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1 GLP-1 decreases Kv1.3 channel contribution to outward cu
2 GLP-1 effects are mediated through binding to the GLP-1
3 GLP-1 induction from engineered mouse cells grafted onto
4 GLP-1 is capable of regulating the blood glucose level b
5 GLP-1 is produced by cells that express proglucagon (GCG
6 GLP-1 neurons may therefore serve as 'satiety sensors' f
7 GLP-1 peptide agonists are efficacious drugs for the tre
8 GLP-1 receptor agonists have a favourable risk-benefit b
9 GLP-1 signalling occurs in the brain; using a newly deve
12 -4 is a long acting glucagon-like peptide 1 (GLP-1) analogue that is an agonist for the GLP-1 recepto
13 l activation of the glucagon-like peptide 1 (GLP-1) and glucagon receptor has the potential to lead t
14 53 increased plasma glucagon-like peptide 1 (GLP-1) and insulin levels and improved glucose tolerance
16 al incretin hormone glucagon-like peptide 1 (GLP-1) by alpha cells and acts directly on beta cells to
17 osis of the hormone glucagon-like peptide 1 (GLP-1) by the intestinal L cell is essential for the inc
19 utic engineering of glucagon-like peptide 1 (GLP-1) has enabled development of new medicines to treat
22 gut hormone called glucagon-like peptide 1 (GLP-1) is a strong moderator of energy homeostasis and c
24 logic properties of glucagon-like peptide 1 (GLP-1) make it a potent candidate drug target in the tre
25 iated the effect of glucagon-like peptide 1 (GLP-1) on glucose-induced insulin secretion, which could
27 of the hypothalamic glucagon-like peptide 1 (GLP-1) receptor (GLP-1R) promotes weight loss and improv
30 )F-DOPA] PET-CT and glucagon-like peptide 1 (GLP-1) receptor imaging), and development of novel medic
33 the hypothesis that glucagon-like peptide 1 (GLP-1) therapies improve cardiac contractile function at
34 clinically relevant glucagon-like peptide 1 (GLP-1) was functionalized with diflunisal, indomethacin,
35 the degradation of glucagon-like peptide 1 (GLP-1), and has been approved for the treatment of type
36 polypeptide (GIP), glucagon-like peptide 1 (GLP-1), and peptide tyrosine tyrosine (PYY)] were measur
39 the stimulation of glucagon-like peptide 1 (GLP-1), which is known to slow gastric emptying, stimula
41 thereby stimulates glucagon-like peptide 1 (GLP-1)-mediated insulin secretion by upregulating interl
42 resent evidence for glucagon-like peptide 1 (GLP-1)-mediated paraventricular hypothalamic circuit coo
46 PP4) inhibitors and glucagon-like peptide-1 (GLP-1) analogs, are important new classes of therapy for
47 y of semaglutide, a glucagon-like peptide-1 (GLP-1) analogue in clinical development, compared with i
48 Semaglutide is a glucagon-like peptide-1 (GLP-1) analogue in phase 3 development for type 2 diabet
50 of both endogenous glucagon-like peptide-1 (GLP-1) and exogenous GLP-1 receptor (GLP-1R) agonists ar
51 , and the incretins glucagon-like peptide-1 (GLP-1) and GIP (glucose-dependent insulinotropic polypep
52 .05]; and increased glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) compared with all other trea
53 ll derived hormones glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) in vitro from mouse and huma
54 l peptides, such as glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), from enteroendocrine cells
55 gical properties of glucagon-like peptide-1 (GLP-1) ensure that it is a promising drug candidate for
58 nicotine activates glucagon-like peptide-1 (GLP-1) neurons in the nucleus tractus solitarius (NTS).
60 Exendin-4 (EX-4), a glucagon-like peptide-1 (GLP-1) receptor agonist, has been shown to reduce food i
68 s while stimulating glucagon-like peptide-1 (GLP-1) secreting enteroendocrine L-cells, we have design
70 ical development of glucagon-like-peptide-1 (GLP-1) spans more than 30 years and includes contributio
72 abetes therapeutic, glucagon-like peptide-1 (GLP-1), and the target of clinical investigation, gastri
73 recombinant microbial delivery vector for a GLP-1 analogue and assess the efficacy of the therapeuti
75 rk, we show that lipid conjugated forms of a GLP-1/GIP/glucagon hybrid peptides stay in circulation f
77 d the safety and efficacy of the long-acting GLP-1 analogue, liraglutide, in patients with non-alcoho
80 that systemic infusion of cocaine activates GLP-1-expressing neurons in the nucleus tractus solitari
81 latory nodes synergistically elevated active GLP-1 to unprecedented concentrations ( approximately 30
84 on-like peptide 1 (GLP-1) receptor agonists (GLP-1-RAs) act on multiple tissues, in addition to the p
85 ndings show cardiovascular safety across all GLP-1 receptor agonist cardiovascular outcome trials and
88 y (2.4 +/- 0.2-fold increase, P < 0.01), and GLP-1 peak increased 3.8 +/- 0.6-, 4.7 +/- 0.8-, and 4.4
89 racellular Ca(2+) levels, cAMP activity, and GLP-1 secretion and improved glucose and lipid metabolis
95 ctreotide formulations, mTOR inhibitors, and GLP-1 receptor antagonists) and surgical therapies (eg,
97 ovements in delivery methods for insulin and GLP-1 receptor agonists are paving the way towards bette
103 y comparable to liraglutide, an antidiabetic GLP-1 analogue that carries a long-chain fatty acid.
