1 subset of hypothalamic neurons are obese and
hyperphagic.
2 lower and more variable, but still regularly
hyperphagic.
3 ice carry leptin mutations and are obese and
hyperphagic.
4 In addition, mice lacking PYY are
hyperphagic and become obese.
5 Transgenic mice overexpressing Pmch are
hyperphagic and develop mild obesity.
6 Interestingly, mutant animals were
hyperphagic and exhibited higher food intake and reduced
7 These mice, as expected, are
hyperphagic and glucose intolerant.
8 GPR7-/- male mice were
hyperphagic and had decreased energy expenditure and loc
9 revealed that virally rescued DDfs mice are
hyperphagic and have modified meal structures compared w
10 The obese mutant mice were
hyperphagic and hyperleptinemic and exhibited reduced lo
11 Further, they are hypermetabolic,
hyperphagic and hyperthermic, all consistent with a brow
12 eatly attenuated diurnal feeding rhythm, are
hyperphagic and obese, and develop a metabolic syndrome
13 L(2.1)KOs are
hyperphagic and obese, whereas I(2.1)KOs are similar to
14 Both db/db and s/s animals are
hyperphagic and obese.
15 (OLETF) rats lack the CCK-1 receptor and are
hyperphagic and obese.
16 b/db mice, lepr(S1138) homozygotes (s/s) are
hyperphagic and obese.
17 c deletion of neuronal insulin receptors are
hyperphagic and obese.
18 n of mu opioid receptors (MOR) makes animals
hyperphagic and selectively increases their preference f
19 OP rats were
hyperphagic and showed a 20% weight gain over OR rats at
20 eek weight gain, is larger, heavier, fatter,
hyperphagic,
and diabetic relative to its randomly selec
21 ditional cilia mutant mice become obese, are
hyperphagic,
and have elevated levels of serum insulin,
22 he melanocortin 4 receptor (MC4R) are obese,
hyperphagic,
and hyperinsulinemic but have been reported
23 s with defective leptin receptors are obese,
hyperphagic,
and hyperinsulinemic.
24 itional knockout (CKO) mice were aggressive,
hyperphagic,
and obese.
25 Site-specific mutants exhibited
hyperphagic behavior and obesity but normal energy expen
26 opmental processes are still ongoing elicits
hyperphagic behavior and obesity in mice.
27 edial hypothalamus (VMH) of mice resulted in
hyperphagic behavior and obesity.
28 Nonetheless, we observed
hyperphagic behavior from increased consumption of the l
29 A similar effect may be contributory to the
hyperphagic behavioral phenotype of obese animal models
30 The mutant mice were not
hyperphagic but developed enlarged and steatotic liver.
31 AdPLA-deficient ob/ob mice remain
hyperphagic but lean, with increased energy expenditure,
32 These mice are
hyperphagic but weigh less than their wild-type litterma
33 edly suppressed serum leptin levels and were
hyperphagic,
but did not gain excess weight.
34 totally (Il18(-/-)) deficient in IL-18 were
hyperphagic by young adulthood, with null mutants then b
35 74% of the non-
hyperphagic cases (n = 23) were anorexic, with a low bod
36 Interestingly, despite being
hyperphagic,
Cav-1 null mice show overt resistance to di
37 These animals are obese,
hyperphagic,
cold intolerant, insulin resistant, and inf
38 hat NPY expression in the DMH during chronic
hyperphagic conditions plays important roles in feeding
39 ut is significantly increased during chronic
hyperphagic conditions such as lactation and diet-induce
40 Untreated diabetic rats were
hyperphagic,
consuming 40% more food (48 +/- 1 g/day; P
41 Phox2b Cre Lepr(flox/flox) mice were
hyperphagic,
displayed increased food intake after fasti
42 Animals treated with a
hyperphagic dose of ghrelin had greater levels of Fos ex
43 negative energy balance and the accompanying
hyperphagic drive are likely to be factors in the suppre
44 st report that diets high in fat inhibit the
hyperphagic effect of ghrelin; these findings indicate t
45 The multiple-day
hyperphagic effect of the melanocortin 3/4 receptor anta
46 Mapping by "Fos plume" methods confirmed the
hyperphagic effect to be anatomically localized to the a
47 its high caloric density, dietary fat has a
hyperphagic effect, in part as a result of its high pala
48 and kappa3 opioid receptors in mediating the
hyperphagic effects of glucoprivation.
49 rmal food intake and body weight, and become
hyperphagic following food deprivation.
50 ous Cep19-knockout mice were morbidly obese,
hyperphagic,
glucose intolerant, and insulin resistant.
51 use models and found that BBS-null mice were
hyperphagic,
had low locomotor activity, and had elevate
52 Data show that Rai1(+/-) mice are
hyperphagic,
have an impaired satiety response and have
53 rt here that THADA knockout flies are obese,
hyperphagic,
have reduced energy production, and are sen
54 erinsulinemic at the time of weaning, become
hyperphagic immediately after weaning, and exhibit impai
55 CTRP13 expression is increased in obese and
hyperphagic leptin-deficient mice, suggesting that it ma
56 cose, p50alpha/p55alpha knockout mice become
hyperphagic like their wild-type littermates.
