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1 mentation of fibroblast growth factor 21 and glucagon-like peptide 1.
2 eased gastric volume capacity and release of glucagon-like peptide 1.
3 d improved glucose tolerance, dependent upon glucagon-like peptide 1.
4 changes in glucose, insulin, peptide YY, and glucagon-like peptide-1.
5 11%, P = 0.002), NEFA (-21%, P = 0.009), and glucagon-like peptide 1 (-31%, P = 0.001) areas under th
6 enome editing to controllably release GLP-1 (glucagon-like peptide 1), a critical incretin that regul
7 together with the beneficial effects of the glucagon-like peptide-1 agonist exendin-4 in transgenic
8 odium-glucose cotransporter 2 inhibitors and glucagon-like peptide-1 agonists, and suggest how such d
9 vestigate the neuroprotective effects of the glucagon-like peptide-1 analog exenatide in resuscitated
11 The cardiovascular effects of semaglutide, a glucagon-like peptide 1 analogue with an extended half-l
12 The cardiovascular effect of liraglutide, a glucagon-like peptide 1 analogue, when added to standard
13 ontrolled trial that compared liraglutide, a glucagon-like peptide 1 analogue, with placebo in patien
14 trophy mice and further demonstrate that the glucagon-like peptide-1 analogue exendin-4, a well-toler
17 f target engagement for clinical trials with glucagon-like peptide-1 analogues in multiple system atr
18 ulation of cells expressing the precursor of glucagon-like peptide 1 and are glutamatergic; able to m
19 with PS-CF and normal control subjects, and glucagon-like peptide 1 and gastric inhibitory polypepti
23 ocrine cells (EECs) produce hormones such as glucagon-like peptide 1 and peptide YY that regulate foo
25 ther dose affected plasma ghrelin, glucagon, glucagon-like peptide 1 and peptide YY, or pyloric and d
26 rolonging the half-life of incretins such as glucagon-like peptide-1 and gastric inhibitory peptide,
27 ates Ca(2+) , cAMP, and insulin responses to glucagon-like peptide-1 and its metabolites following il
28 es of glucose, insulin, C-peptide, glucagon, glucagon-like peptides 1 and 2, gastric inhibitory pepti
29 y reports activation in response to insulin, glucagon-like peptide 1, and agents that raise cAMP leve
30 ve for either prolactin-releasing peptide or glucagon-like peptide 1, and attenuates the activation o
31 onists, including ADP, arginine vasopressin, glucagon-like peptide 1, and forskolin, and, surprisingl
32 ut hormones, fibroblast growth factor 19 and glucagon-like peptide 1, and the BA transport systems, a
33 , insulin, C-peptide, and incretin hormones; glucagon-like peptide-1; and glucose-dependent insulinot
36 of 14.6% +/- 2.6% and elevated postprandial glucagon-like peptide 1 compared with controls (49.2 +/-
37 g, enhanced postprandial cholecystokinin and glucagon-like peptide 1 concentrations, and reduced ghre
38 lunted the body weight-lowering effects of a glucagon-like peptide-1-estrogen (GLP-1-estrogen) conjug
40 w focuses on two peptide drugs - insulin and glucagon-like peptide 1 (GLP-1) - for treatment of type
41 fy 37 T2D patients who were actively using a Glucagon-like peptide 1 (GLP-1) agonist in addition to a
45 ipeptidyl peptidase 4 (DPP-4) inhibitors and glucagon-like peptide 1 (GLP-1) analogues, can increase
50 sized that enteroendocrine L-cells producing glucagon-like peptide 1 (GLP-1) and peptide YY (PYY) may
51 ssed on enteroendocrine L cells that release glucagon-like peptide 1 (GLP-1) and peptide YY (PYY) whe
53 pendent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are secreted postprandia
54 nsulin increased by 120% +/- 15% (P = 0.02), glucagon-like peptide 1 (GLP-1) by 60% +/- 20% (P < 0.01
55 ecretion of the prosurvival incretin hormone glucagon-like peptide 1 (GLP-1) by alpha cells and acts
63 e-dependent insulinotropic peptide (GIP) and glucagon-like peptide 1 (GLP-1) is characterized by thei
