ライフサイエンスコーパス: glucagon

1 ppeared to co-express the alpha-cell marker, glucagon.

2 r islet hormones, including somatostatin and glucagon.

3 d 488 nm laser pulsed at 137 Hz excited FITC-glucagon.

4 e to mobilize stored glycogen in response to glucagon.

5 l nutrition containing amino acids increased glucagon.

6 control subcutaneous delivery of insulin and glucagon.

7 ino acid levels, is critically controlled by glucagon.

8 Circulating concentrations of glucagon, a catabolic hormone that affects these metabol

9 Excessive secretion of glucagon, a functional insulin antagonist, significantly

10 llness and study the role of illness-induced glucagon abundance in the disturbed glucose, lipid, and

11 Glucagon action is transduced by the class B G-protein-c

12 These data suggest that when glucagon activity is blocked in the setting of type 1 di

13 progenitor cells increased the proportion of glucagon(+) alpha relative to insulin(+) beta cells, ass

14 body to healthy individuals increased plasma glucagon and amino acid levels, but did not change circu

15 cells, inhibit the activities of insulin and glucagon and cause T2DM.

16 d with decreased food intake, reduced plasma glucagon and corticosterone concentrations, and decrease

17 ructures of the transmembrane domains of the glucagon and corticotropin releasing factor 1 (CRF1) rec

18 tentiates the gluconeogenic gene response to glucagon and dexamethasone, whereas constitutively activ

19 Both glucagon and GLP-1 are derived from alternate splicing o

20 In obesity fasting levels of both glucagon and insulin are elevated.

21 ersed islet cells secrete aberrant levels of glucagon and insulin at basal and elevated glucose level

22 itate simultaneously stimulates secretion of glucagon and insulin at fasting glucose concentrations.

23 he superficially wasteful zero-sum action of glucagon and insulin but also to enhance/suppress the sy

24 There were also glucagon and insulin co-expressing cells, and beta cells

25 of pancreatic alpha and beta cells producing glucagon and insulin for glucose homeostasis.

26 Here we investigated the mechanism by which glucagon and insulin increased FGF21 gene transcription

27 o simultaneously increase basal secretion of glucagon and insulin positions elevated levels of fatty

28 We conclude that fatty acids enhance both glucagon and insulin secretion at fasting glucose concen

29 othesized that concomitant hypersecretion of glucagon and insulin was also contributed by reduced som

30 Insight in the nutritional regulation of glucagon and its metabolic role during critical illness

31 When hepatic glycogen content was lowered, glucagon and NHGO responses to insulin-induced hypoglyce

32 Metabolic hormone glucagon and nutritional fasting activated CREBH, which

33 Coordinated glucagon and T3 actions synergize to correct hyperlipide

34 Glucagon and thyroid hormone (T3) exhibit therapeutic po

35 ill mice, infusion of amino acids increased glucagon and up-regulated markers of hepatic amino acid

36 heterogenous MAFA expression, and increased glucagon(+) and ghrelin(+) cells compared to grafts from

37 s for multiple gut hormones including GLP-1, glucagon, and gastric inhibitory peptide.

38 action offsets the diabetogenic liability of glucagon, and glucagon-mediated delivery spares the card

39 serum tumor necrosis factor-alpha, cortisol, glucagon, and growth hormone levels increased, and free

40 drenocorticotropic hormone (ACTH), cortisol, glucagon, and nonesterified fatty acid (NEFA) concentrat

41 the islet endocrine hormone markers insulin, glucagon, and somatostatin.

42 ernative islet cell genes including ghrelin, glucagon, and somatostatin.

43 Collectively, these results indicate that glucagon antagonism could i) be a useful adjuvant therap

44 impairs glucose tolerance through effects on glucagon as well as on insulin secretion.

