CB1) receptor antagonists are potent hypophagic agents, but the sites where this acute action
4 tite were also tolerant to three other known hypophagic agents, lipopolysaccharide (LPS), muramyl dip
5          Dopamine-deficient (DD) mice become hypophagic and die of starvation by 3 to 4 weeks of age
6             These mice become hypoactive and hypophagic and die of starvation by 4 weeks of age.
7 cy than wild-type littermates, despite being hypophagic and maintaining normal metabolic rates.
8 n normal but gradually become hypoactive and hypophagic, and die at 3 weeks of age.
9      Pmch-deficient (Pmch-/-) mice are lean, hypophagic, and have an increased metabolic rate.
10                                  Given their hypophagic capacity, PPG neurons might be an attractive
11        Furthermore, orexin knockout mice are hypophagic compared with weight and age-matched litterma
12 he brain histamine system to fully exert its hypophagic effect and that the oxytocin neuron-rich nucl
13     To dissect the mechanisms underlying the hypophagic effect of CB1 receptor blockade, we combined
14 ition of these neurons may contribute to the hypophagic effect of estrogen.
15 ine receptor agonism in the mPFC blocked the hypophagic effect of intra-VTA amylin, and VTA amylin in
16 revent the orexigenic action of MCH, and the hypophagic effect of MCH silencing was maintained after
17  body weight, i.p.) blocked the enterostatin hypophagic effects in these KO mice.
18 deficient, or DD, mice) are resistant to the hypophagic effects of a moderate dose of AMPH (2 microg/
19 lly, blockade of LDTg GLP-1Rs attenuates the hypophagic effects of a systemic GLP-1R agonist.
20  MC4-R, respectively), which may mediate the hypophagic effects of alpha-melanocyte-stimulating hormo
21 med to examine the mechanisms underlying the hypophagic effects of amylin receptor activation in the
22 hypertensive, hyperphagic, less sensitive to hypophagic effects of exendin-4, and expended more energ
23 tly increases food intake and attenuates the hypophagic effects of gastric distension.
24 1R activation contributes to hypothermic and hypophagic effects of hindbrain CART, whereas CART-induc
25 of PYY-Y2 and CCK-1 receptors attenuated the hypophagic effects of pectin, and CCK-1 receptor blockad
26 c brain neurons is dispensable for the acute hypophagic effects of rimonabant.
27 t that the PBN critically contributes to the hypophagic effects of systemically delivered GLP-1R agon
28                                        These hypophagic effects were based on reduced meal size, and
29 ynthesis within MC4R neurons weigh less, are hypophagic, exhibit increased energy expenditure, and ar
30 ncentrating hormone (MCH)-deficient mice are hypophagic, lean, and do not develop hepatosteatosis whe
31       We identified that PRMT2(-/-) mice are hypophagic, lean, and have significantly reduced serum l
32 it growth retardation and the adult mice are hypophagic, lean, and resistant to high-fat diet-induced
33 c beta cells and hypothalamus produced lean, hypophagic mice with increased physical activity and imp
34  increased by up to a factor of 4 during the hypophagic period, when the ingestion rate was greatly r
35 ion of MCH in the hypothalamus with the lean hypophagic phenotype coupled with increased resting meta
36 al loss of AgRP/NPY neurons leads to a lean, hypophagic phenotype.
37 n the amygdala was sufficient to restore the hypophagic property of D-Fen.
38                                          The hypophagic response of Nckx4 knock-out mice is accompani
39 e hypothesized that it may contribute to the hypophagic response to overfeeding.
40  similar home cage food intake and a similar hypophagic response to systemic Exendin-4, a GLP1R agoni
41 ity to leptin and confirmed reports that the hypophagic response to third ventricular (i3vt) leptin i
42  found that, as for leptin, ADX enhanced the hypophagic response via a glucocorticoid-dependent mecha
43 P neurons, and reduces both anxiety-like and hypophagic responses to acute stress.
44 coordinating endocrine and behavioral (i.e., hypophagic) responses to stress.
45  These results indicate that CNS MCs mediate hypophagic signaling in response to involuntary overfeed
46                       Overweight animals are hypophagic, suggesting that IGFII affects fat metabolism