ライフサイエンスコーパス: glucagon

1 dpoint was sensitive to endogenous levels of glucagon.

2 no acid levels in response to high levels of glucagon.

3 ed by the actions of circulating insulin and glucagon.

4 nhibit secretion of AKH, the fly analogue of glucagon.

5 ces that have reshaped the metabolic role of glucagon.

6 cally regulates the secretion of insulin and glucagon.

7 ibitors occur almost entirely independent of glucagon.

8 LIP-seq) in primary hepatocytes induced with glucagon.

9 tudies demonstrated a physiological role for glucagon, acting via the GLP-1 receptor, in paracrine re

10 reas des-His(1)-[Glu(9)]glucagon antagonized glucagon action at the GluR, while having minimal inhibi

11 ontrolling transcript levels associated with glucagon action.

12 on and ketone production, features common to glucagon action.

13 levels of hemoglobin A1c, glucose, insulin, glucagon, adipocytokines, and T-helper (TH) 1-, 2-, and

14 third-party assistance with carbohydrate or glucagon administration, or other resuscitative actions)

15 Moreover, mechanistic studies revealed that glucagon affected the half-life of PCSK9 protein without

16 ype-2 diabetes(1-3), the mechanisms by which glucagon affects hepatic glucose production and mitochon

17 discuss emerging strategies that incorporate glucagon agonism in the pharmacology of treating diabete

18 ve indirectly promoted the integrated use of glucagon agonism with other hormones in a manner that ru

19 The effects of glucagon alone on the induction of thermogenic genes in

20 le for the hyperglycemia in diabetes, making glucagon an attractive target for therapeutic interventi

21 ciated with a significant increase in plasma glucagon and a decrease in the plasma insulin concentrat

22 , signaling, or metabolic function linked to glucagon and fasting responses, but were not the canonic

23 inhibitors LY2409021 and MK 0893 antagonized glucagon and GLP-1 action at the GLP-1R, whereas des-His

24 rmally considered to be highly selective for glucagon and GLP-1, respectively.

25 This effect was paralleled by elevated serum glucagon and hepatic phosphoenolpyruvate carboxykinase 1

26 ansiently activates AMPK, whereas changes in glucagon and insulin levels had no impact on AMPK.

27 Glucagon and insulin maintain blood glucose homeostasis

28 umption show increased circulating levels of glucagon and insulin, and diabetes-like dysregulation of

29 Glucagon and its partner insulin are dually linked in bo

30 Most insulin(low) cells contained abundant glucagon and other alpha-cell markers, suggesting that a

31 es the textbook physiology of both GLP-1 and glucagon and presents a critical paradigm shift for the

32 runs counter to the long-standing pursuit of glucagon antagonism.

33 on at the GLP-1R, whereas des-His(1)-[Glu(9)]glucagon antagonized glucagon action at the GluR, while

34 e and that hepatic amino acid metabolism and glucagon are linked in a mutual feedback cycle, the live

35 cells, we validated a dual agonist action of glucagon at the GluR and GLP-1R.

36 0.001) areas under the curve (AUCs), whereas glucagon AUC increased (+11%, P = 0.030).

37 These results provide insights into glucagon biology and suggest that INSP3R1 may represent

38 ignificant SGLT2 protein colocalization with glucagon but not with insulin or somatostatin.

39 te that 1) the changes in plasma insulin and glucagon concentration after SGLT2i administration are s

40 Previous findings of increased glucagon concentrations and EGP during acute administrat

41 but studies have suggested that circulating glucagon concentrations and endogenous glucose productio

42 while clamping plasma glucose, insulin, and glucagon concentrations at their fasting level.

43 e, chronic physiological increases in plasma glucagon concentrations increased mitochondrial oxidatio

44 (study 2), the change in plasma insulin and glucagon concentrations was comparable in subjects recei

45 and replacement of basal plasma insulin and glucagon concentrations.

46 Glucagon-containing alpha-cells potently regulate glucos

47 aTSC2(KO) was associated with an increase in glucagon content and enhanced glucagon secretion.

48 Insulin and glucagon control plasma macronutrient homeostasis throug

49 Glucagon counters insulin's effects on glucose metabolis

50 ions collectively minimize the complexity of glucagon delivery and enable its application in ways not

51 knockdown of several of these genes affected glucagon-dependent glucose production, a PGC-1alpha-regu

52 inhibitors strongly repressed C-peptide and glucagon during endocrine differentiation.

53 nt between the 2 trials; however, the AUC of glucagon during the OGTT was also significantly greater

54 Treatment of mouse hepatocytes with glucagon, epinephrine, or forskolin stimulated Rpn6 phos

55 Insulin and glucagon exert opposing actions on glucose metabolism, a

56 neovascularization and sustained insulin and glucagon expression up to 80 days posttransplantation.

57 motifs of members of the neuropeptide Y and glucagon families modulate receptor activation propertie

58 Hypersecretion of glucagon from pancreatic alpha-cells strongly contribute

59 inhibitors that blocked production of mature glucagon from proglucagon, beta-cells retained the abili

60 Secretion of glucagon from the pancreatic alpha-cells is conventional

61 ly regulated across all conditions including Glucagon (GCG) and Insulin (INS).

