ライフサイエンスコーパス: GLP

1 GLP and G9a form a heterodimer complex and catalyze mono

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-1R activation also induced a robust reduction in foo

10 -4 is a long acting glucagon-like peptide 1 (GLP-1) analogue that is an agonist for the GLP-1 recepto

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

12 53 increased plasma glucagon-like peptide 1 (GLP-1) and insulin levels and improved glucose tolerance

13 Glucagon-like peptide 1 (GLP-1) and serotonin play critical roles in energy balan

14 al incretin hormone glucagon-like peptide 1 (GLP-1) by alpha cells and acts directly on beta cells to

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

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

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

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

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

20 logic properties of glucagon-like peptide 1 (GLP-1) make it a potent candidate drug target in the tre

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

22 of the hypothalamic glucagon-like peptide 1 (GLP-1) receptor (GLP-1R) promotes weight loss and improv

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

24 Glucagon-like peptide 1 (GLP-1) regulates glucose homeostasis through the control

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

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

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

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

29 Glucagon-like peptide 1 (GLP-1), secreted from intestinal L cells, glucose depend

30 Glucagon-like Peptide 1 (GLP-1)-expressing neurons in the hindbrain send robust p

31 thereby stimulates glucagon-like peptide 1 (GLP-1)-mediated insulin secretion by upregulating interl

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

33 he incretin hormone glucagon-like peptide 1 (GLP-1).

34 Potentiation of glucagon-like peptide-1 (GLP-1) action through selective GLP-1 receptor (GLP-1R)

35 y of semaglutide, a glucagon-like peptide-1 (GLP-1) analogue in clinical development, compared with i

36 Semaglutide is a glucagon-like peptide-1 (GLP-1) analogue in phase 3 development for type 2 diabet

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 .05]; and increased glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) compared with all other trea

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

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

42 Exenatide, a glucagon-like peptide-1 (GLP-1) receptor agonist, has neuroprotective effects in

43 Glucagon-like peptide-1 (GLP-1) receptor agonists are effective glucose-lowering

44 Glucagon-like peptide-1 (GLP-1) receptor agonists are effective therapies for the

45 take inhibitor, and glucagon-like peptide-1 (GLP-1) receptor agonists.

46 s while stimulating glucagon-like peptide-1 (GLP-1) secreting enteroendocrine L-cells, we have design

47 ical development of glucagon-like-peptide-1 (GLP-1) spans more than 30 years and includes contributio

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

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

50 rug candidate for the treatment of T2DM as a GLP-1R agonist.

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

52 ucose in Gipr null and Lepr(db/db) mice in a GLP-1 receptor-dependent manner.

53 this model can be effectively treated with a GLP-1 receptor agonist.

54 P-1R-mediated effects on energy balance, AAV-GLP-1R was injected into the NTS to examine the role of

55 eveloped a novel adeno-associated virus (AAV-GLP-1R) that utilizes short hairpin RNA to chronically k

56 The clinical efficacies of long-acting GLP-1 derivatives strongly support discovery pursuits ai

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

58 icroscopy structure of the peptide-activated GLP-1R-Gs complex at near atomic resolution.

59 latory nodes synergistically elevated active GLP-1 to unprecedented concentrations ( approximately 30

60 To study active GLP-1, glucose-dependent insulinotropic polypeptide rece

61 evaluated whether peripherally administered GLP-1R agonists access the LDTg to affect feeding.

62 or the effects of exogenous GLP-1R agonists (GLP-1RA) or endogenous GLP-1 on these parameters.

63 ndings show cardiovascular safety across all GLP-1 receptor agonist cardiovascular outcome trials and

64 In vitro, all GLP-1 analogues had subnanomolar GLP-1 receptor potency.

65 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

66 racellular Ca(2+) levels, cAMP activity, and GLP-1 secretion and improved glucose and lipid metabolis

67 were observed in GLP-1RKD(DeltaSim1cre) and GLP-1RKD(DeltaPOMCcre) mice.

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

69 0 knockout mice blunted Pcsk1 expression and GLP-1 release from GLUTag cells.

70 e mimic within LIG1 is methylated by G9a and GLP and, compared with H3K9me2/3, more avidly binds UHRF

71 F1, identify a non-histone target of G9a and GLP, and provide an example of a histone mimic that coor

72 afforded the fluorescently labeled GCGR and GLP-1R ECL mutants with labeling yield as high as 68%.

