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1 ivation control the elimination of bioactive GLP-2.
2 d in TPN-fed pigs acutely (4 h) infused with GLP-2.
3 , truncated GLP-1, and N-terminally extended GLP-2.
4 ion (TPN alone), +/- SEN (days 4-6), and +/- GLP-2 (100 mug . kg body wt(-1) . d(-1)).
5 atments and TPN alone (SEN: 15-59% increase; GLP-2: 14-84% increase; and SEN + GLP-2: 63-160% increas
6 /- 10 pmol/L; GLP-2: 59 +/- 31 pmol/L; SEN + GLP-2: 246 +/- 40 pmol/L) and correlated with mucosal gr
7 h saline (control) for 4 hours and then with GLP-2 (500 pmol x kg(-1) x hour(-1), GLP-2) for 4 hours.
8 one: 25 +/- 9 pmol/L; SEN: 29 +/- 10 pmol/L; GLP-2: 59 +/- 31 pmol/L; SEN + GLP-2: 246 +/- 40 pmol/L)
9  increase; GLP-2: 14-84% increase; and SEN + GLP-2: 63-160% increase).
10 a-helices within glucagon and GLP-1, but not GLP-2, act as sorting signals by efficiently directing a
11                                              GLP-2 acutely increased PDV glucose uptake (+90%) and ne
12                                              GLP-2 acutely increased portal-drained visceral (PDV) bl
13   We conclude that in TPN-fed neonatal pigs, GLP-2 acutely stimulates intestinal blood flow and gluco
14 sits 4 weeks apart, to assess the effects of GLP-2 administration on triglyceride-rich lipoprotein (T
15                                              GLP-2 administration resulted in a rapid (within 30 minu
16                                              GLP-2 also enhances gut barrier function and induces pro
17                                              GLP-2 also increased intestinal constitutive nitric oxid
18 pharmacokinetic characteristics, a series of GLP-2 analogues containing Gly substitution at position
19 resence of SCFA sensing in the duodenum with GLP-2 and 5-HT signals further supports the hypothesis t
20        The actions of growth factors such as GLP-2 and EGF are now known to be complex, demonstrating
21 consecutive intravenous infusions of saline, GLP-2, and GLP-2 plus N(G)-Nitro-L-arginine methyl ester
22 d endocrine hormones, especially insulin and GLP-2, and stress.
23                                    GLP-1 and GLP-2 are both cleaved by dipeptidyl peptidase-4 (DPP-4)
24 mine whether the intestinotrophic effects of GLP-2 are mediated by acute up-regulation of intestinal
25                               The actions of GLP-2 are transduced via a single G protein-coupled rece
26        The glucagon-like peptides (GLP-1 and GLP-2) are processed from the proglucagon polypeptide an
27   In the validation study, administration of GLP-2 at 7 hours after the meal, in the absence of addit
28                                              GLP-2 circulates at low basal levels in the fasting peri
29 ndings from both preclinical studies and the GLP-2 clinical development program for short bowel syndr
30 e intestinotrophic response to a low dose of GLP-2 coinfused with PN in a rat model of SBS (60% jejun
31                                    GLP-1 and GLP-2 coinfusion resulted in net increased lipid absorpt
32 peak plasma cholecystokinin, PYY, GLP-1, and GLP-2 concentrations being attained after jejunal feedin
33 tide 1 (GLP-1), and glucagon-like peptide 2 (GLP-2) concentrations was greater after jejunal feeding
34         In contrast, the gut-derived peptide GLP-2, cosecreted from intestinal L cells with GLP-1, ha
35  prolonged (120-min) coinfusion of GLP-1 and GLP-2 decreased postprandial lipemia.
36 s showing no effect and others documenting a GLP-2-dependent delay in gastric emptying.
37 line in circulating glucagon-like peptide 2 (GLP-2) during TPN.
38     The gut hormone glucagon-like peptide-2 (GLP-2) facilitates intestinal absorption of lipids, but
39 en with GLP-2 (500 pmol x kg(-1) x hour(-1), GLP-2) for 4 hours.
