ライフサイエンスコーパス: peptide YY

1 ng receptors specific for neuropeptide Y and peptide YY.

2 ically after birth with rare coexpression of peptide YY.

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

4 eptin and insulin, and lactalbumin increased peptide YY.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

39 Peptide YY coexpression continued in a significant fract

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

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

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

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

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

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

46 40 large T antigen under the control of the peptide YY gene 5' flanking region revealed tumor cells

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 Peptide YY (PYY) and neurotensin responses resembled tho

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

127 in concentrations and significantly enhanced peptide YY release.

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

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

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

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

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

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

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

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

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

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

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