ライフサイエンスコーパス: GLP

1 GLP-1 also exhibits a circadian rhythm, with highest rel

2 GLP-1 is exclusively produced in approximately 50% of al

3 GLP-1 receptor agonist treatment reduced all-cause morta

4 GLP-1(28-36) enters human coronary artery endothelial ce

5 GLP-1(28-36) is a small peptide that targets novel molec

6 GLP-1(28-36) modulates sAC by increasing intracellular A

7 GLP-1-dependent portal glucose signaling was identified,

8 GLP-1R-expressing cells were enriched in several key bra

9 GLP-1R-mApple cells were highly co-expressed with 5-HT3

10 GLP-2 expanded intestinal organoids and reduced expressi

11 Glucagon-like peptide 1 (GLP-1) and cholecystokinin (CCK) are gut-derived peptide

12 Glucagon-like peptide 1 (GLP-1) and glucagon-like peptide 2 (GLP-2) are proglucag

13 lypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are secreted postprandially and contribute import

14 testinally secreted glucagon-like peptide 1 (GLP-1) in regulation of insulin secretion has been quest

15 c peptide (GIP) and glucagon-like peptide 1 (GLP-1) is characterized by their glucose-dependent insul

16 Glucagon-like peptide 1 (GLP-1) is known to suppress glucagon secretion, but the

17 The incretin glucagon-like peptide 1 (GLP-1) is secreted by the intestinal L cell upon nutrien

18 Glucagon-like peptide 1 (GLP-1) mimetics are effective drugs for treatment of typ

19 Liraglutide, a glucagon-like peptide 1 (GLP-1) receptor agonist, and phentermine, a psychostimul

20 otective actions of glucagon-like peptide 1 (GLP-1) were unknown.

21 , lithium chloride, glucagon-like peptide 1 (GLP-1), and leptin shows the precise behavioural changes

22 79; p < 0.001), and glucagon-like peptide-1 (GLP-1) agonists (OR 0.37, 95% CI 0.31-0.44; p < 0.001).

23 de is a once-weekly glucagon-like peptide-1 (GLP-1) analogue for type 2 diabetes.

24 Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide

25 erotonin (5-HT) and glucagon-like peptide-1 (GLP-1) could play a role as upstream effectors involved

26 Glucagon-like peptide-1 (GLP-1) is an incretin hormone with a number of functions

27 Exendin-4 is a glucagon-like peptide-1 (GLP-1) receptor agonist and potent insulinotropic agent

28 ciation between the glucagon-like peptide-1 (GLP-1) receptor agonist dulaglutide and cognitive impair

29 e is the first oral glucagon-like peptide-1 (GLP-1) receptor agonist for glycaemic control in patient

30 iones (glitazones), glucagon-like peptide-1 (GLP-1) receptor agonists and dipeptidyl peptidase 4 (DPP

31 Although glucagon-like peptide-1 (GLP-1) receptor agonists and sodium-glucose cotransporte

32 ence indicates that glucagon-like peptide-1 (GLP-1) receptor agonists reduce drug reinforcement.

33 Two glucagon-like peptide-1 (GLP-1) receptor agonists reduced renal outcomes in peopl

34 d regulation of the glucagon-like peptide-1 (GLP-1) receptor by the non-peptide agonist PF 06882961 a

35 -OAD2, bound to the glucagon-like peptide-1 (GLP-1) receptor.

36 leptin, amylin, and glucagon-like peptide-1 (GLP-1) were assessed using Luminex((R)) technology.

37 he incretin hormone glucagon-like peptide-1 (GLP-1), also release other neuro-transmitters/modulators

38 Glucagon-like peptide-1 (GLP-1), an incretin secreted by L-cells lining the gastr

39 docrine secretions [glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GI

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

41 MRI parameters, and glucagon-like peptide-1 (GLP-1), polypeptide YY (PYY), and cholecystokinin peptid

42 glucagon (GluR) and glucagon-like peptide-1 (GLP-1R) are normally considered to be highly selective f

43 [DPP-4] inhibitors, glucagon-like peptide 1 [GLP-1] receptor agonists, and sodium-glucose cotransport