73 uorescently labeled ECL3 mutants of GCGR and GLP-1R should allow biophysical studies of conformation

74 Several positions in the ECL3s of GCGR and GLP-1R were identified that tolerate SphK mutagenesis an

75 xtracellular loop regions (ECLs) of GCGR and GLP-1R, two members of class B G protein-coupled recepto

76 In contrast, glucose- and GLP-1-stimulated insulin secretion was not affected in i

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

78 RG in beta and L cells increased insulin and GLP-1 secretion up to 50%.

79 y comparable to liraglutide, an antidiabetic GLP-1 analogue that carries a long-chain fatty acid.

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

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

82 Xs were found to control the balance between GLP-1R plasma membrane recycling and lysosomal degradati

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

84 ative allosteric modulators, present in both GLP-1R and GCGR and located outside helices V-VII near t

85 Preclinical studies demonstrate that both GLP-1R agonists and DPP-4 inhibitors exhibit cardioprote

86 w, for we believe the first time, that brain GLP-1R manipulation can result in a robust and chronic b

87 findings support a circuit whereby brainstem GLP-1 activates PVN signaling to mount an appropriate wh

88 eceptors in the hypothalamus were altered by GLP-1R activation.

89 se lowering by these procedures is driven by GLP-1.

90 abolic and emotionality pathways impacted by GLP-1R activation.

91 s the current map of brain areas impacted by GLP-1R activation.

92 a, and fat mass reduction induced by central GLP-1R activation.

93 ng anatomical evidence of endogenous central GLP-1 in the LDTg.

94 y weight are regulated by endogenous central GLP-1.

95 uating oral agents that increase circulating GLP-1.

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

97 gy to investigate the importance of distinct GLP-1R populations in the control of a variety of functi

98 pharmacokinetic investigations of a divalent GLP-1 analogue demonstrated a promising gain in circulat

99 Importantly, divalent GLP-1 analogues showed efficacy comparable to liraglutid

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

101 cose tolerance effects of peripherally dosed GLP-1RA exendin-4 and liraglutide were preserved in all

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

103 loyed following intra-PVT delivery of either GLP-1R agonist, exendin-4 (Ex4), or GLP-1R antagonist, e

104 Both DMG and glutamine alone elicited GLP-1 secretion in GLUTag cells and in vivo, whereas act

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

106 Similar levels of endogenous GLP-1 occur after gastric bypass surgery, and mechanisti

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

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

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

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

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

112 it is necessary for the effects of exogenous GLP-1R agonists (GLP-1RA) or endogenous GLP-1 on these p

113 Conversely, extended GLP-1 microbe intervention improved glucose-dependent in

114 Chow-fed GLP-1RKD(DeltaNkx2.1cre) mice exhibited increased food i

115 de treatment reduced body weight in chow-fed GLP-1RKD(DeltaNkx2.1cre) mice, but this effect was atten

116 that a systemically administered fluorescent GLP-1R agonist accesses the LDTg and is juxtaposed with

117 examined in male and female rats, following GLP-1R activation and pharmacological or genetic GLP-1R

118 tarius (NTS) as a brain region important for GLP-1R-mediated effects on energy balance, AAV-GLP-1R wa

119 ng, role of GLUT2 and glucose metabolism for GLP-1 secretion via an amplifying pathway that increases

120 hich are >30-fold and 140-fold selective for GLP over G9a and other methyltransferases, respectively.

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

122 previously reported potent and selective G9a/GLP dual inhibitors including UNC0638 and UNC0642.

123 1R activation and pharmacological or genetic GLP-1R blockade in the LH.

124 of insulin, glucagon, cholecystokinin, GIP, GLP-1, and PYY, and an increase in total energy intake (

125 ts of glucose, insulin, C-peptide, glucagon, GLP-1, and GIP.

126 under the curve for the satiety gut hormone GLP-1 was significantly increased from 10 days postopera

127 ly regulates release of the incretin hormone GLP-1 and hence insulin secretion after a meal.

128 We investigated how GLP-1 secretion is metabolically coupled in L cells (GLU

129 l residues of a full-length functional human GLP-1R in mammalian cells.

