ライフサイエンスコーパス: GLP-1

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

2 GLP-1 is capable of regulating the blood glucose level b

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

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

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

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

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

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

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

10 l activation of the glucagon-like peptide 1 (GLP-1) and glucagon receptor has the potential to lead t

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

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

13 osis of the hormone glucagon-like peptide 1 (GLP-1) by the intestinal L cell is essential for the inc

14 utic engineering of glucagon-like peptide 1 (GLP-1) has enabled development of new medicines to treat

15 Glucagon-like peptide 1 (GLP-1) immunoreactivity of plasma collected immediately

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

17 Glucagon-like peptide 1 (GLP-1) is a hormone with essential roles in regulating i

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

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

20 Glucagon-like peptide 1 (GLP-1) is secreted by intestinal L-cells, and augments g

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

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

23 The glucagon-like peptide 1 (GLP-1) receptor (GLP-1R) is a key target for type 2 diab

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

25 tes have shown that glucagon-like peptide 1 (GLP-1) receptor agonists prevent beta-cell loss.

26 influenced by local glucagon-like peptide 1 (GLP-1) secretion from alpha-cells, shown by experiments

27 those means induce glucagon-like peptide 1 (GLP-1) secretion.

28 trally administered glucagon-like peptide 1 (GLP-1) supresses food intake.

29 clinically relevant glucagon-like peptide 1 (GLP-1) was functionalized with diflunisal, indomethacin,

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

31 the degradation of glucagon-like peptide 1 (GLP-1), and has been approved for the treatment of type

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

33 polypeptide (GIP), glucagon-like peptide 1 (GLP-1), and peptide tyrosine tyrosine (PYY)] were measur

34 resent evidence for glucagon-like peptide 1 (GLP-1)-mediated paraventricular hypothalamic circuit coo

35 79; p < 0.001), and glucagon-like peptide-1 (GLP-1) agonists (OR 0.37, 95% CI 0.31-0.44; p < 0.001).

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

37 of both endogenous glucagon-like peptide-1 (GLP-1) and exogenous GLP-1 receptor (GLP-1R) agonists ar

38 , and the incretins glucagon-like peptide-1 (GLP-1) and GIP (glucose-dependent insulinotropic polypep

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

40 important peptides: glucagon-like peptide-1 (GLP-1) and the parathyroid hormone (PTH), which respecti

41 (CCK), ghrelin, and glucagon-like peptide-1 (GLP-1) concentrations, appetite perceptions, and gastroi

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

43 suggests a role for glucagon-like peptide-1 (GLP-1) in modulating stress responses.

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

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

46 al formulation of a glucagon-like peptide-1 (GLP-1) receptor agonist developed for the treatment of t

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

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

49 Exendin-4 (EX-4), a glucagon-like peptide-1 (GLP-1) receptor agonist, has been shown to reduce food i

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

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

52 Glucagon-like peptide-1 (GLP-1) receptor agonists are effective treatments for ty

53 Glucagon-like peptide-1 (GLP-1) receptor agonists differ in their structure and d

54 Three different glucagon-like peptide-1 (GLP-1) receptor agonists reduce cardiovascular outcomes

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

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

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

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

59 ulin, C-peptide and glucagon-like peptide-1 (GLP-1) secretion were increased, and the low-density lip

60 Alhough the glucagon-like peptide-1 (GLP-1) system is critical to energy balance control and

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

62 ls (EECs) that were glucagon-like peptide-1 (GLP-1)(+)/Peptide YY (PYY(-)) in the ileum and colon and

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

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

65 abetes therapeutic, glucagon-like peptide-1 (GLP-1), and the target of clinical investigation, gastri

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

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

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

69 whether amylin- and glucagon-like-peptide-1 (GLP-1)-based combination therapies produce greater food

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

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

72 % versus 7.5%), SGLT-2i (10.3% versus 8.1%), GLP-1 RA (3.4% versus 2.4%), and insulin (13.8% versus 9

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

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

75 shown by experiments with MIN6 cells, and a GLP-1 receptor antagonist.

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

77 recombinant microbial delivery vector for a GLP-1 analogue and assess the efficacy of the therapeuti

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

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

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

81 ed the efficacy and safety of semaglutide (a GLP-1 receptor agonist) with canagliflozin (an SGLT2 inh

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

83 Liraglutide, a long-acting GLP-1 receptor agonist, is approved for treatment of obe

84 toxin subunit A substantially reduced active GLP-1 concentrations in brain and spinal cord.