44 ive ghrelin, active glucagon-like peptide 1 [GLP-1], total peptide YY [PYY], cholecystokinin and insu

45 % versus 7.5%), SGLT-2i (10.3% versus 8.1%), GLP-1 RA (3.4% versus 2.4%), and insulin (13.8% versus 9

46 dvances in the current research on the GLP-1/GLP-1R system in beta cells, including the regulation of

47 ing the translational potential of the GLP-1/GLP-1R system in pancreatic beta cells has led to the de

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

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

50 The butyrate-G-protein-coupled receptor 43-GLP-1 pathway in the intestinal crypts may be involved i

51 after GB-IL were mitigated with exendin-9, a GLP-1 receptor antagonist, or cholestyramine, a bile aci

52 n of this series from HTS was supported by a GLP-1R ligand binding model.

53 ated the effects of once-weekly exenatide (a GLP-1 [glucagon-like peptide-1] receptor agonist) versus

54 spiking activity during glucose infusion, a GLP-1r-dependent function.

55 Liraglutide is a GLP-1 receptor agonist recently approved for Type-II dia

56 tched to 79 964 patients initiating use of a GLP-1 agonist.

57 in a 1:1 ratio to those initiating use of a GLP-1 agonist.

58 Methods: Here, we used a GLP-1R knockout mouse model to demonstrate that exocrine

59 Tg circuits attenuated cocaine seeking via a GLP-1R-dependent mechanism.

60 ion with our previously reported long-acting GLP-1 analog is demonstrated in a diet-induced obesity m

61 a peripheral CB1R inhibitor with long-acting GLP-1R agonists achieves greater reduction in body weigh

62 gical studies demonstrated that 19 activates GLP-1R as positive allosteric modulator (PAM) in the pre

63 c glucagon-like peptide-1 receptor agonists (GLP-1 RAs) added to metformin-based background therapy p

64 r glucagon-like peptide-1 receptor agonists (GLP-1 RAs; 3.0%) using three methodologies: drop-in visi

65 ral glucagon-like peptide receptor agonists (GLP-1RA) and sodium-glucose cotransporter-2 inhibitors (

66 All GLP-1 positive strains were identified as Staphylococcus

67 l that the binding sites for PF 06882961 and GLP-1 substantially overlap, whereas CHU-128 adopts a un

68 r by the non-peptide agonist PF 06882961 and GLP-1 that was not observed for another compound, CHU-12

69 ; Trp: 97 +/- 16; C12 + Trp: 229 +/- 22) and GLP-1 (AUC0-90 min, pmol/L*min; control: 102 +/- 41; C12

70 In chow-maintained rats, systemic amylin and GLP-1 combine to reduce meal size.

71 leptin levels and an increase in amylin and GLP-1 levels relative to controls.

72 ts and study their ability to induce CCK and GLP-1 release in enteroendocrine STC-1 cells.

73 combined contributions of endogenous GIP and GLP-1 to the postprandial changes in glucose and glucore

74 Immunohistochemistry (IHC) for GIP and GLP-1 was also done on intestinal biopsies of all acrome

75 a, 2) insulinotropic effects of both GIP and GLP-1, 3) additive to supra-additive effects on insulin

76 2409021 and MK 0893 antagonized glucagon and GLP-1 action at the GLP-1R, whereas des-His(1)-[Glu(9)]g

77 ered to be highly selective for glucagon and GLP-1, respectively.

78 that detect cAMP as a read-out for GluR and GLP-1R activation.

79 o reevaluate prior studies in which GluR and GLP-1R agonists and antagonists were assumed not to exer

80 l agonist action of glucagon at the GluR and GLP-1R.

81 hat the central interaction between 5-HT and GLP-1 is involved in the control of food intake in rats.

82 hether interactions between central 5-HT and GLP-1 signaling are behaviorally and physiologically rel

83 dium glucose cotransporter 2) inhibitors and GLP-1 (glucagon-like peptide-1) receptor agonists, has c

84 sociation between use of DPP4 inhibitors and GLP-1 mimetics and the onset of Parkinson's disease (IRR

85 protective effects with SGLT2 inhibitors and GLP-1 receptor agonists in patients with CKD and T2D.