45 66-79% of participants showed suppression of glucagon at 120 min (fold change glucagon120/0 <1) durin

46 These data suggest that elevated glucagon availability during critical illness increases

47 s, we infused macronutrients and manipulated glucagon availability up and down to investigate its acu

48 The hormones insulin and glucagon both play important roles in the development of

49 g, an increase in concentrations of insulin, glucagon, cholecystokinin, GIP, GLP-1, and PYY, and an i

50 ased proteomics) and show that 29-amino acid glucagon circulates in patients without a pancreas and t

51 rements of circulating glucose, insulin, and glucagon concentrations at 0, 30 and 120 min.

52 ship between insulin sensitivity and fasting glucagon concentrations was nonlinear (P < 0.001).

53 nd were independent of any changes in plasma glucagon concentrations; these effects were abrogated by

54 o chronic rapamycin administration decreased glucagon content and glucagon secretion.

55 Previous studies have shown that glucagon cooperatively interacts with insulin to stimula

56 o marked postsurgery reductions in levels of glucagon, cortisol, and catecholamine and the sympatheti

57 In addition, glucagon deficiency did not impair the natural capacity

58 Glucagon dissociates this interaction, promoting translo

59 r macronutrient infusion can suppress plasma glucagon during critical illness and study the role of i

60 d the association of postchallenge change in glucagon during oral glucose tolerance tests (OGTTs), hy

61 c glucose production, although conditions of glucagon excess or deficiency do not cause changes compa

62 Glucagon exerts its physiological functions through acti

63 in part by increasing insulin and decreasing glucagon expression.

64 glycemia in a setting devoid of insulin and glucagon function remain unclear but may include the hor

65 es to prevent hypoglycemia in the absence of glucagon function.

66 Glucagon (GCG) acutely stimulates energy expenditure (EE

67 on-like peptide-1 (GLP-1) receptor (GLP-1R), glucagon (GCG) receptor (GCGR), and glucose-dependent in

68 ed by rapid demethylation of the insulin and glucagon gene promoters during differentiation of Neurog

69 hylation at the promoters of the insulin and glucagon genes.

70 plasma gut-hormone concentrations [insulin, glucagon, ghrelin, cholecystokinin, gastric inhibitory p

71 measurements of glucose, insulin, C-peptide, glucagon, GLP-1, and GIP.

72 < 0.01 for both), but neither dose affected glucagon, GLP-1, GIP, cholecystokinin, gastric emptying,

73 ma responses of glucose, insulin, C-peptide, glucagon, glucagon-like peptides 1 and 2, gastric inhibi

74 d glycaemic control system using insulin and glucagon has not been shown in a free-living, home-use s

75 w that lipid conjugated forms of a GLP-1/GIP/glucagon hybrid peptides stay in circulation for hours.

76 rs blood glucose but results in compensatory glucagon hypersecretion involving expansion of pancreati

77 Immunoneutralizing glucagon in critically ill mice only transiently affecte

78 tes alpha-cell function and secretion, while glucagon, in turn, regulates amino acid turnover.

79 sting metabolic hormone (insulin, C-peptide, glucagon, incretin, and adipokine) concentrations were m

80 Upon glucagon-induced calcium signaling, calcium/calmodulin-d

81 epatocyte glucose production by antagonizing glucagon-induced expression of the gluconeogenic enzyme

82 imary hepatocytes with exogenous LPA blunted glucagon-induced PEPCK expression and glucose production

83 We found basal glucagon, insulin and somatostatin secretion and respira

84 ells and intestinal L and K cells, secreting glucagon, insulin, and the incretins glucagon-like pepti

85 Glucagon is believed to be a pancreas-specific hormone,

86 Evidence exists that shows glucagon is important for minute-to-minute regulation of

87 ole in glucose regulation, the importance of glucagon is increasingly acknowledged.

88 Glucagon is the primary hormone responsible for increasi

89 Glucagon is usually viewed as an important counterregula

90 TT, whereas 21-34% presented with increasing glucagon levels (fold change glucagon120/0 >/=1).

91 oclonal antibody undergo elevation of plasma glucagon levels and alpha-cell expansion similar to wild

92 In conclusion, increased fasting glucagon levels and delayed glucagon suppression, togeth

93 een-detected diabetes had 30% higher fasting glucagon levels and diminished early glucagon suppressio

94 Glucagon levels are classically suppressed after glucose

95 Ts), hypothesizing that higher postchallenge glucagon levels are observed in subjects with impaired g

96 riglyceride levels, but did not alter plasma glucagon levels or alpha-cell mass.