71 armacological activation of the hypothalamic glucagon-like peptide 1 (GLP-1) receptor (GLP-1R) promot
75 al models of type 2 diabetes have shown that glucagon-like peptide 1 (GLP-1) receptor agonists preven
76 e-18]fluoro-levodopa [(18)F-DOPA] PET-CT and glucagon-like peptide 1 (GLP-1) receptor imaging), and d
80 gon released from pancreatic alpha cells and glucagon-like peptide 1 (GLP-1) released from intestinal
81 proposed pathway was not influenced by local glucagon-like peptide 1 (GLP-1) secretion from alpha-cel
85 enhancing the action of the incretin hormone glucagon-like peptide 1 (GLP-1) therapeutically improve
87 proof-of-principle, the clinically relevant glucagon-like peptide 1 (GLP-1) was functionalized with
90 ty acids (FFAs), insulin, glucose, glucagon, glucagon-like peptide 1 (GLP-1), and gastric inhibitory
91 in plasma cholecystokinin, peptide YY (PYY), glucagon-like peptide 1 (GLP-1), and glucagon-like pepti
92 ) inhibitor that inhibits the degradation of glucagon-like peptide 1 (GLP-1), and has been approved f
93 peptide YY3-36 (PYY3-36), lithium chloride, glucagon-like peptide 1 (GLP-1), and leptin shows the pr
94 kinin, gastric inhibitory polypeptide (GIP), glucagon-like peptide 1 (GLP-1), and peptide tyrosine ty
95 wn at regular intervals for cholecystokinin, glucagon-like peptide 1 (GLP-1), and peptide YY (PYY) an
96 elated to changes in blood peptide YY (PYY), glucagon-like peptide 1 (GLP-1), glucose, or insulin con
97 ing glucose, lipids (fasting only), insulin, glucagon-like peptide 1 (GLP-1), peptide YY (PYY), and g
99 RC1), general control nonrepressed 2 (GCN2), glucagon-like peptide 1 (GLP-1), peptide YY (PYY), serot
101 diabetes associated with the stimulation of glucagon-like peptide 1 (GLP-1), which is known to slow
102 erhans is enhanced by the intestinal hormone glucagon-like peptide 1 (GLP-1), which is secreted from
104 S) in the circulation and thereby stimulates glucagon-like peptide 1 (GLP-1)-mediated insulin secreti
106 studies in subjects with diabetes receiving glucagon-like peptide 1 (GLP-1)-targeted therapies have
111 (OR 0.68, 95% CI 0.58-0.79; p < 0.001), and glucagon-like peptide-1 (GLP-1) agonists (OR 0.37, 95% C
113 dipeptidyl peptidase-4 (DPP4) inhibitors and glucagon-like peptide-1 (GLP-1) analogs, are important n
115 ed the efficacy and safety of semaglutide, a glucagon-like peptide-1 (GLP-1) analogue in clinical dev
120 ate the anorectic effects of both endogenous glucagon-like peptide-1 (GLP-1) and exogenous GLP-1 rece
121 creting glucagon, insulin, and the incretins glucagon-like peptide-1 (GLP-1) and GIP (glucose-depende
123 , Tukey's post hoc, P < 0.05]; and increased glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) com
124 e of enteroendocrine L-cell derived hormones glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) in
125 elease of gastrointestinal peptides, such as glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), fr
126 lation to two clinically important peptides: glucagon-like peptide-1 (GLP-1) and the parathyroid horm
127 circulating glucose, insulin, glucagon, and glucagon-like peptide-1 (GLP-1) concentrations and subje
128 d plasma cholecystokinin (CCK), ghrelin, and glucagon-like peptide-1 (GLP-1) concentrations, appetite
132 The interaction between serotonin (5-HT) and glucagon-like peptide-1 (GLP-1) could play a role as ups
134 In this study, we focused on the function of glucagon-like peptide-1 (GLP-1) in initial responses to
135 Pharmacological evidence suggests a role for glucagon-like peptide-1 (GLP-1) in modulating stress res
136 e acid synthesis and intestinal secretion of glucagon-like peptide-1 (GLP-1) in wild-type, Fxr(-/-),
140 ic polypeptide (GIP) is glucagonotropic, and glucagon-like peptide-1 (GLP-1) is glucagonostatic.