86 ing body fat, SCFAs, early-phase insulin and GLP-1 secretion and the gut microbiota in normal-weight

87 mapping of the tracer uptake and insulin and GLP-1R expression conclusively demonstrated that the obs

88 1 L3740 also increased the L-cell number and GLP-1 levels and improved glucose tolerance in vivo.

89 ates with heightened insulin sensitivity and GLP-1 secretion.

90 G levels restored absolute tracer uptake and GLP-1R expression in beta-cells and the observed loss in

91 dy indicated that >90% of the beta-cells are GLP-1R positive, contradicting the findings with the scR

92 As GLP-1R expression is thought to be influenced by glycemi

93 abolite of GLP-1, was as cardioprotective as GLP-1 and was abolished by scrambling its amino acid seq

94 hree-dimensional structures of GPCRs such as GLP-1R and glucagon receptor has helped to drive the rat

95 e metabolism through the butyrate-associated GLP-1 pathway in the gut, and oral supplementation with

96 antidiabetic effects of currently available GLP-1R agonists.

97 g either SGLT2i or sulfonylureas to baseline GLP-1RA were identified within 3 US claims datasets (201

98 als of SGLT2i versus placebo, where baseline GLP-1RA use was minimal.

99 ynamics of ECD that is necessary for binding GLP-1.

100 Results: Exendin-4-IRDye 800CW binds GLP-1R with a half-maximal inhibitory concentration of 3

101 t reporting of a comprehensive bioanalytical GLP methodology detailing the mass spectrometric quantit

102 k challenges the textbook physiology of both GLP-1 and glucagon and presents a critical paradigm shif

103 NAcylation can improve the stability of both GLP-1 and PTH in serum despite the fact that the O-GlcNA

104 We have previously demonstrated that both GLP-1 and CCK are produced in the endocrine pancreas of

105 tion, including evidence of fetal alpha-cell GLP-1 production and signaling to beta-cells.

106 to beta-cell signaling through the beta-cell GLP-1 receptor.

107 o exert promiscuous effects at the beta-cell GLP-1R, as may occur in the volume-restricted microenvir

108 ntrary to expectations, this loss of central GLP-1 had no significant effect on the ad libitum feedin

109 itarius (NTS), the primary source of central GLP-1, with midbrain and forebrain nuclei known to regul

110 a novel endogenous modulator of the central GLP-1 system and suggest that the central interaction be

111 .7% +/- 0.3% remaining cell viability in CHL-GLP-1R and INS-1 cells, respectively).

112 The tracer accumulates in CHL-GLP-1R xenografts.

113 In vivo NIR fluorescence imaging of CHL-GLP-1R xenografts was performed.

114 Subcutaneous CHL-GLP-1R xenografts were visualized using in vivo NIR fluo

115 in BALB/c nude mice bearing subcutaneous CHL-GLP-1R xenografts.

116 key role for microbiome-dependent circadian GLP-1 secretion in the maintenance of 24-h metabolic hom

117 In this study, we demonstrated GLP-1 receptor (GLP-1R) expression in alpha-cells using

118 e tolerance, and stimulates GPR119-dependent GLP-1 and glucagon secretion in mice.

119 Here, we tested whether islet-derived GLP-1 or CCK is necessary for the full stimulation of in

120 Distal (GLP-1/PYY/NT), but not proximal (CCK/GIP), enteroendocri

121 ence for a role of the microbiome in diurnal GLP-1 release.

122 and human intestinal organoids and elevated GLP-1 secretory capacity.

123 extensive interest in increasing endogenous GLP-1 secretion and L-cell abundance.

124 ated that Hld alone is sufficient to enhance GLP-1 secretion.

