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1 he satiety neuropeptides cholecystokinin and glucagon-like peptide 1.
2 mentation of fibroblast growth factor 21 and glucagon-like peptide 1.
3 changes in glucose, insulin, peptide YY, and glucagon-like peptide-1.
5 e cleavage site, renders peptides, including glucagon-like peptide-1 (7-36) amide (GLP-1) and six oth
10 enome editing to controllably release GLP-1 (glucagon-like peptide 1), a critical incretin that regul
12 by fusion of protease cleavable oligomers of glucagon-like peptide-1, a type-2 diabetes drug, and a t
13 together with the beneficial effects of the glucagon-like peptide-1 agonist exendin-4 in transgenic
14 odium-glucose cotransporter 2 inhibitors and glucagon-like peptide-1 agonists, and suggest how such d
15 e developed that were transfected to produce glucagon-like peptide-1, an incretin hormone with known
17 vestigate the neuroprotective effects of the glucagon-like peptide-1 analog exenatide in resuscitated
18 Here we examine the cardiac effects of the glucagon-like peptide-1 analog liraglutide in a model of
19 ation of beta-cells with an incretin hormone glucagon-like peptide-1 analog or with a fatty acid rece
22 The cardiovascular effects of semaglutide, a glucagon-like peptide 1 analogue with an extended half-l
23 The cardiovascular effect of liraglutide, a glucagon-like peptide 1 analogue, when added to standard
24 ontrolled trial that compared liraglutide, a glucagon-like peptide 1 analogue, with placebo in patien
25 trophy mice and further demonstrate that the glucagon-like peptide-1 analogue exendin-4, a well-toler
27 f target engagement for clinical trials with glucagon-like peptide-1 analogues in multiple system atr
29 with PS-CF and normal control subjects, and glucagon-like peptide 1 and gastric inhibitory polypepti
31 ed with lower glucose and ghrelin and higher glucagon-like peptide 1 and peptide tyrosine-tyrosine re
33 ther dose affected plasma ghrelin, glucagon, glucagon-like peptide 1 and peptide YY, or pyloric and d
34 rolonging the half-life of incretins such as glucagon-like peptide-1 and gastric inhibitory peptide,
35 ysiological effects of the incretin hormones glucagon-like peptide-1 and gastric inhibitory polypepti
36 ieved, not all participants had increases in glucagon-like peptide-1 and gastrin concentrations that
37 ates Ca(2+) , cAMP, and insulin responses to glucagon-like peptide-1 and its metabolites following il
39 ood glucose coefficient of variation for the glucagon-like peptide-1 and saline groups was 18.0% +/-
40 es of glucose, insulin, C-peptide, glucagon, glucagon-like peptides 1 and 2, gastric inhibitory pepti
41 y reports activation in response to insulin, glucagon-like peptide 1, and agents that raise cAMP leve
42 ve for either prolactin-releasing peptide or glucagon-like peptide 1, and attenuates the activation o
43 ut hormones, fibroblast growth factor 19 and glucagon-like peptide 1, and the BA transport systems, a
47 g, enhanced postprandial cholecystokinin and glucagon-like peptide 1 concentrations, and reduced ghre
49 lunted the body weight-lowering effects of a glucagon-like peptide-1-estrogen (GLP-1-estrogen) conjug
51 w focuses on two peptide drugs - insulin and glucagon-like peptide 1 (GLP-1) - for treatment of type
52 fy 37 T2D patients who were actively using a Glucagon-like peptide 1 (GLP-1) agonist in addition to a
57 ipeptidyl peptidase 4 (DPP-4) inhibitors and glucagon-like peptide 1 (GLP-1) analogues, can increase
59 peptide possessing balanced coagonism at the glucagon-like peptide 1 (GLP-1) and glucagon receptors c
62 herapeutic peptide hormone that combines the glucagon-like peptide 1 (GLP-1) and leptin via an IgG-Fc
63 sized that enteroendocrine L-cells producing glucagon-like peptide 1 (GLP-1) and peptide YY (PYY) may
64 ssed on enteroendocrine L cells that release glucagon-like peptide 1 (GLP-1) and peptide YY (PYY) whe
66 nsulin increased by 120% +/- 15% (P = 0.02), glucagon-like peptide 1 (GLP-1) by 60% +/- 20% (P < 0.01