105 imilar safety profile to currently available GLP-1 receptor agonists, representing a potential treatm
107 findings support a circuit whereby brainstem GLP-1 activates PVN signaling to mount an appropriate wh
113 tricle, we highlight a population of central GLP-1 receptors rostral to the hindbrain that are involv
116 y contribute to the mediation of gut-derived GLP-1's effects on food intake, energy homeostasis, and
117 pharmacokinetic investigations of a divalent GLP-1 analogue demonstrated a promising gain in circulat
123 istration of the plasmid DNA (pDNA) encoding GLP-1 decreased diabetic glucose levels to the normoglyc
125 VANs in mediating the effects of endogenous GLP-1 on food intake and glycemia and may promote the fu
128 istochemical analyses reveal that endogenous GLP-1 axons form close synaptic apposition with NTS astr
131 nsufficient to depolarize the cell and evoke GLP-1 secretion in the model, suggesting a crucial role
132 lucagon-like peptide-1 (GLP-1) and exogenous GLP-1 receptor (GLP-1R) agonists are an active area of i
135 R2.60(190) was predicted to be important for GLP-1- and exendin-4-, but not oxyntomodulin-mediated cA
137 ng, role of GLUT2 and glucose metabolism for GLP-1 secretion via an amplifying pathway that increases
138 tonin as a new critical neural substrate for GLP-1 impact on energy homeostasis and expands the curre
139 of insulin, glucagon, cholecystokinin, GIP, GLP-1, and PYY, and an increase in total energy intake (
140 r both), but neither dose affected glucagon, GLP-1, GIP, cholecystokinin, gastric emptying, or energy
143 ulin exocytosis under conditions of glucose, GLP-1, or KCl stimulation through a role in modulating i
144 under the curve for the satiety gut hormone GLP-1 was significantly increased from 10 days postopera
146 prolong the action of the incretin hormones, GLP-1 and glucose-dependent insulinotropic polypeptide (
152 he pKa values of all the ionizable groups in GLP-1 suggest it is the protonation/deprotonation of the
156 pathways can be engaged to robustly increase GLP-1 without invasive surgical or injection regimens.
158 ation phase, LQT2 patients display increased GLP-1, GIP, and insulin secretion and defective glucagon
159 Glucose infusion to the ileum increased GLP-1 and PYY secretion, suppressed aspects of VAS-rated
160 ion of circulating ghrelin levels, increased GLP-1 plasma concentration, and remodeling of gut microb
163 strated a 63% reduction in forskolin-induced GLP-1 release in vitro (P < 0.001) and a 23% reduction i
166 ugs sitagliptin and exenatide, which inhibit GLP-1 breakdown and stimulate GLP-1 receptors, respectiv
167 e-specific IL-6 signaling induces intestinal GLP-1 release to enhance insulin secretion, thereby coun
169 ort the crystal structure of the full-length GLP-1 receptor bound to a truncated peptide agonist.
171 t-friendly alternative to currently marketed GLP-1 injectables and can likely be extended to other pe
176 al mechanisms by which cocaine activates NTS GLP-1-expressing neurons, we microinjected corticosteron
177 gs indicate that increased activation of NTS GLP-1-expressing neurons by corticosterone may represent
178 e show dependence of paraventricular nucleus GLP-1 signaling in the coordination of neuroendocrine, a
179 beta-cell models and blocked the ability of GLP-1 agonists and the depolarizing agent KCl to potenti
180 This might be of relevance for the action of GLP-1 mimetics now widely used in the treatment of diabe
181 ht into the molecular mechanism of action of GLP-1 peptides, here we report the crystal structure of
185 achieved by engineering synthetic analogs of GLP-1 or the more stable exogenous GLP-1R agonist exendi
186 sformed to express a long-acting analogue of GLP-1 or the isogenic control microbe which solely harbo
188 imental findings establishing the biology of GLP-1 as an insulin-stimulating glucoregulatory hormone.