125 HDAC) inhibitor Entinostat (MS-275) enhances GLP-1R agonism to potentiate glucose-stimulated insulin

126 ls has led to the development of established GLP-1R-based therapies for the long-term preservation of

127 nist GIP(3-30)NH(2) and the well-established GLP-1 receptor antagonist exendin(9-39)NH(2) During 4-h

128 erodorsal tegmental nucleus (LDTg) expresses GLP-1Rs and functions as a neuroanatomical hub connectin

129 tive positive allosteric modulator (PAM) for GLP-1R based on a 3,4,5,6-tetrahydro-1H-1,5-epiminoazoci

130 ed from healthy individuals and screened for GLP-1 modulation by incubating bacterial cell-free super

131 re represents a snapshot of the peptide-free GLP-1R and provides insights into the activation pathway

132 identification of a novel chemotype for G9a/GLP inhibitors, based on the underinvestigated 2-alkyl-5

133 radation of the H3K9 methyltransferases, G9a/GLP, and the DNA methyltransferase, DNMT1, which both co

134 ates cocaine seeking and highlight GABAergic GLP-1R-expressing circuits in the midbrain as important

135 The O-GlcNAcylated GLP-1 and PTH also displayed significantly improved in v

136 nist strategy with which to target the GluR, GLP-1R, and NPY2R.

137 dentified an endocrine profile of heightened GLP-1 and PP but lower ghrelin that differentiated rats

138 ess the Glp1r gene, supporting heterogeneous GLP-1R expression.

139 des triggered CCK release, while the highest GLP-1 response was found with a hydrophobic positively c

140 n increased intestinal secretion of hormones GLP-1 and anorexigenic PYY, which is believed to contrib

141 e crystal structure of the full-length human GLP-1R in an inactive state, which reveals a unique clos

142 eater in CD participants, compared with HVs [GLP-1, CD 50 +/- 8 ug/mL versus HV 13 +/- 3 ug/mL (P <=

143 in GLP-1 positive supernatants but absent in GLP-1 neutral supernatants.

144 Furthermore, the changes in GLP-1 secretion were shown to be essential for the maint

145 The tracer accumulates dose-dependently in GLP-1R-positive tumors.

146 caused significant specific phototoxicity in GLP-1R-positive cells (2.3% +/- 0.8% and 2.7% +/- 0.3% r

147 3 kDa peptide, Hld (delta-toxin), present in GLP-1 positive supernatants but absent in GLP-1 neutral

148 t insulin resistance, through a reduction in GLP-1r density, leads to functional portal desensitizati

149 lets, which was paralleled by a reduction in GLP-1R expression.

150 a-cell Glp1r expression, but no reduction in GLP-1R protein levels or GLP-1R-mediated insulin secreti

151 d gastric emptying rate as well as increased GLP-1 response.

152 proximately 45 strains capable of increasing GLP-1 were discovered.

153 unication is exemplified by secretin-induced GLP-1 secretion.

154 e effect of L3740 on L cells required intact GLP-1 receptor and serotonin 5-hydroxytryptamine recepto

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

156 d highlight the critical role of intra-islet GLP-1 signaling in the regulation of human beta-cell fun

157 ified, in vivo, using a novel (68)Ga-labeled GLP-1r positron-emitting probe that supplied a quantitat

158 s study was to characterize the role of LDTg GLP-1R-expressing neurons and their projections to the v

159 1(9-36)NH(2) of the potent endogenous ligand GLP-1(7-36)NH(2).

160 ncomitant with increased levels of lymphatic GLP-1 in the fasted state and increased levels of intest

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

162 with 2) infusions of GIP (1.5 pmol/kg/min), GLP-1 (0.5 pmol/kg/min), or saline (NaCl).

163 data suggest the potential of small molecule GLP-1R PAMs for T2DM treatment, further optimization is

164 tablished that glucagon is a nonconventional GLP-1R agonist, an effect inhibited by the GLP-1R orthos

165 , P < 0.01) and NT (+32%, P < 0.01), but not GLP-1 (+5%; 95% CI: -2.9%, 13%; P = 0.22), whereas the e

166 IHC positivity for GIP, but not GLP-1, staining cells in duodenum and colon was signific

167 ition with sacubitril blunted the ability of GLP-1 to increase cAMP levels in coronary vascular cells

168 1(28-36) and demonstrate that the ability of GLP-1(28-36) to shift substrate utilization from oxygen-

169 of oxycodone, suggesting that activation of GLP-1 receptors attenuated opioid reinforcement without

170 is not an agonist or allosteric activator of GLP-1R but enhances the sustained receptor-mediated sign

171 atekeepers that limit the bioavailability of GLP-1.

