1 ice carry leptin mutations and are obese and
hyperphagic.
2 lower and more variable, but still regularly
hyperphagic.
3 subset of hypothalamic neurons 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 and categories of ED (restrictive, bulimic,
hyperphagic,
and other types of EDs) were determined wit
26 Site-specific mutants exhibited
hyperphagic behavior and obesity but normal energy expen
27 opmental processes are still ongoing elicits
hyperphagic behavior and obesity in mice.
28 edial hypothalamus (VMH) of mice resulted in
hyperphagic behavior and obesity.
29 Nonetheless, we observed
hyperphagic behavior from increased consumption of the l
30 A similar effect may be contributory to the
hyperphagic behavioral phenotype of obese animal models
31 Thus,
hyperphagic behaviors are captured by the HQ-CT for most
32 interventional studies to assess changes in
hyperphagic behaviors in individuals with Prader-Willi s
33 ation reduced the frequency and intensity of
hyperphagic behaviors measured by HQ-CT.
34 The mutant mice were not
hyperphagic but developed enlarged and steatotic liver.
35 AdPLA-deficient ob/ob mice remain
hyperphagic but lean, with increased energy expenditure,
36 These mice are
hyperphagic but weigh less than their wild-type litterma
37 edly suppressed serum leptin levels and were
hyperphagic,
but did not gain excess weight.
38 totally (Il18(-/-)) deficient in IL-18 were
hyperphagic by young adulthood, with null mutants then b
39 74% of the non-
hyperphagic cases (n = 23) were anorexic, with a low bod
40 Interestingly, despite being
hyperphagic,
Cav-1 null mice show overt resistance to di
41 These animals are obese,
hyperphagic,
cold intolerant, insulin resistant, and inf
42 hat NPY expression in the DMH during chronic
hyperphagic conditions plays important roles in feeding
43 ut is significantly increased during chronic
hyperphagic conditions such as lactation and diet-induce
44 Untreated diabetic rats were
hyperphagic,
consuming 40% more food (48 +/- 1 g/day; P
45 rring in leptin receptor-deficient obese and
hyperphagic db/db mice.
46 disorders (OR: 4.38; 95% CI: 3.66, 5.23) and
hyperphagic disorders (OR: 2.91; 95% CI: 2.56, 3.31).
47 Phox2b Cre Lepr(flox/flox) mice were
hyperphagic,
displayed increased food intake after fasti
48 Animals treated with a
hyperphagic dose of ghrelin had greater levels of Fos ex
49 negative energy balance and the accompanying
hyperphagic drive are likely to be factors in the suppre
50 st report that diets high in fat inhibit the
hyperphagic effect of ghrelin; these findings indicate t
51 The multiple-day
hyperphagic effect of the melanocortin 3/4 receptor anta
52 Mapping by "Fos plume" methods confirmed the
hyperphagic effect to be anatomically localized to the a
53 its high caloric density, dietary fat has a
hyperphagic effect, in part as a result of its high pala
54 aling that VAN signaling is required for the
hyperphagic effects of ghrelin administered at dark onse
55 and kappa3 opioid receptors in mediating the
hyperphagic effects of glucoprivation.
56 rmal food intake and body weight, and become
hyperphagic following food deprivation.
57 ous Cep19-knockout mice were morbidly obese,
hyperphagic,
glucose intolerant, and insulin resistant.
58 use models and found that BBS-null mice were
hyperphagic,
had low locomotor activity, and had elevate
59 Data show that Rai1(+/-) mice are
hyperphagic,
have an impaired satiety response and have
60 rt here that THADA knockout flies are obese,
hyperphagic,
have reduced energy production, and are sen
61 erinsulinemic at the time of weaning, become
hyperphagic immediately after weaning, and exhibit impai
62 CTRP13 expression is increased in obese and
hyperphagic leptin-deficient mice, suggesting that it ma
63 found that the SHRSP rats were hypertensive,
hyperphagic,
less sensitive to hypophagic effects of exe
64 cose, p50alpha/p55alpha knockout mice become
hyperphagic like their wild-type littermates.
65 on in chow-fed but not high-fat (HF)-induced
hyperphagic male rats.
66 rotect against insulin resistance in the GTG
hyperphagic model of rodent obesity.
67 In several
hyperphagic models, including lactation, in which hypoth
68 ere, we demonstrate that when expressed on a
hyperphagic ob/ob background, the P465L PPARgamma mutant
69 ist, hexarelin, improved the metabolism in a
hyperphagic obese mouse model.
70 balance and reproduction-Crtc1(-/-) mice are
hyperphagic,
obese and infertile.
71 n LETO control animals are attenuated in the
hyperphagic,
obese OLETF rat.
72 spontaneous null mutation of the CCK1R, are
hyperphagic,
obese, and predisposed to type 2 diabetes.
73 tants that survived the neonatal period were
hyperphagic,
obese, diabetic, and infertile.