57 rotect against insulin resistance in the GTG
hyperphagic model of rodent obesity.
58 In several
hyperphagic models, including lactation, in which hypoth
59 ere, we demonstrate that when expressed on a
hyperphagic ob/ob background, the P465L PPARgamma mutant
60 balance and reproduction-Crtc1(-/-) mice are
hyperphagic,
obese and infertile.
61 n LETO control animals are attenuated in the
hyperphagic,
obese OLETF rat.
62 spontaneous null mutation of the CCK1R, are
hyperphagic,
obese, and predisposed to type 2 diabetes.
63 tants that survived the neonatal period were
hyperphagic,
obese, diabetic, and infertile.
64 Using the
hyperphagic,
obese, Otsuka Long-Evans Tokushima Fatty (O
65 the sudden cessation of daily exercise in a
hyperphagic/
obese model activates a subgroup of precurso
66 Four-week-old,
hyperphagic/
obese Otsuka Long-Evans Tokushima Fatty rats
67 Sim1 haploinsufficiency in mice induces
hyperphagic obesity and developmental abnormalities of t
68 ied germ line Sim1 heterozygotes, displaying
hyperphagic obesity and increased length.
69 n of the PVN or its projections and that the
hyperphagic obesity in Sim1-deficient mice may be attrib
70 nerability to certain eating problems (e.g.,
hyperphagic obesity).
71 ism, mice hypomorphic for Rpgrip1l exhibited
hyperphagic obesity, as the result of diminished leptin
72 Among the canonical PWS phenotypes are
hyperphagic obesity, central hypogonadism, and low growt
73 ion of LepRb (Lepr(Nos1KO)) in mice produces
hyperphagic obesity, decreased energy expenditure and hy
74 Humans and mice deficient in PC1 display
hyperphagic obesity, hypogonadism, decreased GH, and hyp
75 1alpha, which stimulate PLC, leads to severe
hyperphagic obesity, increased linear growth, and inacti
76 truncated long Bdnf 3' UTR developed severe
hyperphagic obesity, which was completely reversed by vi
77 levels of neuropeptides, resulting in severe
hyperphagic obesity.
78 amma of the PI3K complex, and attenuates the
hyperphagic obesity.
79 NS deficiency of Sim1 is sufficient to cause
hyperphagic obesity.
80 eems to result in a unique human syndrome of
hyperphagic obesity.
81 Also, we found that OP rats were
hyperphagic on a regular chow diet and gained more weigh
82 Hyperphagic Otsuka Long-Evans Tokushima fatty rats fed a
83 uggesting that beneficial effects of rhGH in
hyperphagic patients might be achieved without glutamine
84 upregulation of NPY mRNA consistent with the
hyperphagic phenotype and suggests a critical role of Sn
85 Hyperphagic POMC-deficient mice were more sensitive than
86 libitum access to food and manifest a normal
hyperphagic response after fasting, suggesting that othe
87 Conversely, the
hyperphagic response elicited by central glucoprivation
88 resistant to obesity and have an attenuated
hyperphagic response to ghrelin.
89 resistant to obesity and have an attenuated
hyperphagic response to ghrelin.
90 high-fat-diet (HFD)-fed rats and blocked the
hyperphagic response to oral TZD treatment.
91 treatment is necessary for expression of the
hyperphagic response to SHU9119, or alternatively, wheth
92 Here, we demonstrate a
hyperphagic response to stimulation of GHS-R in the caud
93 To investigate NPY's role in the
hyperphagic response to uncontrolled diabetes, streptozo
94 ot POMC neurons, was sufficient to cause the
hyperphagic response.
95 led diabetes, Npy(--/--) mice exhibit intact
hyperphagic responses to fasting.
96 ostweaning feeding and growth, and disrupted
hyperphagic responses to NPY.
97 eased food intake in wild-type mice, but the
hyperphagic responses were blunted in D3R-/- mice.
98 DIO rats were
hyperphagic selectively at the dark cycle onset, showing
99 ntal criteria by which the novel syndrome of
hyperphagic short stature may be recognised clinically.
100 , ingest excess dietary fat that can produce
hyperphagic steatorrhea.
101 ency spontaneously resolved only in formerly
hyperphagic subjects.
102 Although DOR-KO mice were
hyperphagic,
they showed higher energy expenditure (P<0.
103 resses; we show that Gfral knockout mice are
hyperphagic under stressed conditions and are resistant
104 Caloric matching of
hyperphagic VMHL rats to SL controls did not reduce thei
105 Insulin-deficient diabetic rats are markedly
hyperphagic when fed a high-carbohydrate (HC) diet, but
106 Surprisingly, Mch1r-/- mice are
hyperphagic when maintained on regular chow, and their l