172 Fasting concentrations of GLP-1 and PYY were significantly greater in CD participa

173 we sought to understand the consequences of GLP-1 resistance on glucose portal signaling.

174 d the effects of L3740, acting downstream of GLP-1.

175 ypes that mediate the suppressive effects of GLP-1R agonists on cocaine-seeking behavior are largely

176 However, the efficacy of GLP-1 receptor agonists in attenuating opioid-mediated b

177 is manuscript, we provide detailed images of GLP-1R-mApple expression and distribution within the bra

178 sibility of targeted fluorescence imaging of GLP-1R-positive lesions.

179 The FIGHT (Functional Impact of GLP-1 [glucagon-like peptide-1] for Heart Failure Treatm

180 d in vitro in cells with different levels of GLP-1R expression.

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

182 dase-generated (NEP-generated) metabolite of GLP-1, was as cardioprotective as GLP-1 and was abolishe

183 hat metabolic stress decreases the number of GLP-1R-positive beta-cells.

184 ein-alpha (MTPalpha) as a binding partner of GLP-1(28-36) and demonstrate that the ability of GLP-1(2

185 The circadian pattern of GLP-1 release was found to be dependent on the oral rout

186 regional and cellular expression patterns of GLP-1R expressing cells in the CNS, using double-label i

187 We also examined the expression patterns of GLP-1R in mouse models of metabolic stress.

188 anisms is the anti-inflammatory potential of GLP-1 receptor (Glp1r) agonism.

189 sely mimic the pharmacological properties of GLP-1.

190 mulation, and whole-cell patch recordings of GLP-1 receptor-expressing PVH neurons revealed enhanced

191 ials have reported on the concomitant use of GLP-1 receptor agonists with sodium-glucose cotransporte

192 cohort of patients with diabetes already on GLP-1RA, addition of SGLT2i conferred greater cardiovasc

193 lucagon products, with a particular focus on GLP-1, in the context of their roles in insulin secretio

194 he impact of visceral sensory information on GLP-1 receptor-expressing neurons in the PVH.

195 d the effect of blood glucose (BG) levels on GLP-1R-mediated exendin uptake in both murine and human

196 expression of 5-HT2C and 5-HT3 receptors on GLP-1-producing preproglucagon (PPG) neurons in the medi

197 eatic islets secrete GLP-1 and CCK, but only GLP-1 acts locally within the islet to promote insulin r

198 bitors versus DPP-4 inhibitors (cohort 1) or GLP-1 agonists (cohort 2).

199 ffer from controls in glucose-, alanine-, or GLP-1-stimulated insulin secretion during perifusion.

200 The use of DPP4 inhibitors and/or GLP-1 mimetics is associated with a lower rate of Parkin

201 ed with glitazones or DPP4 inhibitors and/or GLP-1 receptor agonists to individuals treated with othe

202 ng mouse models with genetic loss of CB1R or GLP-1R, we demonstrate that these two metabolic receptor

203 The effect of SUs together with GIP or GLP-1, respectively, on insulin and glucagon secretion i

204 minimal inhibitory action versus glucagon or GLP-1 at the GLP-1R.

205 thermore, systemic administration of GluR or GLP-1R agonists and antagonists at high doses may lead t

206 but no reduction in GLP-1R protein levels or GLP-1R-mediated insulin secretion.

207 Overall, GLP-1 receptor agonist treatment reduced MACE by 12% (HR

208 oned, and a physiological role of pancreatic GLP-1 in regulation of insulin secretion has been propos

209 e L-cell differentiation through a paracrine GLP-1-dependent and serotonin-mediated mechanism.

210 -day- and diet-dependent changes paralleling GLP-1 secretion.

211 Glucagon-like peptide (GLP)-1 analogs such as liraglutide improved albuminuria

212 DPP4 and increase in Glucagon-like peptide (GLP)-1 levels as compared to the placebo-treated group,

213 The therapeutic success of peptidic GLP-1 receptor agonists for treatment of type 2 diabetes

214 ffects than C8-dietary oil on AUCs of plasma GLP-1 (+32%; 95% CI: 23%, 43%; P < 0.01), CCK (+53%, P <

215 This reflected a reduction in portal GLP-1r binding potential, particularly between the splen

216 edure hormones fasting ghrelin, postprandial GLP-1, postprandial PYY, and fasting GIP levels were inc

217 relin levels decreased, whereas postprandial GLP-1 and PYY increased after sleeve gastrectomy.