67 ecretion of the prosurvival incretin hormone glucagon-like peptide 1 (GLP-1) by alpha cells and acts
80 armacological activation of the hypothalamic glucagon-like peptide 1 (GLP-1) receptor (GLP-1R) promot
83 al models of type 2 diabetes have shown that glucagon-like peptide 1 (GLP-1) receptor agonists preven
84 e-18]fluoro-levodopa [(18)F-DOPA] PET-CT and glucagon-like peptide 1 (GLP-1) receptor imaging), and d
88 gon released from pancreatic alpha cells and glucagon-like peptide 1 (GLP-1) released from intestinal
91 pendent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) secretion, on glucose lo
93 enhancing the action of the incretin hormone glucagon-like peptide 1 (GLP-1) therapeutically improve
97 proof-of-principle, the clinically relevant glucagon-like peptide 1 (GLP-1) was functionalized with
99 Upon a nutrient challenge, L cells produce glucagon-like peptide 1 (GLP-1), a powerful stimulant of
100 ty acids (FFAs), insulin, glucose, glucagon, glucagon-like peptide 1 (GLP-1), and gastric inhibitory
101 nificant elevations in postprandial insulin, glucagon-like peptide 1 (GLP-1), and glucagon coincident
102 in plasma cholecystokinin, peptide YY (PYY), glucagon-like peptide 1 (GLP-1), and glucagon-like pepti
103 poststimulation levels of glucose, insulin, glucagon-like peptide 1 (GLP-1), and glucose-dependent i
104 ) inhibitor that inhibits the degradation of glucagon-like peptide 1 (GLP-1), and has been approved f
105 kinin, gastric inhibitory polypeptide (GIP), glucagon-like peptide 1 (GLP-1), and peptide tyrosine ty
106 wn at regular intervals for cholecystokinin, glucagon-like peptide 1 (GLP-1), and peptide YY (PYY) an
107 been linked to the exaggerated secretion of glucagon-like peptide 1 (GLP-1), but causality has not b
108 elated to changes in blood peptide YY (PYY), glucagon-like peptide 1 (GLP-1), glucose, or insulin con
109 ing glucose, lipids (fasting only), insulin, glucagon-like peptide 1 (GLP-1), peptide YY (PYY), and g
111 RC1), general control nonrepressed 2 (GCN2), glucagon-like peptide 1 (GLP-1), peptide YY (PYY), serot
114 diabetes associated with the stimulation of glucagon-like peptide 1 (GLP-1), which is known to slow
115 erhans is enhanced by the intestinal hormone glucagon-like peptide 1 (GLP-1), which is secreted from
117 S) in the circulation and thereby stimulates glucagon-like peptide 1 (GLP-1)-mediated insulin secreti
119 studies in subjects with diabetes receiving glucagon-like peptide 1 (GLP-1)-targeted therapies have
130 dipeptidyl peptidase-4 (DPP4) inhibitors and glucagon-like peptide-1 (GLP-1) analogs, are important n
131 ed the efficacy and safety of semaglutide, a glucagon-like peptide-1 (GLP-1) analogue in clinical dev
133 al insulin analogue insulin degludec and the glucagon-like peptide-1 (GLP-1) analogue liraglutide has
137 ate the anorectic effects of both endogenous glucagon-like peptide-1 (GLP-1) and exogenous GLP-1 rece
138 creting glucagon, insulin, and the incretins glucagon-like peptide-1 (GLP-1) and GIP (glucose-depende
140 esponses to glucose and to incretins such as glucagon-like peptide-1 (GLP-1) and glucose-dependent in
141 , Tukey's post hoc, P < 0.05]; and increased glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) com
142 e of enteroendocrine L-cell derived hormones glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) in
143 elease of gastrointestinal peptides, such as glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), fr
145 circulating glucose, insulin, glucagon, and glucagon-like peptide-1 (GLP-1) concentrations and subje
152 In this study, we focused on the function of glucagon-like peptide-1 (GLP-1) in initial responses to
153 Pharmacological evidence suggests a role for glucagon-like peptide-1 (GLP-1) in modulating stress res
154 e acid synthesis and intestinal secretion of glucagon-like peptide-1 (GLP-1) in wild-type, Fxr(-/-),
160 ic polypeptide (GIP) is glucagonotropic, and glucagon-like peptide-1 (GLP-1) is glucagonostatic.