74 Using the
hyperphagic,
obese, Otsuka Long-Evans Tokushima Fatty (O
75 the sudden cessation of daily exercise in a
hyperphagic/
obese model activates a subgroup of precurso
76 Four-week-old,
hyperphagic/
obese Otsuka Long-Evans Tokushima Fatty rats
77 Sim1 haploinsufficiency in mice induces
hyperphagic obesity and developmental abnormalities of t
78 ied germ line Sim1 heterozygotes, displaying
hyperphagic obesity and increased length.
79 n of the PVN or its projections and that the
hyperphagic obesity in Sim1-deficient mice may be attrib
80 ranscriptional dysregulation associated with
hyperphagic obesity of adolescent onset with variable ND
81 Ablating Lepr from LepRbGlp1r cells provoked
hyperphagic obesity without impairing energy expenditure
82 nerability to certain eating problems (e.g.,
hyperphagic obesity).
83 ism, mice hypomorphic for Rpgrip1l exhibited
hyperphagic obesity, as the result of diminished leptin
84 Among the canonical PWS phenotypes are
hyperphagic obesity, central hypogonadism, and low growt
85 ion of LepRb (Lepr(Nos1KO)) in mice produces
hyperphagic obesity, decreased energy expenditure and hy
86 MRAP2 variants are pathogenic for monogenic
hyperphagic obesity, hyperglycemia and hypertension.
87 Humans and mice deficient in PC1 display
hyperphagic obesity, hypogonadism, decreased GH, and hyp
88 1alpha, which stimulate PLC, leads to severe
hyperphagic obesity, increased linear growth, and inacti
89 truncated long Bdnf 3' UTR developed severe
hyperphagic obesity, which was completely reversed by vi
90 ntricular hypothalamus (PVH) leads to severe
hyperphagic obesity.
91 f the primary cilium and is characterized by
hyperphagic obesity.
92 levels of neuropeptides, resulting in severe
hyperphagic obesity.
93 amma of the PI3K complex, and attenuates the
hyperphagic obesity.
94 NS deficiency of Sim1 is sufficient to cause
hyperphagic obesity.
95 eems to result in a unique human syndrome of
hyperphagic obesity.
96 Also, we found that OP rats were
hyperphagic on a regular chow diet and gained more weigh
97 Hyperphagic Otsuka Long-Evans Tokushima fatty rats fed a
98 uggesting that beneficial effects of rhGH in
hyperphagic patients might be achieved without glutamine
99 upregulation of NPY mRNA consistent with the
hyperphagic phenotype and suggests a critical role of Sn
100 Hyperphagic POMC-deficient mice were more sensitive than
101 libitum access to food and manifest a normal
hyperphagic response after fasting, suggesting that othe
102 us application of N/OFQ further elevated the
hyperphagic response and increased meal size during the
103 Conversely, the
hyperphagic response elicited by central glucoprivation
104 nexpectedly caused a marked reduction in the
hyperphagic response of ZSF1 obese animals.
105 cally important role for AgRP neurons in the
hyperphagic response to cold exposure.
106 resistant to obesity and have an attenuated
hyperphagic response to ghrelin.
107 AMPK inhibition occluded the amplified
hyperphagic response to glucocorticoids in FAAH A/A mice
108 high-fat-diet (HFD)-fed rats and blocked the
hyperphagic response to oral TZD treatment.
109 treatment is necessary for expression of the
hyperphagic response to SHU9119, or alternatively, wheth
110 Here, we demonstrate a
hyperphagic response to stimulation of GHS-R in the caud
111 To investigate NPY's role in the
hyperphagic response to uncontrolled diabetes, streptozo
112 A
hyperphagic response was also seen in Nnat(+/-p) mice in
113 ot POMC neurons, was sufficient to cause the
hyperphagic response.
114 led diabetes, Npy(--/--) mice exhibit intact
hyperphagic responses to fasting.
115 ostweaning feeding and growth, and disrupted
hyperphagic responses to NPY.
116 eased food intake in wild-type mice, but the
hyperphagic responses were blunted in D3R-/- mice.
117 DIO rats were
hyperphagic selectively at the dark cycle onset, showing
118 ntal criteria by which the novel syndrome of
hyperphagic short stature may be recognised clinically.
119 , ingest excess dietary fat that can produce
hyperphagic steatorrhea.
120 ency spontaneously resolved only in formerly
hyperphagic subjects.
121 Although DOR-KO mice were
hyperphagic,
they showed higher energy expenditure (P<0.
122 resses; we show that Gfral knockout mice are
hyperphagic under stressed conditions and are resistant
123 Caloric matching of
hyperphagic VMHL rats to SL controls did not reduce thei
124 Because ob mice are
hyperphagic,
we hypothesized that activating PPP1R17 neu
125 Insulin-deficient diabetic rats are markedly
hyperphagic when fed a high-carbohydrate (HC) diet, but
126 Surprisingly, Mch1r-/- mice are
hyperphagic when maintained on regular chow, and their l
127 Here, using two pre-clinical CKM models, the
hyperphagic ZSF1 obese rat and the uninephrectomized SDT
128 Leptin-deficient
hyperphagic Zucker (fa/fa) rats were modeled to test the