97 Glucagon levels were measured during OGTT in a total of

98 increasing insulin secretion and suppressing glucagon levels.

99 l muscle, which acts as a myokine to control glucagon-like adipokinetic hormone (AKH) secretion from

100 ABSTACT: The gut hormone glucagon-like peptide (GLP)-1 and its analogues represen

101 Hypoglycemia can be avoided with glucagon-like peptide (GLP)-1 receptor agonists, which a

102 Growing evidence suggests that agonists of glucagon-like peptide (GLP-1) receptor exert neuroprotec

103 r suggested the presence of the gut hormone, glucagon-like peptide (GLP-1), in deep short axon cells

104 e effect of diacetyl on the satiety hormone, glucagon-like peptide (GLP-1), using the enteroendocrine

105 Glucagon-like peptide 1 (GLP-1) agonists have shown card

106 Exendin-4 is a long acting glucagon-like peptide 1 (GLP-1) analogue that is an agon

107 Dual activation of the glucagon-like peptide 1 (GLP-1) and glucagon receptor ha

108 In contrast, AR231453 increased plasma glucagon-like peptide 1 (GLP-1) and insulin levels and i

109 Glucagon-like peptide 1 (GLP-1) and serotonin play criti

110 ecretion of the prosurvival incretin hormone glucagon-like peptide 1 (GLP-1) by alpha cells and acts

111 Exocytosis of the hormone glucagon-like peptide 1 (GLP-1) by the intestinal L cell

112 Since glucagon-like peptide 1 (GLP-1) exerts neuroprotective e

113 Therapeutic engineering of glucagon-like peptide 1 (GLP-1) has enabled development

114 Glucagon-like peptide 1 (GLP-1) immunoreactivity of plas

115 Glucagon-like peptide 1 (GLP-1) is a hormone with essent

116 Glucagon-like peptide 1 (GLP-1) is secreted by intestina

117 The physiologic properties of glucagon-like peptide 1 (GLP-1) make it a potent candida

118 Moreover, ANP potentiated the effect of glucagon-like peptide 1 (GLP-1) on glucose-induced insul

119 The glucagon-like peptide 1 (GLP-1) receptor (GLP-1R) is a k

120 armacological activation of the hypothalamic glucagon-like peptide 1 (GLP-1) receptor (GLP-1R) promot

121 Glucagon-like peptide 1 (GLP-1) receptor agonists (GLP-1

122 al models of type 2 diabetes have shown that glucagon-like peptide 1 (GLP-1) receptor agonists preven

123 e-18]fluoro-levodopa [(18)F-DOPA] PET-CT and glucagon-like peptide 1 (GLP-1) receptor imaging), and d

124 Glucagon-like peptide 1 (GLP-1) regulates glucose homeos

125 in from adipocytes and by those means induce glucagon-like peptide 1 (GLP-1) secretion.

126 This study tested the hypothesis that glucagon-like peptide 1 (GLP-1) therapies improve cardia

127 proof-of-principle, the clinically relevant glucagon-like peptide 1 (GLP-1) was functionalized with

128 ) inhibitor that inhibits the degradation of glucagon-like peptide 1 (GLP-1), and has been approved f

129 kinin, gastric inhibitory polypeptide (GIP), glucagon-like peptide 1 (GLP-1), and peptide tyrosine ty

130 Glucagon-like peptide 1 (GLP-1), secreted from intestina

131 diabetes associated with the stimulation of glucagon-like peptide 1 (GLP-1), which is known to slow

132 Glucagon-like Peptide 1 (GLP-1)-expressing neurons in th

133 S) in the circulation and thereby stimulates glucagon-like peptide 1 (GLP-1)-mediated insulin secreti

134 Here, we present evidence for glucagon-like peptide 1 (GLP-1)-mediated paraventricular

135 elease of the incretin and satiating peptide glucagon-like peptide 1 (GLP-1).