130 This demonstrates that the hypothalamic GLP-1R is sufficient but does not show whether it is nec

131 lp1r expression throughout the hypothalamus (GLP-1RKD(DeltaNkx2.1cre)).

132 In GLP-1 and GIP, a single thioamide near the scissile bond

133 None of these phenotypes were observed in GLP-1RKD(DeltaSim1cre) and GLP-1RKD(DeltaPOMCcre) mice.

134 Finally, we summarize recent progress in GLP biology, highlighting emerging concepts and scientif

135 upled receptor trafficking for their role in GLP-1R potentiation of insulin secretion in pancreatic b

136 agonists for multiple gut hormones including GLP-1, glucagon, and gastric inhibitory peptide.

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

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

139 ation phase, LQT2 patients display increased GLP-1, GIP, and insulin secretion and defective glucagon

140 Glucose infusion to the ileum increased GLP-1 and PYY secretion, suppressed aspects of VAS-rated

141 otes beta-cell function through IL-6-induced GLP-1 production in alpha-cells.

142 strated a 63% reduction in forskolin-induced GLP-1 release in vitro (P < 0.001) and a 23% reduction i

143 of the mechanisms underlying glucose-induced GLP-1 secretion from human small intestine.

144 ugs sitagliptin and exenatide, which inhibit GLP-1 breakdown and stimulate GLP-1 receptors, respectiv

145 e-specific IL-6 signaling induces intestinal GLP-1 release to enhance insulin secretion, thereby coun

146 Direct activation of LDTg GLP-1R suppresses food intake through a reduction in ave

147 Pharmacological blockade of LDTg GLP-1Rs with exendin-(9-39) dose-dependently increases f

148 Together, these data indicate that LDTg GLP-1R signaling controls energy balance and underscores

149 ort the crystal structure of the full-length GLP-1 receptor bound to a truncated peptide agonist.

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

151 ersely, acute pharmacological blockade of LH GLP-1R increased food motivation but only in male rats.

152 Chronic knockdown of LH GLP-1R induced by intraparenchymal delivery of an adeno-

153 d motivation was reduced by activation of LH GLP-1R.

154 as molecular and efferent targets, of the LH GLP-1R activation were also evaluated.

155 Our data identify the LH GLP-1R as an indispensable element of normal food reinfo

156 that vCA1-targeted RNA interference-mediated GLP-1R knockdown increases motivated operant responding

157 and developing orally active, small-molecule GLP-1 receptor (GLP-1R) agonists.

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

159 taSim1cre)) and proopiomelanocortin neurons (GLP-1RKD(DeltaPOMCcre)).

160 In addition, NTS GLP-1R knockdown significantly increased self-administra

161 ignificantly increased following chronic NTS GLP-1R knockdown.

162 he NTS to examine the role of endogenous NTS GLP-1R signaling in energy balance control.

163 , these data demonstrate that endogenous NTS GLP-1R signaling is required for the control of food int

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

165 lei/cell types, the paraventricular nucleus (GLP-1RKD(DeltaSim1cre)) and proopiomelanocortin neurons

166 ht into the molecular mechanism of action of GLP-1 peptides, here we report the crystal structure of

167 Here we review the cardiovascular actions of GLP-1R agonists and DPP-4 inhibitors, with a focus on th

168 Chemogenetic activation of GLP-1 neurons in NTS similarly decreased nicotine intake

169 Activation of GLP-1 receptors in the MHb-IPN circuit abolished nicotin

170 The advantages of GLP-1 for the avoidance of hypoglycemia and the control

171 ify and characterize a novel oral agonist of GLP-1R (i.e., myricetin).

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

173 Important attributes of GLP-1 action and enteroendocrine science are reviewed, w

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

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

176 Finally, we show that postnatal depletion of GLP-1R in the PVN increases food intake and causes obesi

177 No significant effect of GLP-1 receptor agonists was identified on fatal and non-

178 prising because of the beneficial effects of GLP-1R analogs reported in experimental models of DR.

179 ot individually necessary for the effects of GLP-1RA on nutrient homeostasis.

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

181 amino acid glutamine is a potent elicitor of GLP-1 secretion, the responsible mechanism remains uncle

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

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

184 altered the serum lipidome, independently of GLP-1 secretion.