189 1) to examine the expression and content of GLP-1 receptor (GLP-1R) in human and db/db mice retinas;
191 e of non-viral vector based oral delivery of GLP-1 gene through enterohepatic recycling pathways of b
194 als that assessed the safety and efficacy of GLP-1 receptor agonists compared with placebo in adult p
195 amino acid glutamine is a potent elicitor of GLP-1 secretion, the responsible mechanism remains uncle
196 hoton microscopy revealed that exocytosis of GLP-1 is biphasic, with a first peak at 1-6 min and a se
200 tor 5 antagonist, which blunts inhibition of GLP-1 release, and agonists for TGR5 and GPR40, which st
202 y, four trials of cardiovascular outcomes of GLP-1 receptor agonists were identified: ELIXA (lixisena
204 peptides combining the N-terminal portion of GLP-1 or Ex-4 and the C-terminal segment of the helix-pr
206 ters can induce Ca(2+) influx and release of GLP-1 as a result of electrical activity, while glucose
207 c or regulate propionate-mediated release of GLP-1 from mouse colonic preparations defined this physi
211 tcome trials showed cardiovascular safety of GLP-1 receptor agonists, but results for cardiovascular
213 olitarius (NTS), the major central source of GLP-1, with the other nuclei in the midbrain and forebra
216 tide hormones share the overall structure of GLP-1 and Ex-4, with a C-terminal helical segment and a
220 effects of 5 wk of resveratrol treatment on GLP-1 secretion, gastric emptying, and glycemic control
222 decreased hepatic glucose production, other GLP-1-associated effects were not observed - e.g., activ
223 ests that agonists of glucagon-like peptide (GLP-1) receptor exert neuroprotective and neurorestorati
224 e of the gut hormone, glucagon-like peptide (GLP-1), in deep short axon cells (Cajal cells) of the ol
229 eased serum insulin, serum C-peptide, plasma GLP-1, and plasma GIP responses (P=0.03-0.001) and decre
236 xr(-/-) and Tgr5(-/-) mice exhibited reduced GLP-1 secretion, which was stimulated by INT-767 in the
239 x(9-39)NH2, were compared with the reference GLP-1 receptor agonist [Nle(14),Lys(40)(Ahx-DOTA-(68)Ga)
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 mia-induced PC1 expression thereby releasing GLP-1, which in turn increases beta cell mass and functi
243 dependence prevents hypoglycemia, rendering GLP-1 analogs a useful and safe treatment modality in ty
244 issue specimens, we showed a dose-responsive GLP-1 secretion in the ileum at >/=200 mmol/L glucose.
245 glucagon were engineered into the selective GLP-1 receptor agonist exendin-4, resulting in hybrid pe
246 e peptide-1 (GLP-1) action through selective GLP-1 receptor (GLP-1R) agonism or by prevention of enzy
247 s first applied as drug carrier to stabilize GLP-1 against protease degradation by forming a cavity.
248 which inhibit GLP-1 breakdown and stimulate GLP-1 receptors, respectively, decreased nicotine intake
249 Ca(2+) levels and cAMP activity to stimulate GLP-1 secretion and improve hepatic glucose and lipid me
250 agonists for TGR5 and GPR40, which stimulate GLP-1 secretion, were investigated alone and in combinat
253 d a 23% reduction in oral glucose-stimulated GLP-1 secretion (P < 0.05) in association with impairmen
256 When added to metformin and sulfonylurea, GLP-1 receptor agonists were associated with the lowest
260 Using optogenetic stimulation, we show that GLP-1 excites medial habenular (MHb) projections to the
267 er, is produced in the DTC and activates the GLP-1/Notch receptor on adjacent germ cells to maintain
269 ide in cyclic AMP activation assays, but the GLP-1 thiopeptides have much lower beta-arrestin potency
270 (GLP-1) analogue that is an agonist for the GLP-1 receptor, a G-protein coupled receptor (GPCR).
271 nding of peptide-mediated signaling from the GLP-1 receptor and the key role that the central polar n
273 efficacy and safety of co-initiation of the GLP-1 receptor agonist exenatide and the SGLT2 inhibitor
275 receptors to develop improved models of the GLP-1 receptor that predict additional key molecular int
276 able signaling and secretory capacity of the GLP-1 system, we sought to discover mechanisms that incr
277 EC-1/BECN1/Beclin1 acts independently of the GLP-1/Notch or DAF-7/TGF-beta pathways but together with
279 effects are mediated through binding to the GLP-1 receptor (GLP-1R), a class B G-protein-coupled rec
280 PP-4) inhibition (vildagliptin) by using the GLP-1 receptor antagonist exendin [9-39] in patients wit
284 ns that were activated by food intake; these GLP-1 fibers formed close appositions to putative GLP-1R
286 ules were able to confer albumin affinity to GLP-1 and indicated that affinity is increased for dival
287 yperglycemia-induced switch from glucagon to GLP-1 synthesis in human and mouse islet alpha cells by
288 and beta cells by switching from glucagon to GLP-1 to restore beta cell mass and function under hyper
289 ucose, glucose tolerance, insulin tolerance, GLP-1 and insulin secretion), and decreased blood lipids
291 sting a crucial role for SGLT1 in triggering GLP-1 release in agreement with experimental studies.
292 the ability of exendin-4, a clinically used GLP-1 analog, to reduce body weight in rats, suggesting
294 target for the peptide was determined using GLP-1 receptor binding assays, immunocytochemistry for t
295 Finally, AAV-shRNA-mediated knockdown of VTA GLP-1 receptors was sufficient to augment cocaine self-a
298 Here we investigated mechanisms by which GLP-1 and serotonin interact at the level of the central
299 analogs by GDH in the L cell may explain why GLP-1 secretion, but not that of insulin, is activated b
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