164 The multiple physiological properties of glucagon-like peptide-1 (GLP-1) make it a promising drug
167 impaired; this impairment is ameliorated by glucagon-like peptide-1 (GLP-1) or by GLP-1 receptor ago
175 table therapy, clinicians can choose between glucagon-like peptide-1 (GLP-1) receptor agonists and ba
176 New drugs for the treatment of diabetes, glucagon-like peptide-1 (GLP-1) receptor agonists and in
186 Recent evidence indicates that activation of glucagon-like peptide-1 (GLP-1) receptors in the ventral
189 oid these systemic effects while stimulating glucagon-like peptide-1 (GLP-1) secreting enteroendocrin
190 021 to be an especially potent stimulator of glucagon-like peptide-1 (GLP-1) secretion in vitro.
195 an 11-residue analogue of the N-terminus of glucagon-like peptide-1 (GLP-1) to investigate effects o
197 ecystokinin (CCK); peptide YY3-36 (PYY3-36); glucagon-like peptide-1 (GLP-1)) excite vagal afferent n
198 , we use the validated diabetes therapeutic, glucagon-like peptide-1 (GLP-1), and the target of clini
199 hormones, such as cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1), are released following
200 -dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), cholecystokinin (CCK) a
201 We measured tastant-dependent secretion of glucagon-like peptide-1 (GLP-1), glucagon, and neuropept
202 lucose, plasma insulin, C-peptide, glucagon, glucagon-like peptide-1 (GLP-1), glucose-dependent insul
203 bolically-related peptide hormone receptors: glucagon-like peptide-1 (GLP-1), glucose-dependent insul
205 lowering effects of a gut-released hormone, glucagon-like peptide-1 (GLP-1), has been reported in th
206 tropyloroduodenal motility, cholecystokinin, glucagon-like peptide-1 (GLP-1), insulin, glucagon, bloo
213 haracterization, and clinical development of glucagon-like-peptide-1 (GLP-1) spans more than 30 years
214 rs prevent degradation of incretin hormones (glucagon-like peptide 1 [GLP-1] and glucose-dependent in
218 oss-reactivity with related peptides such as glucagon-like peptide-1, glucagon-like peptide-2, gastri
219 , we investigated the effects of G49, a dual glucagon-like peptide-1/glucagon receptor agonist, on NA
221 se-dependent insulinotropic polypeptide, and glucagon-like peptide 1), glucose, and multiple AAs, inc
222 nsional ultrasound), plasma cholecystokinin, glucagon-like peptide 1, glucose-dependent insulinotropi
223 ood glucose ranged from 7.2% to 30.4% in the glucagon-like peptide-1 group and from 19.8% to 56.8% in
225 mmol/L) in both groups were low (one in the glucagon-like peptide-1 group, three in the saline group
226 n of a long-acting analog of the gut-hormone glucagon-like peptide-1 highlights the therapeutic poten
228 h plasma concentrations of acylated ghrelin, glucagon-like peptide 1, insulin, glucose, and nonesteri
230 entrations of total ghrelin, peptide YY, and glucagon-like peptide-1, leptin, adiponectin, expired 13
231 ulted in elevated C-peptide levels, elevated glucagon like peptide-1 levels and a reduction in dipept
232 in human beta-cells, using forskolin or the glucagon-like peptide 1 mimetic Exendin-4, inhibits the
233 eceptor activation, whereas responses to the glucagon-like peptide-1 or the glucagon-like peptide-1 r