185 dent responsiveness does not reflect loss of GLP-1R signaling in adult islets, since Ex-4 treatment s

186 eural connections and cellular mechanisms of GLP-1R signaling on PVT-to-nucleus accumbens (NAc) proje

187 e 2 diabetes requires positive modulation of GLP-1R to inhibit glucagon secretion and stimulate insul

188 We thus identify key modulators of GLP-1R trafficking and signaling that might provide nove

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

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

191 Given the established role of GLP-1 in promoting beta-cell survival, we hypothesized t

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

193 hibition in vivo of GDH blocked secretion of GLP-1 in response to DMG.

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

195 Here, we describe that stimulation of GLP-1 afferent fibers within the PVN is sufficient to su

196 The cocrystal structures of GLP and G9a in the complex with either 4 or 18 displayed

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

198 This dampening effect on GLP-1 appears to be mediated by increasing intracellular

199 Glucose also has an effect on GLP-1 secretion downstream of electrical activity.

200 f either GLP-1R agonist, exendin-4 (Ex4), or GLP-1R antagonist, exendin-9-39 (Ex9).

201 th a safety profile similar to that of other GLP-1 receptor agonists.

202 decreased hepatic glucose production, other GLP-1-associated effects were not observed - e.g., activ

203 TACT: The gut hormone glucagon-like peptide (GLP)-1 and its analogues represent a new generation of a

204 a can be avoided with glucagon-like peptide (GLP)-1 receptor agonists, which are expensive and requir

205 ests that agonists of glucagon-like peptide (GLP-1) receptor exert neuroprotective and neurorestorati

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

207 Compared with placebo, GLP-1 receptor agonist treatment showed a significant 10

208 s infusion was sufficient to increase plasma GLP-1 levels.

209 eased serum insulin, serum C-peptide, plasma GLP-1, and plasma GIP responses (P=0.03-0.001) and decre

210 Three months postoperatively, GLP-1 area under the curve was associated with early sat

211 G9a-like protein (GLP) and G9a are highly homologous protein lysine methyl

212 fibers formed close appositions to putative GLP-1R-expressing PVT cells that project to the NAc.

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

214 PVT GLP-1R agonism reduced food intake, food-motivation, and

215 food-seeking, while blocking endogenous PVT GLP-1R signaling increased meal size and food intake.

216 cal data illuminate a novel function for PVT GLP-1R signaling in food intake control and suggest a ro

217 -NAc pathway in mediating the effects of PVT GLP-1R activation.

218 t control, we tested the hypothesis that PVT GLP-1R signaling contributes to food intake and reward i

219 PVT neurons receive GLP-1 innervation from nucleus tractus solitarius prepro

220 Although the Notch receptor GLP-1 was implicated in both interactions, the molecular

221 We also show that GLP-1 receptor (GLP-1R) activation augments excitatory synaptic strength

222 the energy balance impact of GLP-1 receptor (GLP-1R) activation.

223 nipulating glucagon-like peptide-1 receptor (GLP-1R) activity selectively in the LH can profoundly af

224 -1) action through selective GLP-1 receptor (GLP-1R) agonism or by prevention of enzymatic degradatio

225 tide-1 (GLP-1) and exogenous GLP-1 receptor (GLP-1R) agonists are an active area of investigation.

226 Glucagon-like peptide 1 receptor (GLP-1R) agonists are increasingly being used as treatmen

227 rally active, small-molecule GLP-1 receptor (GLP-1R) agonists.

228 The glucagon-like peptide-1 receptor (GLP-1R) and the glucagon receptor (GCGR) are members of

229 The glucagon-like peptide-1 receptor (GLP-1R) is a key therapeutic target in the management of

230 penetrant glucagon-like peptide-1 receptor (GLP-1R) noncompetitive antagonist.

231 Glucagon-like peptide 1 receptor (GLP-1R) signaling in the CNS has been linked to reduced

232 iated through binding to the GLP-1 receptor (GLP-1R), a class B G-protein-coupled receptor (GPCR) tha

233 ist of the glucagon-like peptide 1 receptor (GLP-1R), stimulates human beta cell proliferation in juv

234 he glucagon-like peptide 1 (GLP-1) receptor (GLP-1R) is a key target for type 2 diabetes (T2D) treatm

235 ic glucagon-like peptide 1 (GLP-1) receptor (GLP-1R) promotes weight loss and improves glucose tolera

236 A to chronically knock down GLP-1 receptors (GLP-1R) in rats.

237 s express glucagon-like peptide-1 receptors (GLP-1R), which are critical to feeding and body weight c

238 xr(-/-) and Tgr5(-/-) mice exhibited reduced GLP-1 secretion, which was stimulated by INT-767 in the

239 Moreover, reduced GLP-1 levels are associated with increased obesity progr

240 ferential effects were attributed to reduced GLP-1 receptor expression in diabetic islets.

