ライフサイエンスコーパス: GLP-2

1 IL-6 mirrored the time course of GLP-2.

2 tric oxide (NO) in the absorptive actions of GLP-2.

3 es more effectively compared to the native l-GLP-2.

4 ivation control the elimination of bioactive GLP-2.

5 d in TPN-fed pigs acutely (4 h) infused with GLP-2.

6 , truncated GLP-1, and N-terminally extended GLP-2.

7 ion (TPN alone), +/- SEN (days 4-6), and +/- GLP-2 (100 mug . kg body wt(-1) . d(-1)).

8 atments and TPN alone (SEN: 15-59% increase; GLP-2: 14-84% increase; and SEN + GLP-2: 63-160% increas

9 /- 10 pmol/L; GLP-2: 59 +/- 31 pmol/L; SEN + GLP-2: 246 +/- 40 pmol/L) and correlated with mucosal gr

10 h saline (control) for 4 hours and then with GLP-2 (500 pmol x kg(-1) x hour(-1), GLP-2) for 4 hours.

11 one: 25 +/- 9 pmol/L; SEN: 29 +/- 10 pmol/L; GLP-2: 59 +/- 31 pmol/L; SEN + GLP-2: 246 +/- 40 pmol/L)

12 increase; GLP-2: 14-84% increase; and SEN + GLP-2: 63-160% increase).

13 a-helices within glucagon and GLP-1, but not GLP-2, act as sorting signals by efficiently directing a

14 GLP-2 acutely increased PDV glucose uptake (+90%) and ne

15 GLP-2 acutely increased portal-drained visceral (PDV) bl

16 We conclude that in TPN-fed neonatal pigs, GLP-2 acutely stimulates intestinal blood flow and gluco

17 sits 4 weeks apart, to assess the effects of GLP-2 administration on triglyceride-rich lipoprotein (T

18 GLP-2 administration resulted in a rapid (within 30 minu

19 Treatment with the GLP-2 agonist, teduglutide, reduced de novo acute GVHD a

20 r stability to protease degradation of our d-GLP-2 agonists helps us envision their potential applica

21 All the d-GLP-2 agonists increased the protein kinase B phosphoryl

22 Here, we designed three d-GLP-2 agonists that activated the glucagon-like peptide-

23 GLP-2 also enhances gut barrier function and induces pro

24 GLP-2 also increased intestinal constitutive nitric oxid

25 press receptors for glucagon-like peptide-2 (GLP-2)-an intestinotrophic growth factor released by ent

26 The most effective d-GLP-2 analogue boosted the AKT phosphorylation 2.28 time

27 pharmacokinetic characteristics, a series of GLP-2 analogues containing Gly substitution at position

28 ncement in the p-AKT levels induced by the d-GLP-2 analogues could be explained by GLP-2R's more prol

29 more prolonged activation, given that the d-GLP-2 analogues induce a lower beta-arrestin recruitment

30 resence of SCFA sensing in the duodenum with GLP-2 and 5-HT signals further supports the hypothesis t

31 The actions of growth factors such as GLP-2 and EGF are now known to be complex, demonstrating

32 GLP-2 and GIP levels increased significantly in the cont

33 Using variants of the hormone GLP-2 and the designed clinical agonist glepaglutide (GL

34 Glucagon-Like Peptide-2 (GLP-2) and Glucose-dependent Insulinotropic Peptide (GIP

35 consecutive intravenous infusions of saline, GLP-2, and GLP-2 plus N(G)-Nitro-L-arginine methyl ester

36 d endocrine hormones, especially insulin and GLP-2, and stress.

37 GLP-1 and GLP-2 are both cleaved by dipeptidyl peptidase-4 (DPP-4)

38 mine whether the intestinotrophic effects of GLP-2 are mediated by acute up-regulation of intestinal

39 The actions of GLP-2 are transduced via a single G protein-coupled rece

40 The glucagon-like peptides (GLP-1 and GLP-2) are processed from the proglucagon polypeptide an

41 ptide 1 (GLP-1) and glucagon-like peptide 2 (GLP-2) are proglucagon derived peptides that are release

42 In the validation study, administration of GLP-2 at 7 hours after the meal, in the absence of addit

43 eviously shown that glucagon-like peptide 2 (GLP-2) augments dietary fat uptake and chylomicron produ

44 e that L cells are a target of GVHD and that GLP-2-based treatment of acute GVHD restores intestinal

45 GLP-2 circulates at low basal levels in the fasting peri

46 ndings from both preclinical studies and the GLP-2 clinical development program for short bowel syndr

47 e intestinotrophic response to a low dose of GLP-2 coinfused with PN in a rat model of SBS (60% jejun

48 GLP-1 and GLP-2 coinfusion resulted in net increased lipid absorpt

49 peak plasma cholecystokinin, PYY, GLP-1, and GLP-2 concentrations being attained after jejunal feedin

50 tide 1 (GLP-1), and glucagon-like peptide 2 (GLP-2) concentrations was greater after jejunal feeding

51 In contrast, the gut-derived peptide GLP-2, cosecreted from intestinal L cells with GLP-1, ha

52 ptide-1 (GLP-1) and glucagon-like peptide-2 (GLP-2) critically affect hepatic regeneration in rodent

53 prolonged (120-min) coinfusion of GLP-1 and GLP-2 decreased postprandial lipemia.

54 GLP-1 and GLP-2 demonstrated a rapid and consistently inverse time

55 s showing no effect and others documenting a GLP-2-dependent delay in gastric emptying.