234 rs in hippocampal neurons to reduce (leptin, glucagon-like peptide-1) or increase (ghrelin) food inta
235 eptide ligands, including endogenous ligands glucagon-like peptide-1, oxyntomodulin, and the clinical
237 igher early postprandial cholecystokinin and glucagon-like peptide 1 peaks than did the other partici
238 l motility, plasma ghrelin, cholecystokinin, glucagon-like peptide 1, peptide YY, insulin, glucagon,
243 abetic C57BL/6J mice treated with either the glucagon-like peptide 1 receptor (GLP-1R) agonist liragl
245 like peptide-1 (GLP-1) signaling through the glucagon-like peptide 1 receptor (GLP-1R) is a key regul
247 und that exendin-4 (Ex-4), an agonist of the glucagon-like peptide 1 receptor (GLP-1R), stimulates hu
248 ron oxide-based nanoparticle probe targeting glucagon-like peptide 1 receptor (GLP-1R), which is high
251 ctivities of NRTN relative to liraglutide, a glucagon-like peptide 1 receptor agonist, in Zucker diab
252 cagon was elevated, and cells expressing the glucagon-like peptide 1 receptor were more abundant in R
255 ffects of LiCl appear to be mediated through glucagon-like peptide-1 receptor (GLP-1R) activation, we
258 ble incretin mimetic based upon the specific glucagon-like peptide-1 receptor (GLP-1R) agonist liragl
263 Therapeutic intervention to activate the glucagon-like peptide-1 receptor (GLP-1R) enhances gluco
264 We have shown previously that the incretin glucagon-like peptide-1 receptor (GLP-1R) internalizes f
268 first orally bioavailable and CNS penetrant glucagon-like peptide-1 receptor (GLP-1R) noncompetitive
269 tivated positive allosteric modulator of the glucagon-like peptide-1 receptor (GLP-1R), a class B GPC
270 f intraduodenal metformin, and both duodenal glucagon-like peptide-1 receptor (Glp-1r)-protein kinase
272 mpare the efficacy and safety of long-acting glucagon-like peptide-1 receptor agonist dulaglutide wit
273 ponses to the glucagon-like peptide-1 or the glucagon-like peptide-1 receptor agonist exendin-4 were
274 smotic pump to give continuous delivery of a glucagon-like peptide-1 receptor agonist for 6-12 months
277 ons in the dipeptidyl peptidase-4 inhibitor, glucagon-like peptide-1 receptor agonist, and sodium-glu
283 f dipeptidyl peptidase-4 inhibitors and some glucagon-like peptide-1 receptor agonists, at least in t
285 CT in combination with CT (SPECT/CT) with a glucagon-like peptide-1 receptor avid radiotracer, and c
287 in vivo We further demonstrate that an ileal glucagon-like peptide-1 receptor-dependent neuronal netw
289 tidyl-peptidase 4-inhibitor sitagliptin, the glucagon-like peptide 1-receptor agonist lixisenatide ba
290 We assessed the effects of lixisenatide, a glucagon-like peptide 1-receptor agonist, on cardiovascu
292 In nonfasted rats, central antagonism of glucagon-like peptide 1 receptors partially mimics the e
295 urgery, beta-cell function, weight loss, and glucagon-like peptide 1 response were all predictors of
296 e/isoleucine, methionine, phenylalanine, and glucagon-like peptide 1 response were associated with ch
297 ly reported for LCFAs, including stimulating glucagon-like peptide-1 secretion from enteroendocrine c
299 that the addition of continuous infusion of glucagon-like peptide-1 to intensive insulin therapy wou
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