142 The multiple physiological properties of glucagon-like peptide-1 (GLP-1) make it a promising drug
145 impaired; this impairment is ameliorated by glucagon-like peptide-1 (GLP-1) or by GLP-1 receptor ago
152 maglutide is the first oral formulation of a glucagon-like peptide-1 (GLP-1) receptor agonist develop
153 d to investigate the association between the glucagon-like peptide-1 (GLP-1) receptor agonist dulaglu
157 exposed to thiazolidinediones (glitazones), glucagon-like peptide-1 (GLP-1) receptor agonists and di
158 New drugs for the treatment of diabetes, glucagon-like peptide-1 (GLP-1) receptor agonists and in
165 body of preclinical evidence indicates that glucagon-like peptide-1 (GLP-1) receptor agonists reduce
170 rlap between signaling and regulation of the glucagon-like peptide-1 (GLP-1) receptor by the non-pept
173 Recent evidence indicates that activation of glucagon-like peptide-1 (GLP-1) receptors in the ventral
175 oid these systemic effects while stimulating glucagon-like peptide-1 (GLP-1) secreting enteroendocrin
176 021 to be an especially potent stimulator of glucagon-like peptide-1 (GLP-1) secretion in vitro.
177 etate and early-phase insulin, C-peptide and glucagon-like peptide-1 (GLP-1) secretion were increased
181 an 11-residue analogue of the N-terminus of glucagon-like peptide-1 (GLP-1) to investigate effects o
182 lasma levels of insulin, leptin, amylin, and glucagon-like peptide-1 (GLP-1) were assessed using Lumi
183 CK in enteroendocrine cells (EECs) that were glucagon-like peptide-1 (GLP-1)(+)/Peptide YY (PYY(-)) i
184 for their production of the incretin hormone glucagon-like peptide-1 (GLP-1), also release other neur
186 , we use the validated diabetes therapeutic, glucagon-like peptide-1 (GLP-1), and the target of clini
187 hormones, such as cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1), are released following
188 lucose, plasma insulin, C-peptide, glucagon, glucagon-like peptide-1 (GLP-1), glucose-dependent insul
189 bolically-related peptide hormone receptors: glucagon-like peptide-1 (GLP-1), glucose-dependent insul
190 FAs and 2-OG, on enteroendocrine secretions [glucagon-like peptide-1 (GLP-1), glucose-dependent insul
192 on of glucose-regulating hormones, including glucagon-like peptide-1 (GLP-1), peptide YY (PYY), and i
193 ll-bowel motility, other MRI parameters, and glucagon-like peptide-1 (GLP-1), polypeptide YY (PYY), a
195 ed receptors (GPCRs) for glucagon (GluR) and glucagon-like peptide-1 (GLP-1R) are normally considered
196 haracterization, and clinical development of glucagon-like-peptide-1 (GLP-1) spans more than 30 years
197 Here, we investigated whether amylin- and glucagon-like-peptide-1 (GLP-1)-based combination therap
198 , dipeptidyl peptidase 4 [DPP-4] inhibitors, glucagon-like peptide 1 [GLP-1] receptor agonists, and s
199 ite-related hormones (active ghrelin, active glucagon-like peptide 1 [GLP-1], total peptide YY [PYY],
200 tus and obesity, exemplified by the licensed glucagon-like peptide 1 (GLP1) mimetics and dipeptidyl p
203 visceral or cognitive threats that increase glucagon-like peptide-1 (GLP1) signaling from the caudal
204 , we investigated the effects of G49, a dual glucagon-like peptide-1/glucagon receptor agonist, on NA
206 nsional ultrasound), plasma cholecystokinin, glucagon-like peptide 1, glucose-dependent insulinotropi
207 n of a long-acting analog of the gut-hormone glucagon-like peptide-1 highlights the therapeutic poten
209 h plasma concentrations of acylated ghrelin, glucagon-like peptide 1, insulin, glucose, and nonesteri
210 in human beta-cells, using forskolin or the glucagon-like peptide 1 mimetic Exendin-4, inhibits the
211 Strikingly, when P-NT was combined with the glucagon-like peptide 1 mimetic liraglutide, the two pep
212 eceptor activation, whereas responses to the glucagon-like peptide-1 or the glucagon-like peptide-1 r
213 rs in hippocampal neurons to reduce (leptin, glucagon-like peptide-1) or increase (ghrelin) food inta
215 igher early postprandial cholecystokinin and glucagon-like peptide 1 peaks than did the other partici
216 accompanied by higher secretion of insulin, glucagon-like peptide 1, peptide YY, and cholecystokinin
217 l motility, plasma ghrelin, cholecystokinin, glucagon-like peptide 1, peptide YY, insulin, glucagon,
219 nt research has indicated a crucial role for glucagon-like peptide-1-producing preproglucagon (PPG) n
220 us of the solitary tract (cNTS) that produce glucagon-like peptide-1; published work in rodents indic
221 udy assessing the occupancy of the dual GCGR/glucagon like peptide-1 receptor agonist SAR425899.