218 s, but not free amino acids, showed a potent GLP-1 secretagogue effect, while proteins only had a mod

219 Thus, GPBAR1 agonists and other powerful GLP-1 secretagogues facilitate L-cell differentiation th

220 methyltransferases G9a and G9a-like protein (GLP) have been reported.

221 in-4 penetrated the brain and bound putative GLP-1 receptors on dopamine D1 receptor- and dopamine D2

222 -1R antibody, and flow cytometry to quantify GLP-1R promoter activity, gene expression, and protein e

223 ization, and treatment with the radiolabeled GLP-1R agonist exendin.

224 dy weight, glucagon-like peptide 1 receptor (GLP-1R) agonism has emerged as a preferred treatment for

225 Glucagon-like peptide 1 receptor (GLP-1R) agonists effectively improve glycemia and body w

226 in part by glucagon-like peptide 1 receptor (GLP-1R) and not the G protein-coupled receptor GPR40.

227 ecules that can activate the GLP-1 receptor (GLP-1R) as a well-validated target for T2DM.

228 this study, we demonstrated GLP-1 receptor (GLP-1R) expression in alpha-cells using both antibody-de

229 Glucagon-like peptide 1 receptor (GLP-1R) imaging with radiolabeled exendin has proven to

230 actions of glucagon-like peptide 1 receptor (GLP-1R) in beta-cells have made it a useful target to ma

231 Glucagon-like peptide-1 receptor (GLP-1R) is a class B G protein-coupled receptor that pla

232 inomas, the glucagonlike peptide-1 receptor (GLP-1R) is a potential target for diagnosis, localizatio

233 The glucagon-like peptide-1 receptor (GLP-1R), a key pharmacological target in type 2 diabetes

234 imaging of glucagonlike peptide 1 receptor (GLP-1R)-positive lesions, using the GLP-1 agonist exendi

235 argets the glucagon-like peptide-1 receptor (GLP-1R).

236 activated glucagon-like peptide 1 receptor (GLP-1r).

237 geting the glucagon-like peptide 1 receptor (GLP-1R).

238 g central glucagon-like peptide-1 receptors (GLP-1Rs) may represent a novel approach to treating coca

239 area was maintained in spite of the reduced GLP-1R expression levels.

240 In most regions, GLP-1R primarily colocalized with GABAergic neurons, exc

241 confirm that mouse pancreatic islets secrete GLP-1 and CCK, but only GLP-1 acts locally within the is

242 Conclusion: Selective GLP-1R blocking, which improves contrast between healthy

243 cell-based activation assays, while several GLP-1 analogs were biased agonists relative to GLP-1.

244 GSC) regulation are the same for both sexes: GLP-1/Notch signaling from the mesenchymal distal tip ce

245 A novel alpha-cell-specific GLP-1R knockout (alphaGLP-1R(-/-)) mouse model was creat

246 metformin-based background therapy, specific GLP-1 RAs and SGLT-2 inhibitors have a favorable effect

247 C12, but not Trp, stimulated GLP-1 (P < 0.05) and phasic pyloric pressures (P < 0.05)

248 sulin secretion when combining SU+GIP and SU+GLP-1, respectively, and 4) increased fasting and argini

249 safety profile consistent with subcutaneous GLP-1 receptor agonists.

250 Further characterization of Hld suggests GLP-1 stimulatory action of Hld occurs via calcium signa

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

252 as the incretin receptors and indicate that GLP-1R is widely expressed in beta-cells, absent in alph

253 Taken together, these findings suggest that GLP-1 receptors could serve as potential molecular targe

254 also demonstrated, for the first time, that GLP-1Rs are expressed primarily on GABAergic neurons in

255 The GLP-1 system is known to be impaired in insulin-resistan

256 ilable small molecules that can activate the GLP-1 receptor (GLP-1R) as a well-validated target for T

257 antagonized glucagon and GLP-1 action at the GLP-1R, whereas des-His(1)-[Glu(9)]glucagon antagonized

258 itory action versus glucagon or GLP-1 at the GLP-1R.