85 d combined-treated groups, without affecting GLP-1 receptor, preproglucagon or amylin-receptor gene e

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

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

88 All GLP-1 positive strains were identified as Staphylococcus

89 s (OR 0.50, 95% CI 0.39-0.65; p < 0.001) and GLP-1 agonists (OR 0.45, 95% CI 0.35-0.57; p < 0.001).

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

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

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

93 Furthermore, the amylin and GLP-1 analogs salmon calcitonin (sCT) and liraglutide pr

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

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

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

97 ptide YY (PYY(-)) in the ileum and colon and GLP-1(-)/PYY(-) in the cecum.

98 tiotemporal glucose and Ca(2+) dynamics, and GLP-1 secretion.

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

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

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

102 2409021 and MK 0893 antagonized glucagon and GLP-1 action at the GLP-1R, whereas des-His(1)-[Glu(9)]g

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

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

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

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

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

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

109 r wild-type littermates, whereas insulin and GLP-1 levels remained similar.

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

111 demonstrating glucose-dependent insulin and GLP-1 secretion in vitro.

112 1 L3740 also increased the L-cell number and GLP-1 levels and improved glucose tolerance in vivo.

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

114 ozin (14.5 events per 1000 person-years) and GLP-1 agonists (16.1 events per 1000 person-years) (over

115 lozin (2.2 events per 1000 person-years) and GLP-1 agonists (2.3 events per 1000 person-years), with

116 As GLP-1 mimetics are administered systemically in humans,

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

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

119 imilar safety profile to currently available GLP-1 receptor agonists, representing a potential treatm

120 At week 9, basal GLP-1 was decreased only in males (P < 0.001), whereas p

121 or medullary thyroid cancer reported between GLP-1 receptor agonist treatment and placebo.

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

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

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

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

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

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

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

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

130 nous hindbrain 5-HT are dependent on central GLP-1 receptor signaling.

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

132 ts as an endogenous modulator of the central GLP-1 system to mediate satiation and malaise in rats.

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

134 ion, the gene encoding PC1/3, which controls GLP-1 production, was decreased in knockout mice.

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

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

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

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

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

140 In lean mice, the divalent GLP-1 analogues were superior to monovalent analogues wi

141 short hairpin RNA to chronically knock down GLP-1 receptors (GLP-1R) in rats.

142 Widely used antidiabetic drugs (GLP-1 receptor agonists and sulfonylureas) activate this

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

144 istration of the plasmid DNA (pDNA) encoding GLP-1 decreased diabetic glucose levels to the normoglyc

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

146 r-population-mediating effects of endogenous GLP-1 signaling are not fully understood.

147 TS) are the predominant source of endogenous GLP-1 within the brain.

148 nous GLP-1R agonists (GLP-1RA) or endogenous GLP-1 on these parameters.

149 s and insulin secretion more than endogenous GLP-1, but the hormones contribute additively to postpra

150 peptidyl peptidase 4 inhibitors that enhance GLP-1 levels in patients with type 2 diabetes.

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

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

153 nsufficient to depolarize the cell and evoke GLP-1 secretion in the model, suggesting a crucial role

154 lucagon-like peptide-1 (GLP-1) and exogenous GLP-1 receptor (GLP-1R) agonists are an active area of i

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

156 tonin as a new critical neural substrate for GLP-1 impact on energy homeostasis and expands the curre

157 sure indices of IS, beta-cell function, GIP, GLP-1 and glucagon response.

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

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

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

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

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

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

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

165 3 kDa peptide, Hld (delta-toxin), present in GLP-1 positive supernatants but absent in GLP-1 neutral

166 pathways can be engaged to robustly increase GLP-1 without invasive surgical or injection regimens.

167 sought to discover mechanisms that increase GLP-1 pharmacologically.

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

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

170 ends on the enteroendocrine-derived incretin GLP-1(2), which is normally controlled by IELs through e

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

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

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

174 ed glucose tolerance and circulating leptin, GLP-1, and insulin levels were reduced.

175 1(9-36)NH(2) of the potent endogenous ligand GLP-1(7-36)NH(2).

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

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

178 r glycemic control surpassing that of native GLP-1.

179 , 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

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

181 Oral semaglutide, a novel GLP-1 agonist, was compared with subcutaneous liraglutid

182 e show dependence of paraventricular nucleus GLP-1 signaling in the coordination of neuroendocrine, a

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

184 1(28-36) and demonstrate that the ability of GLP-1(28-36) to shift substrate utilization from oxygen-

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

186 sformed to express a long-acting analogue of GLP-1 or the isogenic control microbe which solely harbo

187 atekeepers that limit the bioavailability of GLP-1.

188 imental findings establishing the biology of GLP-1 as an insulin-stimulating glucoregulatory hormone.