136 stimulates secretion of the incretin hormone glucagon-like peptide 1 (GLP-1).

137 We describe this method using dulaglutide, a glucagon-like peptide 1 (GLP1)-Fc fusion protein.

138 ontrolled trial that compared liraglutide, a glucagon-like peptide 1 analogue, with placebo in patien

139 with PS-CF and normal control subjects, and glucagon-like peptide 1 and gastric inhibitory polypepti

140 improves glucose tolerance while stimulating glucagon-like peptide 1 and insulin secretion.

141 Mean changes in serum glucagon-like peptide 1 and peptide YY were 106.6% +/- 2

142 in human beta-cells, using forskolin or the glucagon-like peptide 1 mimetic Exendin-4, inhibits the

143 ted depletion, which could not be rescued by glucagon-like peptide 1 pretreatment.

144 abetic C57BL/6J mice treated with either the glucagon-like peptide 1 receptor (GLP-1R) agonist liragl

145 Glucagon-like peptide 1 receptor (GLP-1R) agonists are i

146 Glucagon-like peptide 1 receptor (GLP-1R) signaling in t

147 und that exendin-4 (Ex-4), an agonist of the glucagon-like peptide 1 receptor (GLP-1R), stimulates hu

148 Glucagon-like peptide 1 receptor (GLP1R) agonists are wi

149 The short-acting glucagon-like peptide 1 receptor agonist exenatide reduc

150 ctivities of NRTN relative to liraglutide, a glucagon-like peptide 1 receptor agonist, in Zucker diab

151 enome editing to controllably release GLP-1 (glucagon-like peptide 1), a critical incretin that regul

152 y reports activation in response to insulin, glucagon-like peptide 1, and agents that raise cAMP leve

153 ut hormones, fibroblast growth factor 19 and glucagon-like peptide 1, and the BA transport systems, a

154 h plasma concentrations of acylated ghrelin, glucagon-like peptide 1, insulin, glucose, and nonesteri

155 mentation of fibroblast growth factor 21 and glucagon-like peptide 1.

156 Potentiation of glucagon-like peptide-1 (GLP-1) action through selective

157 dipeptidyl peptidase-4 (DPP4) inhibitors and glucagon-like peptide-1 (GLP-1) analogs, are important n

158 ed the efficacy and safety of semaglutide, a glucagon-like peptide-1 (GLP-1) analogue in clinical dev

159 Semaglutide is a glucagon-like peptide-1 (GLP-1) analogue in phase 3 deve

160 Glucagon-like peptide-1 (GLP-1) analogues reduce hepatic

161 ate the anorectic effects of both endogenous glucagon-like peptide-1 (GLP-1) and exogenous GLP-1 rece

162 creting glucagon, insulin, and the incretins glucagon-like peptide-1 (GLP-1) and GIP (glucose-depende

163 , Tukey's post hoc, P < 0.05]; and increased glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) com

164 e of enteroendocrine L-cell derived hormones glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) in

165 elease of gastrointestinal peptides, such as glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), fr

166 Multiple physiological properties of glucagon-like peptide-1 (GLP-1) ensure that it is a prom

167 Pharmacological evidence suggests a role for glucagon-like peptide-1 (GLP-1) in modulating stress res

168 e acid synthesis and intestinal secretion of glucagon-like peptide-1 (GLP-1) in wild-type, Fxr(-/-),

169 Here we show that nicotine activates glucagon-like peptide-1 (GLP-1) neurons in the nucleus t

170 Glucagon-like peptide-1 (GLP-1) receptor (GLP-1R), gluca

171 Exendin-4 (EX-4), a glucagon-like peptide-1 (GLP-1) receptor agonist, has be

172 Exenatide, a glucagon-like peptide-1 (GLP-1) receptor agonist, has ne

173 Glucagon-like peptide-1 (GLP-1) receptor agonists and so

174 Glucagon-like peptide-1 (GLP-1) receptor agonists are ef

175 Glucagon-like peptide-1 (GLP-1) receptor agonists are ef

176 amine-norepinephrine reuptake inhibitor, and glucagon-like peptide-1 (GLP-1) receptor agonists.