223 icacy and ability to reduce the body weight, glucagon-like peptide 1 receptor (GLP-1R) agonism has em
224 abetic C57BL/6J mice treated with either the glucagon-like peptide 1 receptor (GLP-1R) agonist liragl
230 like peptide-1 (GLP-1) signaling through the glucagon-like peptide 1 receptor (GLP-1R) is a key regul
232 und that exendin-4 (Ex-4), an agonist of the glucagon-like peptide 1 receptor (GLP-1R), stimulates hu
235 ering glucose, incretin drugs, which include glucagon-like peptide 1 receptor (GLP1R) agonists and di
237 treatment with thiazolidinedione therapy or glucagon-like peptide 1 receptor agonism alone or in com
239 ctivities of NRTN relative to liraglutide, a glucagon-like peptide 1 receptor agonist, in Zucker diab
241 odium glucose cotransporter 2 inhibitors and glucagon-like peptide 1 receptor agonists have consisten
243 ffects of LiCl appear to be mediated through glucagon-like peptide-1 receptor (GLP-1R) activation, we
246 ble incretin mimetic based upon the specific glucagon-like peptide-1 receptor (GLP-1R) agonist liragl
251 Therapeutic intervention to activate the glucagon-like peptide-1 receptor (GLP-1R) enhances gluco
252 We have shown previously that the incretin glucagon-like peptide-1 receptor (GLP-1R) internalizes f
256 first orally bioavailable and CNS penetrant glucagon-like peptide-1 receptor (GLP-1R) noncompetitive
257 tivated positive allosteric modulator of the glucagon-like peptide-1 receptor (GLP-1R), a class B GPC
259 f intraduodenal metformin, and both duodenal glucagon-like peptide-1 receptor (Glp-1r)-protein kinase
263 mpare the efficacy and safety of long-acting glucagon-like peptide-1 receptor agonist dulaglutide wit
264 ponses to the glucagon-like peptide-1 or the glucagon-like peptide-1 receptor agonist exendin-4 were
265 smotic pump to give continuous delivery of a glucagon-like peptide-1 receptor agonist for 6-12 months
268 e available for the subcutaneous form of the glucagon-like peptide-1 receptor agonist semaglutide but
269 we evaluated the efficacy of a short-course glucagon-like peptide-1 receptor agonist therapy-specifi
270 als, including cholecystokinin, exendin-4 (a glucagon-like peptide-1 receptor agonist), amylin, and m
272 ons in the dipeptidyl peptidase-4 inhibitor, glucagon-like peptide-1 receptor agonist, and sodium-glu
274 lucose-lowering medication occurred, and for glucagon-like peptide-1 receptor agonists (GLP-1 RAs; 3.
277 However, the distinction may be crucial for glucagon-like peptide-1 receptor agonists and other anti
278 es and consensus statements have recommended glucagon-like peptide-1 receptor agonists and sodium-glu
280 Indeed, in several of the new statements, glucagon-like peptide-1 receptor agonists are suggested
282 to dramatic weight loss in combination with glucagon-like peptide-1 receptor agonists in preclinical
286 f dipeptidyl peptidase-4 inhibitors and some glucagon-like peptide-1 receptor agonists, at least in t
287 to micelles, and these micelles activate the glucagon-like peptide-1 receptor with a potency comparab
288 in vivo We further demonstrate that an ileal glucagon-like peptide-1 receptor-dependent neuronal netw
289 ucose cotransporter 2) inhibitors and GLP-1 (glucagon-like peptide-1) receptor agonists, has changed
290 tidyl-peptidase 4-inhibitor sitagliptin, the glucagon-like peptide 1-receptor agonist lixisenatide ba
291 We assessed the effects of lixisenatide, a glucagon-like peptide 1-receptor agonist, on cardiovascu
292 e effects of once-weekly exenatide (a GLP-1 [glucagon-like peptide-1] receptor agonist) versus placeb
294 In nonfasted rats, central antagonism of glucagon-like peptide 1 receptors partially mimics the e
296 l literature suggests that targeting central glucagon-like peptide-1 receptors (GLP-1Rs) may represen
297 us of the stria terminalis (alBST) expresses glucagon-like peptide-1 receptors (GLP1Rs) and receives
299 ntragastric infusion test sessions), whereas glucagon-like peptide 1 responses to milkshake intake we