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

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

191 e of non-viral vector based oral delivery of GLP-1 gene through enterohepatic recycling pathways of b

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

193 als that assessed the safety and efficacy of GLP-1 receptor agonists compared with placebo in adult p

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

195 hoton microscopy revealed that exocytosis of GLP-1 is biphasic, with a first peak at 1-6 min and a se

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

197 cal mediator of the energy balance impact of GLP-1 receptor (GLP-1R) activation.

198 ld potentially lead to earlier initiation of GLP-1 receptor agonist therapy in the diabetes treatment

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

200 y, four trials of cardiovascular outcomes of GLP-1 receptor agonists were identified: ELIXA (lixisena

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

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

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

204 sely mimic the pharmacological properties of GLP-1.

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

206 ters can induce Ca(2+) influx and release of GLP-1 as a result of electrical activity, while glucose

207 tcome trials showed cardiovascular safety of GLP-1 receptor agonists, but results for cardiovascular

208 olitarius (NTS), the major central source of GLP-1, with the other nuclei in the midbrain and forebra

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

210 mic control by increasing concentrations of "GLP-1 equivalents" ( approximately 50 pmol/L).

211 both of these receptors is also dependent on GLP-1 signaling.

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

213 pears to have a greater beneficial impact on GLP-1 in females.

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

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

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

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

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

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

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

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

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

223 e long-term impact on glucose-stimulated, or GLP-1 potentiated insulin secretion.

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

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

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

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

228 the satiety hormone, glucagon-like peptide (GLP-1), using the enteroendocrine cell line, STC-1.

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

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

231 Basal and postprandial GLP-1 and postprandial PYY (all P < 0.05) were significa

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

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

234 y in males (P < 0.001), whereas postprandial GLP-1 was increased only in females (P < 0.001).

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

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

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

238 duced anxiety-like behavior, implicating PVN GLP-1 signaling in behavioral stress reactivity.

239 iguanides, glucagon-like peptide 1 receptor (GLP-1) agonists, dipeptidyl peptidase 4 (DPP-4) inhibito

240 linagliptin treatment increased the relative GLP-1 vs glucagon production in both non-diabetic and di

241 iated genome editing to controllably release GLP-1 (glucagon-like peptide 1), a critical incretin tha

242 dependence prevents hypoglycemia, rendering GLP-1 analogs a useful and safe treatment modality in ty

243 issue specimens, we showed a dose-responsive GLP-1 secretion in the ileum at >/=200 mmol/L glucose.

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

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

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

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

248 e of SGLT1 in controlling glucose-stimulated GLP-1 release in human ileal L cells.

249 olon, 300 mmol/L glucose potently stimulated GLP-1 release.

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

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

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

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

254 Here we demonstrate that GLP-1-producing (PPG) neurons in the nucleus tractus sol

255 Taken together, this study demonstrates that GLP-1 (via GLP-1R in alpha-cells) plays a bidirectional

256 It is known that GLP-1 secreting cells can sense glucose to promote elect

257 We also show that GLP-1 receptor (GLP-1R) activation augments excitatory s

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

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

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

261 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.

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

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

264 We assessed the long-term effect of the GLP-1 receptor agonist dulaglutide on renal outcomes in

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

266 Using a targeted knockdown of the GLP-1 receptor in the single-minded 1 neurons, we show d

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

268 controlled by IELs through expression of the GLP-1 receptor.

269 able signaling and secretory capacity of the GLP-1 system, we sought to discover mechanisms that incr

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

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

272 EC-1/BECN1/Beclin1 acts independently of the GLP-1/Notch or DAF-7/TGF-beta pathways but together with

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

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

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

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

277 Cotreatment with the GLP-1 receptor agonist exendin-4 reversed the lysosomal

278 Importantly, treatment with the GLP-1 receptor antagonist exendin 9-39 abolished the obs

279 Initial tests show that a thioamide GLP-1 analogue is biologically active in rats, with an i

280 ules were able to confer albumin affinity to GLP-1 and indicated that affinity is increased for dival

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

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

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

284 sting a crucial role for SGLT1 in triggering GLP-1 release in agreement with experimental studies.

285 the ability of exendin-4, a clinically used GLP-1 analog, to reduce body weight in rats, suggesting

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

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

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

289 5% CI -1.884 to -1.089, I = 91.95%), whereas GLP-1 and PYY increased post-procedure (Hedge g 1.095, 9

290 Whether GLP-1 mediates beta-cell survival via the key lysosomal-

291 Here we investigated mechanisms by which GLP-1 and serotonin interact at the level of the central

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

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

294 analogs by GDH in the L cell may explain why GLP-1 secretion, but not that of insulin, is activated b

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

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

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

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

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