40  functional connection to vascular action of GLP-2 in the gut.
41 nical role of glutamine, growth hormone, and GLP-2 in the treatment of short-bowel syndrome.
42                                              GLP-2 increased PDV indispensable amino acid uptake by 2
43                                              GLP-2 increases mesenteric blood flow and activates proa
44 ction, with GLP-1 significantly reducing and GLP-2 increasing postprandial chylomicronemia.
45           Combination treatment with SEN and GLP-2 induced a synergistic response resulting in greate
46                                        SEN + GLP-2 induced dramatic mucosal growth and greater plasma
47                         We conclude that the GLP-2-induced stimulation of blood flow is mediated by v
48 active GLP-2 were significantly greater with GLP-2 infusion (TPN alone: 25 +/- 9 pmol/L; SEN: 29 +/-
49                            In neonatal pigs, GLP-2 infusion dose-dependently stimulated intestinal bl
50                                        Hence GLP-2 integrates nutrient-derived signals to optimize mu
51 greater plasma concentration of GLP-2 (SEN x GLP-2 interaction, P < 0.0001).
52 ion, food intake, and satiety signaling, and GLP-2 is implicated in regulating small-bowel growth.
53 c, dipolar alpha-helix, whereas the helix in GLP-2 is not dipolar.
54                     Glucagon-like peptide-2 (GLP-2) is a 33-amino-acid proglucagon-derived peptide se
55                     Glucagon-like peptide 2 (GLP-2) is a nutrient-dependent, proglucagon-derived gut
56                     Glucagon-like peptide-2 (GLP-2) is a nutrient-responsive hormone that exerts dive
57                  These findings suggest that GLP-2 may play an important physiological role in the re
58     Previous studies assessing the effect of GLP-2 on gastric emptying in humans have yielded inconsi
59 ning retinyl palmitate and were given either GLP-2 or placebo 7 hours later with measurement of TRL t
60 onse, including possible hypersensitivity to GLP-2 or reduced sensitivity to GLP-1.
61                                              GLP-2 plays a key role in the control of energy absorpti
62                               Co-infusion of GLP-2 plus L-NAME did not increase either PDV blood flow
63  intravenous infusions of saline, GLP-2, and GLP-2 plus N(G)-Nitro-L-arginine methyl ester (L-NAME, 5
64 ) inhibition, at the same time as increasing GLP-2 portal blood concentrations.
65 e the intestinotrophic response to exogenous GLP-2, possibly by stimulating enterocyte proliferation
66 mal physiological conditions, the actions of GLP-2 predominate; however, when GLP-1 activity is susta
67                           The discovery that GLP-2 promotes mucosal growth in the intestine is descri
68                                 In search of GLP-2 receptor agonists with better pharmacokinetic char
69 anced by DPPIV inhibition and inhibited by a GLP-2 receptor antagonist.
70 od flow and that nitric oxide is involved in GLP-2 receptor function.
71 ve FFA1 agonist increased DBS accompanied by GLP-2 release, enhanced by DPPIV inhibition and inhibite
72 O3(-) exchanger inhibition without affecting GLP-2 release, implicating acetate absorption in the par
73 nd presumably FFA3 by SCFA increased DBS via GLP-2 release, whereas FFA2 activation stimulated DBS vi
74     A short (30-min) intravenous infusion of GLP-2 resulted in a marked increase in postprandial apol
75       In vitro receptor potency at the human GLP-2, selectivity vs the human GLP-1 and GCG receptors,
76 l growth and greater plasma concentration of GLP-2 (SEN x GLP-2 interaction, P < 0.0001).
77 actions of glucagon-like peptide (GLP)-1 and GLP-2, the two major enteroendocrine L-cell peptides.
78                            Administration of GLP-2 to men causes the release of chylomicrons that com
79  the apparent paradoxical roles of GLP-1 and GLP-2 under physiological conditions in the Syrian golde
80           Plasma concentrations of bioactive GLP-2 were significantly greater with GLP-2 infusion (TP

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