ライフサイエンスコーパス: peptide YY

1 ibitory peptide, glucagon-like peptides, and peptide YY).

2 ctant protein-1, pancreatic polypeptide, and peptide YY.

3 ng receptors specific for neuropeptide Y and peptide YY.

4 ically after birth with rare coexpression of peptide YY.

5 eptin and insulin, and lactalbumin increased peptide YY.

6 appetite are linked to acetate, lactate and peptide YY.

7 genous YR agonists pancreatic polypeptide or peptide YY.

8 sponded to all the substances tested, except peptide YY.

9 prefers pancreatic polypeptide over NPY and peptide YY.

10 pelin, endocannabinoids, leptin, insulin and peptide YY.

11 ones such as GIP, ghrelin, oxyntomodulin and peptide YY.

12 sulinotropic peptide, as well as ghrelin and peptide YY.

13 -h levels of the satiety hormones leptin and peptide-YY.

14 ed to examine the feasibility of using [125I]peptide YY ([125I]PYY) to measure neuropeptide Y (NPY) Y

15 rticular, the discovery that the gut hormone peptide YY 3-36 (PYY3-36) reduced feeding in obese roden

16 eripheral injection of the satiety-signaling peptide YY 3-36 increased 5-HT turnover in the LH and am

17 effects of peripheral administration of both peptide YY(3-36) (PYY(3-36)) and glucagon-like peptide-1

18 Peptide YY(3-36) (PYY(3-36)) is released by endocrine ce

19 Peptide YY(3-36) (PYY(3-36)), a Y2 receptor agonist, and

20 Peptide YY(3-36) (PYY(3-36)), a Y2R agonist, is released

21 esponse to neuropeptide Y (NPY), the related peptide YY(3-36) (PYY(3-36)), and pancreatic polypeptide

22 s, while glucagon-like peptide-1 (GLP-1) and peptide YY(3-36) [PYY(3-36)] inhibit, food intake and ga

23 Despite the anorectic effects of exogenous peptide YY(3-36) following intraperitoneal administratio

24 Anorectic activity of peptide YY(3-36) has been confirmed in a number of anima

25 e, energy expenditure, and responsiveness to peptide YY(3-36).

26 hotoflow reactor on a recombinantly prepared peptide YY analogue and a GLP-1/amylin co-agonist precur

27 Plasma peptide YY and ghrelin (enzyme-linked immunosorbent assa

28 To compare the circulating plasma levels of peptide YY and ghrelin in control subjects and in critic

29 pathophysiologic role of the enterohormones peptide YY and ghrelin is supported by preclinical data.

30 r extent and weight gain via enteroendocrine peptide YY and glucagon pathways to a lesser extent.

31 gion revealed tumor cells producing not only peptide YY and glucagon, but also neurotensin, cholecyst

32 of pancreatic secretion by the gut hormones peptide YY and pancreatic polypeptide.

33 weight-loss, enhances lipid-induced BPP and peptide YY and reduces food intake, suggesting that ener

34 en, and lipid-stimulated cholecystokinin and peptide YY and the desire to eat were greater in both gr

35 cholesterol, triglycerides, leptin, ghrelin, peptide YY, and adiponectin.

36 in, and incretins; and increases in ghrelin, peptide YY, and adiponectin.

37 cretion of insulin, glucagon-like peptide 1, peptide YY, and cholecystokinin after RYGB, whereas leve

38 lucose and plasma concentrations of insulin, peptide YY, and ghrelin were assayed every 30 minutes.

39 ostprandial concentrations of total ghrelin, peptide YY, and glucagon-like peptide-1, leptin, adipone

40 e by consistent changes in glucose, insulin, peptide YY, and glucagon-like peptide-1.

41 agon-like peptide(7-36), acyl-ghrelin, total peptide YY, and leptin.

42 least three endogenous peptides, i.e., NPY, peptide YY, and pancreatic polypeptide (PP), the latter

43 lecystokinin, vasoactive intestinal peptide, peptide YY, and somatostatin.