177 The glucagon-like peptide-1 (GLP-1) receptor and the glucose

178 oid these systemic effects while stimulating glucagon-like peptide-1 (GLP-1) secreting enteroendocrin

179 Alhough the glucagon-like peptide-1 (GLP-1) system is critical to en

180 , we use the validated diabetes therapeutic, glucagon-like peptide-1 (GLP-1), and the target of clini

181 together with the beneficial effects of the glucagon-like peptide-1 agonist exendin-4 in transgenic

182 odium-glucose cotransporter 2 inhibitors and glucagon-like peptide-1 agonists, and suggest how such d

183 vestigate the neuroprotective effects of the glucagon-like peptide-1 analog exenatide in resuscitated

184 Glucagon-like peptide-1 analogs are approved for type 2

185 trophy mice and further demonstrate that the glucagon-like peptide-1 analogue exendin-4, a well-toler

186 f target engagement for clinical trials with glucagon-like peptide-1 analogues in multiple system atr

187 ates Ca(2+) , cAMP, and insulin responses to glucagon-like peptide-1 and its metabolites following il

188 n of a long-acting analog of the gut-hormone glucagon-like peptide-1 highlights the therapeutic poten

189 Here we hypothesize that manipulating glucagon-like peptide-1 receptor (GLP-1R) activity selec

190 The glucagon-like peptide-1 receptor (GLP-1R) and the glucag

191 Therapeutic intervention to activate the glucagon-like peptide-1 receptor (GLP-1R) enhances gluco

192 The glucagon-like peptide-1 receptor (GLP-1R) is a key thera

193 first orally bioavailable and CNS penetrant glucagon-like peptide-1 receptor (GLP-1R) noncompetitive

194 tivated positive allosteric modulator of the glucagon-like peptide-1 receptor (GLP-1R), a class B GPC

195 hibits food-motivated behaviors through vCA1 glucagon-like peptide-1 receptor (GLP-1R).

196 To determine the effects of the glucagon-like peptide-1 receptor agonist liraglutide add

197 ons in the dipeptidyl peptidase-4 inhibitor, glucagon-like peptide-1 receptor agonist, and sodium-glu

198 Both glucagon-like peptide-1 receptor agonists and dipeptidyl

199 More recently, the glucagon-like peptide-1 receptor agonists liraglutide an

200 f dipeptidyl peptidase-4 inhibitors and some glucagon-like peptide-1 receptor agonists, at least in t

201 in vivo We further demonstrate that an ileal glucagon-like peptide-1 receptor-dependent neuronal netw

202 Given that PVT neurons express glucagon-like peptide-1 receptors (GLP-1R), which are cr

203 rs in hippocampal neurons to reduce (leptin, glucagon-like peptide-1) or increase (ghrelin) food inta

204 , we investigated the effects of G49, a dual glucagon-like peptide-1/glucagon receptor agonist, on NA

205 Dual-acting glucagon-like peptide-1/glucagon receptor agonists such

206 Glucagon-like peptide-2 receptor agonists have therapeut

207 es of glucose, insulin, C-peptide, glucagon, glucagon-like peptides 1 and 2, gastric inhibitory pepti

208 haracterization, and clinical development of glucagon-like-peptide-1 (GLP-1) spans more than 30 years

209 the diabetogenic liability of glucagon, and glucagon-mediated delivery spares the cardiovascular sys

210 During nutrient deprivation, glucagon-mediated increase in calcium (Ca(2+)) levels, v

211 Mechanistically, LPA antagonized glucagon-mediated inhibition of STAT3, a transcriptional

212 and adipocytes, cGAMP weakens the effects of glucagon on stimulating hepatocyte gluconeogenic enzyme

213 we show that islet cells expressing insulin, glucagon, or somatostatin share a lack of methylation at

214 es in both plasma epinephrine (P = 0.01) and glucagon (P = 0.01).