259 l GLP-1R agonist, an effect inhibited by the GLP-1R orthosteric antagonist exendin(9-39) (Ex(9-39)).

260 luorescent protein (mApple) is driven by the GLP-1R promoter.

261 din-4-IRDye700DX has a high affinity for the GLP-1R, with a half-maximal inhibitory concentration of

262 s (IR, 2.15), compared with 87 events in the GLP-1 agonist group (IR, 2.96) (HR, 0.72 [CI, 0.53 to 0.

263 l gastric volume interventions increased the GLP-1 response, none of the interventions, except VSG, s

264 We assessed the effect of the GLP-1 receptor agonist dulaglutide on major adverse card

265 e showed that systemic administration of the GLP-1 receptor agonist exendin-4 reduced oxycodone self-

266 rimarily mediated through stimulation of the GLP-1 receptor.

267 companied by inappropriate activation of the GLP-1 target sygl-1 in PGCs.

268 arnessing the translational potential of the GLP-1/GLP-1R system in pancreatic beta cells has led to

269 Here, we showed that administration of the GLP-1R agonist exendin-4 (Ex-4) directly into the LDTg s

270 cent advances in the current research on the GLP-1/GLP-1R system in beta cells, including the regulat

271 eceptor (GLP-1R)-positive lesions, using the GLP-1 agonist exendin-4 labeled with IRDye 800CW, was ex

272 siological role for glucagon, acting via the GLP-1 receptor, in paracrine regulation of insulin secre

273 luding renal safety, was consistent with the GLP-1 receptor agonist class.

274 amster lung (CHL) cells transfected with the GLP-1R.

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

276 apeutic potential of MS-275 as an adjunct to GLP-1R therapy in the treatment of diabetes and obesity.

277 tion in tracer uptake directly correlates to GLP-1R expression levels.

278 ear-normalized for at least 3 weeks prior to GLP-1R agonist treatment or quantitative radiolabeled ex

279 P-1 analogs were biased agonists relative to GLP-1.

280 olic stress reduces beta-cell sensitivity to GLP-1, yet the underlying mechanisms are unknown.

281 ns unknown whether the addition of SGLT2i to GLP-1RA therapy has further cardiovascular benefits.

282 Intestinal digests triggered GLP-1 release at a higher rate than gastric digests.

283 the relevance of this process in fine-tuning GLP-1R responses in pancreatic beta cells to control ins

284 nd 4 per 10 000 person-years in 10 684 using GLP-1 mimetics, 6861 of whom were prescribed GTZ and/or

285 ed GTZ and/or DPP4 inhibitors prior to using GLP-1 mimetics.

286 nts with Glp1r reporter mice and a validated GLP-1R antibody indicated that >90% of the beta-cells ar

287 oupled with quantitative RT-PCR, a validated GLP-1R antibody, and flow cytometry to quantify GLP-1R p

288 ocrine binding of exendin is exclusively via GLP-1R (~1,000/cell) and not any other receptor.

289 n (high-fat/high-sucrose) diet for 16 weeks, GLP-1 secretion was markedly increased but arrhythmic ov

290 5% CI -1.884 to -1.089, I = 91.95%), whereas GLP-1 and PYY increased post-procedure (Hedge g 1.095, 9

291 ucagon secretion, but the mechanism by which GLP-1 exerts this effect is unclear.

292 he lateral septum, the brain region in which GLP-1R is most highly expressed.

293 Interestingly, while GLP-1 is well known to stimulate insulin secretion by th

294 This shift explains why GLP-1, which signals via Gq, but not GIP, which signals

295 th increased risk for fracture compared with GLP-1 agonists.

296 e set out to identify microbial strains with GLP-1 stimulatory activity as potential metabolic diseas

297 de that L-cells co-secrete ATP together with GLP-1 and PYY, and that ATP acts as an additional signal

298 se hamster lung (CHL) cells transfected with GLP-1R.

299 Treatment with GLP-1 receptor agonists has beneficial effects on cardio

300 odels of ischemic injury that treatment with GLP-1(28-36), a neutral endopeptidase-generated (NEP-gen