44 ipid-induced basal pyloric pressures (BPPs), peptide YY, and the desire to eat were greater (P < 0.05

45 es in absolute concentrations of ghrelin and peptide YY between the 2 HPWL diets, although the respon

46 oncentrations of glucagon-like peptide-2 and peptide YY, but not gastrin, increased significantly bet

47 ion-based cell lineage trace to determine if peptide YY cells were progenitors for gastrointestinal e

48 Peptide YY(+) cells gave rise to all L-type enteroendocr

49 creatic alpha and rare beta cells arose from peptide YY(+) cells, suggesting that most beta cells and

50 dies to perform a meta-analysis for ghrelin, peptide YY, cholecystokinin, insulin, and pancreatic pol

51 Peptide YY coexpression continued in a significant fract

52 P, reduced daily ghrelin and increased daily peptide YY concentrations compared with BS.

53 The plasma levels of peptide YY did not differ between patients (6.4 [0-18.1]

54 te hormones (focusing on ghrelin, leptin and peptide-YY), energy expenditure, food intake and choice,

55 educed numbers of somatostatin (D-cells) and peptide YY-expressing cells (L-cells).

56 atic polypeptide (PP) cells, indicating that peptide YY expression was not required for terminal diff

57 Compounds also displaced radiolabeled peptide YY from the Y2R with high affinity (K(i) values

58 kinins A and B, neurotensin, neuropeptide Y, peptide YY, gastrin-releasing peptide, somatostatin, and

59 40 large T antigen under the control of the peptide YY gene 5' flanking region revealed tumor cells

60 ions suggest that targeted disruption of the peptide YY gene does not perturb terminal endocrine cell

61 created mice with a targeted deletion of the peptide YY gene.

62 gon-like peptide 1 (GLP-1), cholecystokinin, peptide YY, ghrelin, blood glucose, serum insulin, and a

63 jority of alpha cells are not descendants of peptide YY(+)/glucagon-positive/insulin-positive cells t

64 e were no significant changes in circulating peptide YY, glucagon-like peptide 1, oxyntomodulin, panc

65 appetite indices ([leptin], [acyl ghrelin], [peptide YY], [glucagon-like peptide-1]); and gut microbi

66 tivity is NPY > or = [Leu31,Pro34]NPY > or = peptide YY > NPY2-36 > NPY13-36 > NPY18-36 > or = NPY26-

67 cy: human PP = bovine PP > or = human [Pro34]peptide YY > rat PP > human peptide YY = human neuropept

68 In the colon, peptide YY has been frequently identified in glucagon-ex

69 r = human [Pro34]peptide YY > rat PP > human peptide YY = human neuropeptide Y.

70 In order to better understand the role of peptide YY in energy homeostasis and development, we cre

71 fy an unappreciated role for the EEC hormone peptide YY in regulating ion-coupled absorption of gluco

72 n, cholecystokinin, glucagon-like peptide 1, peptide YY, insulin, glucagon, blood glucose, appetite p

73 These data suggest that peptide YY is a key regulator of macronutrient absorptio

74 The gastrointestinal hormone peptide YY is a potent inhibitor of food intake and is e

75 These studies indicate that expression of peptide YY is an early event in colonic endocrine differ

76 We have previously shown that peptide YY is coexpressed in all four islet cell types i

77 The hormone peptide YY is produced by endocrine cells in the pancrea

78 We find that peptide YY is required in the small intestine to maintai

79 cells (producing glucagon-like peptide 1 and peptide YY), long-chain fatty acid receptor FFAR1 was hi

80 ne concentrations of ghrelin (large effect), peptide YY (medium effect), and cholecystokinin (medium

81 Preproglucagon, somatostatin, and peptide YY messenger RNA (mRNA) levels also were reduced

82 Plasma peptide YY or ghrelin did not differ between fasting and

83 l-ghrelin, but no differences were found for peptide YY or leptin.

84 Similar effects were observed using peptide YY or the NPY analog [Leu31, Pro34]NPY.

85 relin, glucagon, glucagon-like peptide 1 and peptide YY, or pyloric and duodenal pressures.

86 nin, glucagon-like peptide 1, oxyntomodulin, peptide YY, orexin A and ghrelin.

87 n concentrations of insulin (P = 0.0024) and peptide YY (P < 0.0001), not seen with continuous feedin

88 d between the temporal profile of ghrelin or peptide YY plasma concentration with bedside functional

89 ple enteroendocrine lineages were related to peptide YY-producing cells.

90 when they first appear, suggesting a common peptide YY-producing progenitor.

