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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.                                                  
  
     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)
  
    10 a-helices within glucagon and GLP-1, but not GLP-2, act as sorting signals by efficiently directing a
  
  
    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
  
  
  
    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
  
    21 consecutive intravenous infusions of saline, GLP-2, and GLP-2 plus N(G)-Nitro-L-arginine methyl ester
  
  
    24 mine whether the intestinotrophic effects of GLP-2 are mediated by acute up-regulation of intestinal 
  
  
    27   In the validation study, administration of GLP-2 at 7 hours after the meal, in the absence of addit
  
    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
  
    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 
  
  
  
  
  
  
  
  
  
  
  
  
  
  
    48 active GLP-2 were significantly greater with GLP-2 infusion (TPN alone: 25 +/- 9 pmol/L; SEN: 29 +/- 
  
  
  
    52 ion, food intake, and satiety signaling, and GLP-2 is implicated in regulating small-bowel growth.   
  
  
  
  
  
    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
  
  
  
    63  intravenous infusions of saline, GLP-2, and GLP-2 plus N(G)-Nitro-L-arginine methyl ester (L-NAME, 5
  
    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
  
  
  
  
    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
  
  
    77 actions of glucagon-like peptide (GLP)-1 and GLP-2, the two major enteroendocrine L-cell peptides.   
  
    79  the apparent paradoxical roles of GLP-1 and GLP-2 under physiological conditions in the Syrian golde
  
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