215 s emphasize the existence of extrapancreatic glucagon (perhaps originating from the gut) in man and s

216 Glucagon plays a major role in the regulation of glucose

217 These results demonstrate that glucagon plus insulin increases FGF21 transcription by s

218 Transfection analyses demonstrated that glucagon plus insulin induction of FGF21 transcription w

219 A and PI3K/Akt/mTORC1 mediates the effect of glucagon plus insulin on ATF4 expression.

220 Glucagon plus insulin stimulated a 5-fold increase in AT

221 of ATF4 expression suppressed the ability of glucagon plus insulin to increase FGF21 expression.

222 complex 1 (mTORC1) suppressed the ability of glucagon plus insulin to stimulate ATF4 and FGF21 expres

223 In patients with glucagon-producing tumors (glucagonomas), the most consp

224 in treatment increased the relative GLP-1 vs glucagon production in both non-diabetic and diabetic is

225 glucose, insulin, C-peptide, the insulin-to-glucagon ratio, and HOMA-insulin resistance in fasted ad

226 tivity and clearance, and the portal insulin:glucagon ratio.The addition of lactisole to the OGTT cau

227 Recent studies report that mice lacking glucagon receptor (Gcgr(-/-)) do not develop diabetes fo

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

229 Glucagon receptor (GcgR) blockade has been proposed as a

230 Using this model, we show that glucagon receptor (GCGR) inhibition with a monoclonal an

231 transduced by the class B G-protein-coupled glucagon receptor (GCGR), which is located on liver, kid

232 ological functions through activation of the glucagon receptor (GCGR).

233 ng in hybrid peptides with potent dual GLP-1/glucagon receptor activity.

234 fects of G49, a dual glucagon-like peptide-1/glucagon receptor agonist, on NASH and hepatic regenerat

235 Dual-acting glucagon-like peptide-1/glucagon receptor agonists such as G49 represent a novel

236 ds and their transport into alpha-cells link glucagon receptor blockage to alpha-cell hyperplasia.

237 n of the glucagon-like peptide 1 (GLP-1) and glucagon receptor has the potential to lead to a novel t

238 These data show that Angptl4 does not link glucagon receptor inhibition to compensatory hyperglucag

239 angiopoietin-like protein 4 (Angptl4) links glucagon receptor inhibition to hyperglucagonemia and al

240 that Angptl4(-/-) mice treated with an anti-glucagon receptor monoclonal antibody undergo elevation

241 The human glucagon receptor, GCGR, belongs to the class B G-protei

242 subjects with inactivating mutations of the glucagon receptor, pancreatic swelling may be the first

243 Furthermore, administration of glucagon receptor-blocking antibody to healthy individua

244 epends on enhanced signaling through hepatic glucagon receptors (GCGRs).

245 In addition, the diabetogenic role of glucagon released from alpha-cells plays a major role in

246 Because this glucagon response is impaired early in type 1 diabetes,

247 e sensing, noted by impaired epinephrine and glucagon responses and impaired c-fos activation in the

248 ects had lower acute insulin, C-peptide, and glucagon responses compared with PS-CF and normal contro

249 LQT2 patients had defective glucagon responses to low glucose, P=0.008.

250 e applied novel analytical methods of plasma glucagon (sandwich ELISA and mass spectrometry-based pro

251 ine cells of the pancreatic islet, including glucagon secreting alpha-cells, but particularly in insu

252 Since FFAR1 is also present on glucagon-secreting alpha-cells, we hypothesized that pal

253 g, stimulate insulin secretion, and suppress glucagon secretion and energy intake.

254 f mTORC1 in nutrient-dependent regulation of glucagon secretion and identify a role for mTORC1 in con

255 res positive modulation of GLP-1R to inhibit glucagon secretion and stimulate insulin secretion in a

256 Regulation of glucagon secretion by factors secreted by neighbouring b

257 accounts for up to 23% of the suppression of glucagon secretion by high glucose.