241 Although they are closely related, GLP and G9a possess distinct physiological and pathophys

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

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

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

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

246 report the discovery of potent and selective GLP inhibitors including 4 (MS0124) and 18 (MS012), whic

247 e peptide-1 (GLP-1) action through selective GLP-1 receptor (GLP-1R) agonism or by prevention of enzy

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

251 d a 23% reduction in oral glucose-stimulated GLP-1 secretion (P < 0.05) in association with impairmen

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

253 vitro, all GLP-1 analogues had subnanomolar GLP-1 receptor potency.

254 s contributing to food palatability suppress GLP-1.

255 as required for the coupling of cell surface GLP-1R activation with clathrin-dependent endocytosis, t

256 Short-term GLP-1 microbe intervention in rats reduced serum low-den

257 The discovery that GLP-2 promotes mucosal growth in the intestine is descri

258 and forebrain, we tested the hypothesis that GLP-1R signaling in the LDTg controls food intake.

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

260 cordings of PVT-to-NAc neurons revealed that GLP-1R activation reduced their excitability, mediated i

261 Using optogenetic stimulation, we show that GLP-1 excites medial habenular (MHb) projections to the

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

263 Immunohistochemical data show that GLP-1-producing neurons in the NTS project to the LDTg,

264 We show that GLP-1R stimulation in DR is sufficient to induce hypopha

265 These data support that GLP-1 agonism augments cardiac efficiency via attenuatio

266 The GLP-1 receptor (Glp1r) in mice was knocked down in neuro

267 er, is produced in the DTC and activates the GLP-1/Notch receptor on adjacent germ cells to maintain

268 ndings from both preclinical studies and the GLP-2 clinical development program for short bowel syndr

269 ide in cyclic AMP activation assays, but the GLP-1 thiopeptides have much lower beta-arrestin potency

270 orsal tegmental nucleus (LDTg) expresses the GLP-1R and represents a potential neuroanatomical hub co

271 (GLP-1) analogue that is an agonist for the GLP-1 receptor, a G-protein coupled receptor (GPCR).

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

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

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

275 lated N-terminal extracellular domain of the GLP-1R in complex with exendin(9-39), revealing both sim

276 knowledge linking biological activity of the GLP-1R with the molecular structure of an intact, full-l

277 e insulinoma MIN6B1 cells in response to the GLP-1 analog exendin-4.

278 effects are mediated through binding to the GLP-1 receptor (GLP-1R), a class B G-protein-coupled rec

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

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

281 eutic strategy for type 2 diabetes, with the GLP-1 signaling pathway as a potential focus.

282 major adverse cardiovascular event) with the GLP-1R agonists liraglutide (LEADER trial [Liraglutide E

283 ns that were activated by food intake; these GLP-1 fibers formed close appositions to putative GLP-1R

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

285 Thus, GLP or G9a selective small-molecule inhibitors are usefu

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

287 ucose, glucose tolerance, insulin tolerance, GLP-1 and insulin secretion), and decreased blood lipids

288 iacetyl decreased proglucagon mRNA and total GLP-1 from glucose stimulated STC-1 cells.

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

290 lacking Glp1r expression specifically in two GLP-1RA-responsive hypothalamic feeding nuclei/cell type

291 and nonpolar labels onto a fully unprotected GLP-1R agonist through a linear 7 A diynyl linker.

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

293 lts of two outstanding clinical trials using GLP-1R agonists addressing this issue (Liraglutide Effec

294 ake and body weight reduction following vCA1 GLP-1R activation.

295 logical experiments further reveal that vCA1 GLP-1R activation reduces food intake and inhibits impul

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

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

298 tive, an overview of the mechanisms by which GLP-1R activation exerts its effects in preventing or ar

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

300 tropin-releasing hormone (CRH) neurons, with GLP-1R activation promoting a protein kinase A (PKA)-dep