91 that were glucagon-like peptide-1 (GLP-1)(+)/Peptide YY (PYY(-)) in the ileum and colon and GLP-1(-)/

92 We have found that peptide YY (PYY(1-36)), but not endocrine PYY(3-36), act

93 inhibitory polypeptide (GIP) (P = 0.00004), peptide YY (PYY) (P = 0.01), and beta-hydroxybutyrate (P

94 dependently glucagon-like peptide-1 (GLP-1), peptide YY (PYY) 3-36, and glucagon; MHP produced 10%, 7

95 7 containing glucagon fused to a fragment of peptide YY (PYY) acted as a triagonist at the GluR, GLP-

96 okinin, glucagon-like peptide 1 (GLP-1), and peptide YY (PYY) analysis.

97 Peptide YY (PYY) and [Leu31,Pro34]NPY did not mimic the

98 tion of Y2 receptor (Y2R) agonism-engaged by peptide YY (PYY) and belonging to the structurally diver

99 ition, and assessed whether the gut hormones peptide YY (PYY) and cholecystokinin (CCK) play a role i

100 at release serotonin or L-cells that release peptide YY (PYY) and glucagon-like peptide 1 (GLP-1), bo

101 rted that intracisternal (i.c.) injection of peptide YY (PYY) and low doses of thyrotropin-releasing

102 Peptide YY (PYY) and neuropeptide Y (NPY) are peptides t

103 Peptide YY (PYY) and neuropeptide Y (NPY) are regulatory

104 Peptide YY (PYY) and neurotensin responses resembled tho

105 hat the other two natural ligands of Y(5) R, peptide YY (PYY) and pancreatic polypeptide (PP) dock to

106 Peptide YY (PYY) and pancreatic polypeptide (PPY) are me

107 Ghrelin and peptide YY (PYY) are gut hormones involved in appetite r

108 Although the role of peptide YY (PYY) as a regulator of energy homeostasis wa

109 o maternal leptin, adiponectin, ghrelin, and peptide YY (PYY) at 3 years postpartum among 570 partici

110 Peptide YY (PYY) belongs to a family of peptides includi

111 ncreased glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) compared with all other treatments (Tuk

112 es increased fasting and postprandial plasma peptide YY (PYY) concentrations, and attenuated fasting

113 Total plasma peptide YY (PYY) excursions during OFTT were 3-fold larg

114 tides (PPs) such as neuropeptide Y (NPY) and peptide YY (PYY) exert profound, vagally mediated effect

115 ediator of this response is not established, peptide YY (PYY) has been considered the most likely pep

116 Peptide YY (PYY) has been implicated in the control of f

117 discovered the presence of the gut satiation peptide YY (PYY) in saliva of mice and humans and define

118 ut models and the specific reconstitution of peptide YY (PYY) in saliva using gene therapy protocols

119 Central injection of peptide YY (PYY) in sated rats produces the most powerfu

120 hormones glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) in vitro from mouse and human colons.

121 The cellular target for peptide YY (PYY) inhibition of gastric acid secretion is

122 Peptide YY (PYY) is a gut hormone that inhibits secretio

123 Peptide YY (PYY) is an important gut hormone synthesized

124 In the pancreas, peptide YY (PYY) is expressed by a subpopulation of nonb

125 The gastrointestinal-derived hormone peptide YY (PYY) is released from intestinal L-cells pos

126 Peptide YY (PYY) levels are reported to be decreased in

127 roducing glucagon-like peptide 1 (GLP-1) and peptide YY (PYY) may be a target of AVP and contribute t

128 tions in glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) only following meals with very high lip

129 ibited the cardiovascular changes induced by peptide YY (PYY) or CCh microinjection into the PHN.

130 g approaches, three new neuropeptide Y (NPY)/peptide YY (PYY) receptors have been described in rodent

131 prandial glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) responses (time x treatment, P = 0.001

132 lucose-dependent insulinotropic peptide, and peptide YY (PYY) were measured.

133 release glucagon-like peptide 1 (GLP-1) and peptide YY (PYY) when activated by short-chain fatty aci

134 Peptide YY (PYY), a member of the NPY superfamily of pep

135 Fasting leptin, peptide YY (PYY), and ghrelin concentrations were obtain

136 dial plasma glucagon-like peptide 1 (GLP-1), peptide YY (PYY), and ghrelin immunoreactivity were meas

137 in, leptin, glucagon-like peptide 1 (GLP-1), peptide YY (PYY), and ghrelin were measured at baseline

138 ), insulin, glucagon-like peptide 1 (GLP-1), peptide YY (PYY), and ghrelin.

139 equent dieting, and GIBP surgery on ghrelin, peptide YY (PYY), and glucagon-like peptide-1 (GLP-1).