258 improved understanding of the modulation of glucagon secretion can provide novel therapeutic routes

259 etion together with reciprocal inhibition of glucagon secretion contributes to glucose tolerance.

260 Glucagon secretion dysregulation in diabetes fosters hyp

261 Moreover, temporal insulin and glucagon secretion exhibited distinct oscillatory profil

262 However, the mechanisms that regulate glucagon secretion from alpha-cells are still unclear.

263 The recovery of regulated glucagon secretion from alpha-cells in small pseudoislet

264 rtant for regulating alpha-cell activity and glucagon secretion in human islets, we constructed compu

265 pear to be required for proper inhibition of glucagon secretion in response to glucose.

266 t 23% of the inhibitory effect of glucose on glucagon secretion is mediated by beta-cells via gap jun

267 In alphaRaptorKO mice, impaired glucagon secretion occurred in response to different sec

268 Therefore, the increased epinephrine and glucagon secretion with declining plasma glucose concent

269 -1, GIP, and insulin secretion and defective glucagon secretion, causing decreased plasma glucose and

270 othalamus differentially control insulin and glucagon secretion, potentially in partnership to help m

271 a- and beta-cell mass as well as insulin and glucagon secretion.

272 as a major regulator of alpha cell mass and glucagon secretion.

273 by glucose-dependent control of insulin and glucagon secretion.

274 exaggerated counter-regulatory response for glucagon secretion.

275 dministration decreased glucagon content and glucagon secretion.

276 PLPP1 activity and hepatocyte LPA levels in glucagon sensitivity via a mechanism involving STAT3.

277 hormone and metabolic factors that influence glucagon sensitivity.

278 ic disruption or pharmacologic inhibition of glucagon signaling effectively lowers blood glucose but

279 mechanism by which AMPK antagonizes hepatic glucagon signalling via phosphorylation-induced PDE4B ac

280 ly maintain distinct mono-hormonal insulin+, glucagon+, somatostatin+ and PP+ cells and glucose-respo

281 previously been shown to antagonize hepatic glucagon-stimulated cyclic AMP (cAMP) signalling indepen

282 Importantly, LPA did not blunt glucagon-stimulated glucose production or PEPCK expressi

283 (O-GlcNAc) transferase (OGT) is required for glucagon-stimulated liver autophagy and metabolic adapta

284 Lower glucagon suppression after oral glucose administration i

285 Longitudinal changes in glucagon suppression were investigated in 50 participant

286 early glucagon suppression, but greater late glucagon suppression when compared with individuals with

287 fasting glucagon levels and diminished early glucagon suppression, but greater late glucagon suppress

288 ncreased fasting glucagon levels and delayed glucagon suppression, together with increased circulatin

289 e and functionally comparable to the insulin-glucagon system for regulating blood Glc levels in anima

290 ABSTRACT: Glucagon, the body's principal hyperglycaemic hormone, i

291 Treatment with MIA-602 normalized GLP-1 and glucagon to control levels in T1D rats.

292 ugmented a hyperglycemia-induced switch from glucagon to GLP-1 synthesis in human and mouse islet alp

293 KA-selective agonist mimicked the ability of glucagon to stimulate ATF4 and FGF21 expression.

294 ogranin A, neuron-specific enolase, gastrin, glucagon, vasoactive intestinal peptide, pancreatic poly

295 rmalities, and immunostaining of insulin and glucagon was similar to that from wild-type pancreata.

296 ructure-based design, structural elements of glucagon were engineered into the selective GLP-1 recept

297 infusing glucose with insulin did not lower glucagon, whereas parenteral nutrition containing amino

298 ell hyperplasia with gross hypersecretion of glucagon, which according to recent groundbreaking resea

299 al and 4-Pal) enhanced aqueous solubility of glucagon while maintaining biological properties.

300 A bioactive peptide that combines glucagon with the thyroid hormone T3 lowers lipid levels

301 no acids in the liver, mediated by increased glucagon, without preventing muscle wasting.