56 gest dynamic inverse regulation of GLP-1 and GLP-2 during liver regeneration, rather caused by an inc

57 line in circulating glucagon-like peptide 2 (GLP-2) during TPN.

58 parameters were present and correlated with GLP-2 dynamics.

59 GLP-2 expanded intestinal organoids and reduced expressi

60 The gut hormone glucagon-like peptide-2 (GLP-2) facilitates intestinal absorption of lipids, but

61 en with GLP-2 (500 pmol x kg(-1) x hour(-1), GLP-2) for 4 hours.

62 ations and dynamics of circulating GLP-1 and GLP-2 in patients undergoing liver resections, focusing

63 functional connection to vascular action of GLP-2 in the gut.

64 nical role of glutamine, growth hormone, and GLP-2 in the treatment of short-bowel syndrome.

65 GLP-2 increased PDV indispensable amino acid uptake by 2

66 GLP-2 increases mesenteric blood flow and activates proa

67 ction, with GLP-1 significantly reducing and GLP-2 increasing postprandial chylomicronemia.

68 Combination treatment with SEN and GLP-2 induced a synergistic response resulting in greate

69 SEN + GLP-2 induced dramatic mucosal growth and greater plasma

70 We conclude that the GLP-2-induced stimulation of blood flow is mediated by v

71 active GLP-2 were significantly greater with GLP-2 infusion (TPN alone: 25 +/- 9 pmol/L; SEN: 29 +/-

72 In neonatal pigs, GLP-2 infusion dose-dependently stimulated intestinal bl

73 Hence GLP-2 integrates nutrient-derived signals to optimize mu

74 greater plasma concentration of GLP-2 (SEN x GLP-2 interaction, P < 0.0001).

75 GLP-1, GLP-2, Interleukin-6 (IL-6) and parameters of lipid meta

76 ion, food intake, and satiety signaling, and GLP-2 is implicated in regulating small-bowel growth.

77 c, dipolar alpha-helix, whereas the helix in GLP-2 is not dipolar.

78 Glucagon-like peptide-2 (GLP-2) is a 33-amino-acid proglucagon-derived peptide se

79 Glucagon-like peptide 2 (GLP-2) is a nutrient-dependent, proglucagon-derived gut

80 Glucagon-like peptide-2 (GLP-2) is a nutrient-responsive hormone that exerts dive

81 Glucagon-like-peptide-2 (GLP-2) is an enteroendocrine tissue hormone produced by

82 observed that acute GVHD reduced intestinal GLP-2 levels in mice and patients developing GVHD.

83 These findings suggest that GLP-2 may play an important physiological role in the re

84 sm in which nNOS-generated NO is crucial for GLP-2-mediated lipid absorption and chylomicron producti

85 ta implicate an nNOS-PKG-mediated pathway in GLP-2-mediated stimulation of dietary fat absorption and

86 Previous studies assessing the effect of GLP-2 on gastric emptying in humans have yielded inconsi

87 ignificant decrease of GLP-1 and increase of GLP-2 on POD1.

88 tion in WT mice also abrogated the effect of GLP-2 on postprandial lipid accumulation.

89 ning retinyl palmitate and were given either GLP-2 or placebo 7 hours later with measurement of TRL t

90 onse, including possible hypersensitivity to GLP-2 or reduced sensitivity to GLP-1.

91 GLP-2 plays a key role in the control of energy absorpti

92 Co-infusion of GLP-2 plus L-NAME did not increase either PDV blood flow

93 intravenous infusions of saline, GLP-2, and GLP-2 plus N(G)-Nitro-L-arginine methyl ester (L-NAME, 5

94 ) inhibition, at the same time as increasing GLP-2 portal blood concentrations.

95 e the intestinotrophic response to exogenous GLP-2, possibly by stimulating enterocyte proliferation

96 mal physiological conditions, the actions of GLP-2 predominate; however, when GLP-1 activity is susta

97 GLP-2 promotes intestinal TSLP in mouse and human intest

98 The discovery that GLP-2 promotes mucosal growth in the intestine is descri

99 In search of GLP-2 receptor agonists with better pharmacokinetic char

100 anced by DPPIV inhibition and inhibited by a GLP-2 receptor antagonist.

101 od flow and that nitric oxide is involved in GLP-2 receptor function.

102 ve FFA1 agonist increased DBS accompanied by GLP-2 release, enhanced by DPPIV inhibition and inhibite

103 O3(-) exchanger inhibition without affecting GLP-2 release, implicating acetate absorption in the par

104 nd presumably FFA3 by SCFA increased DBS via GLP-2 release, whereas FFA2 activation stimulated DBS vi

105 A short (30-min) intravenous infusion of GLP-2 resulted in a marked increase in postprandial apol

106 In vitro receptor potency at the human GLP-2, selectivity vs the human GLP-1 and GCG receptors,

107 l growth and greater plasma concentration of GLP-2 (SEN x GLP-2 interaction, P < 0.0001).

108 Mechanistically GLP-2 substitution promoted regeneration of PCs and ISCs

109 actions of glucagon-like peptide (GLP)-1 and GLP-2, the two major enteroendocrine L-cell peptides.

110 Administration of GLP-2 to men causes the release of chylomicrons that com

111 GLP-2 treatment in wild-type (WT) mice significantly inc

112 the apparent paradoxical roles of GLP-1 and GLP-2 under physiological conditions in the Syrian golde

113 intestinal biopsies and high serum levels of GLP-2 were associated with a higher incidence of nonrela

114 Plasma concentrations of bioactive GLP-2 were significantly greater with GLP-2 infusion (TP