140 , including glucagon-like peptide-1 (GLP-1), peptide YY (PYY), and insulin, in serum.

141 ic polypeptide (GIP), cholecystokinin (CCK), peptide YY (PYY), and neurotensin (NT)] and on glucose,

142 ptides, which includes neuropeptide Y (NPY), peptide YY (PYY), and pancreatic polypeptide (PP), are f

143 family that includes the endocrine peptides, peptide YY (PYY), and pancreatic polypeptide (PP).

144 such as glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), from enteroendocrine cells in the smal

145 postprandial rise in plasma cholecystokinin, peptide YY (PYY), glucagon-like peptide 1 (GLP-1), and g

146 vations were not related to changes in blood peptide YY (PYY), glucagon-like peptide 1 (GLP-1), gluco

147 nd blood samples for analyses of plasma TAG, peptide YY (PYY), glucagon-like peptide-1 (GLP-1), ghrel

148 al-stimulated responses of insulin, ghrelin, peptide YY (PYY), glucagon-like-peptide-1 (GLP-1), and p

149 rexigenic actions of neuropeptide Y (NPY) or peptide YY (PYY), indicating that these neuromodulators

150 In addition, appetite and plasma GLP-1, peptide YY (PYY), insulin, glucagon, and blood glucose c

151 dy mass index (BMI), % body fat (BF), plasma peptide YY (PYY), leptin, ghrelin, and resistin for all

152 been proposed based on preferences for NPY, peptide YY (PYY), or pancreatic polypeptide (PP).

153 (NEUROG3), chromogranin A (CgA), serotonin, peptide YY (PYY), oxyntomodulin (enteroglucagon), pancre

154 d 2 (GCN2), glucagon-like peptide 1 (GLP-1), peptide YY (PYY), serotonin, and insulin.

155 The development of peptide YY (PYY)-based approaches to treat obesity are n

156 way in which two enteroendocrine cell types, peptide YY (PYY)-expressing L cells and serotonergic EC

157 6)-stimulates Toll-like receptor 5 (TLR5) in peptide YY (PYY)-labelled colonic neuropod cells.

158 lunted response to central administration of peptide YY (PYY).

159 and the Y2 receptor agonist NPY 13-36 and by peptide YY (PYY).

160 hormones amylin, cholecystokinin (CCK), and peptide YY (PYY).

161 ncluding glucagon-like peptide 1 (GLP-1) and peptide YY (PYY).

162 The family of mammalian neuropeptide Y (NPY)/peptide YY (PYY)/pancreatic polypeptide (PP) receptors c

163 Exogenous NPY [as well as its homolog, peptide YY (PYY)] augmented GDNF-dependent budding in th

164 Peptide-YY (PYY) is secreted from endocrine L-cells of t

165 ctive glucagon-like peptide 1 [GLP-1], total peptide YY [PYY], cholecystokinin and insulin), and subj

166 rectic response to the acute satiety factors peptide YY (PYY3-36) and cholecystokinin (CCK) and the l

167 in concentrations and significantly enhanced peptide YY release.

168 epithelial layers, functional Y1 and Y1T361* peptide YY responses became more transient as the agonis

169 holecystokinin, glucagon-like peptide 1, and peptide YY responses compared with placebo.

170 intraperitoneal administration, mice lacking peptide YY showed normal growth, food intake, energy exp

171 hormones such as glucagon-like peptide 1 and peptide YY that regulate food absorption, insulin secret

172 levels of gastric inhibitory polypeptide and peptide YY that were induced following DSS treatment.

173 BP1c, whereas AMPK induced the expression of peptide YY, the early endocrine pancreas marker.

174 Administration of peptide YY to EEC-deficient mice restores normal electro

175 Application of NPY and peptide YY to SCN slices at circadian time (CT) 7.5-8.5

176 gastrin and somatostatin first appeared and peptide YY was coexpressed in each cell type at this tim

177 ntiation in nontransgenic mice revealed that peptide YY was the first hormone to appear during develo

178 changes in serum glucagon-like peptide 1 and peptide YY were 106.6% +/- 208.5 and 17.8% +/- 54.8 at 1

179 and satiety hormones ghrelin and leptin, and peptide YY, which signaled excess energy stores.

180 e cells developed normally in the absence of peptide YY with the exception of pancreatic polypeptide

181 ng PDX1 and the nonclassical hormone markers peptide YY (YY) and islet amyloid polypeptide (IAPP) in