62 hormones [somatostatin (SST), insulin (INS), Glucagon (GCG)], differentiation markers [Forkhead box O

63 G protein-coupled receptors (GPCRs) for glucagon (GluR) and glucagon-like peptide-1 (GLP-1R) are

64 locks exhibit strongly disrupted insulin and glucagon granule docking and exocytosis.

65 tion structure of fibrils of synthetic human glucagon grown at pharmaceutically relevant low pH.

66 ole in the regulation of glucose metabolism, glucagon has been described to promote ketosis in the fa

67 ced white adipose tissue (WAT) browning, but glucagon has largely been ignored.

68 9-39) in combination with des-His(1)-[Glu(9)]glucagon in INS-1 832/13 cells, we validated a dual agon

69 Here, we directly test the ketogenic role of glucagon in mice, demonstrating that neither fasting- no

70 ly, islets from three donors did not secrete glucagon in response to either 1 mmol/L glucose or dapag

71 o cadaveric alpha cells, express and secrete glucagon in response to glucose and some glucagon secret

72 inducing insulin secretion and resistance to glucagon in the liver.

73 d that reductions in the ratio of insulin to glucagon in the portal vein have a major role in the dys

74 in fasted liver and hepatocytes treated with glucagon, in a PGC1alpha-dependent manner.

75 th the negative group (P <= 0.0001), whereas glucagon increased from EU to HYPO only in the high C-pe

76 Although both insulin and glucagon induced AMPKalpha phosphorylation at its Ser(48

77 cumulation, decreased glycemia, and hampered glucagon-induced gluconeogenesis, thus preventing a prop

78 ls in murine primary hepatocytes facilitates glucagon-induced glucose production and enhances the exp

79 lpha depletion decreased a fraction of these glucagon-induced messenger RNA (mRNA) transcript levels.

80 er, both before and after fasting and during glucagon infusion.

81 d by modifications in glucose levels and the glucagon/insulin ratio in the bloodstream.

82 than the related hormonal changes (i.e. the glucagon/insulin ratio), sensitize AMPK activation to th

83 Finally, we argue that glucagon is a bona fide postprandial hormone that evolve

84 n of a conserved liver-alpha-cell axis where glucagon is a critical regulator of amino acid homeostas

85 Glucagon is a key hormone that regulates the adaptive me

86 This analysis established that glucagon is a nonconventional GLP-1R agonist, an effect

87 ptor (GCGR) activated by the peptide hormone glucagon is a seven-transmembrane G protein-coupled rece

88 Glucagon is classically described as a counterregulatory

89 Glucagon is historically described as the counterregulat

90 er, it is becoming clear that the biology of glucagon is much more complex and extends beyond hepatic

91 inconsistencies with the canonical view that glucagon is primarily a hyperglycemic agent driven by fa

92 A and C resulted in higher glucagon levels and faster gastric emptying.

93 Elevation of glucagon levels and increase in alpha-cell mass are asso

94 nd 4) increased fasting and arginine-induced glucagon levels compared with control subjects without d

95 ter surgery, indices of IS improved, GIP and glucagon levels decreased significantly in both the grou

96 P-1R(-/-) mice both showed higher nonfasting glucagon levels than their wild-type littermates, wherea

97 ass index) or other biomarkers (e.g., plasma glucagon levels).

98 ody weight, blood glucose, plasma insulin or glucagon levels, glucose tolerance or arginine tolerance

99 udy assessing the occupancy of the dual GCGR/glucagon like peptide-1 receptor agonist SAR425899.

100 Glucagon-like peptide (GLP)-1 analogs such as liraglutid

101 eduction in circulating DPP4 and increase in Glucagon-like peptide (GLP)-1 levels as compared to the

102 11%, P = 0.002), NEFA (-21%, P = 0.009), and glucagon-like peptide 1 (-31%, P = 0.001) areas under th

103 Glucagon-like peptide 1 (GLP-1) and cholecystokinin (CCK

104 Glucagon-like peptide 1 (GLP-1) and glucagon-like peptid

105 pendent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are secreted postprandia

106 The role of intestinally secreted glucagon-like peptide 1 (GLP-1) in regulation of insulin

107 e-dependent insulinotropic peptide (GIP) and glucagon-like peptide 1 (GLP-1) is characterized by thei

108 Glucagon-like peptide 1 (GLP-1) is known to suppress glu

109 The incretin glucagon-like peptide 1 (GLP-1) is secreted by the intes

110 Glucagon-like peptide 1 (GLP-1) mimetics are effective d

111 Liraglutide, a glucagon-like peptide 1 (GLP-1) receptor agonist, and ph

112 proposed pathway was not influenced by local glucagon-like peptide 1 (GLP-1) secretion from alpha-cel

113 Centrally administered glucagon-like peptide 1 (GLP-1) supresses food intake.

114 ms mediating the cardioprotective actions of glucagon-like peptide 1 (GLP-1) were unknown.

115 peptide YY3-36 (PYY3-36), lithium chloride, glucagon-like peptide 1 (GLP-1), and leptin shows the pr

116 , dipeptidyl peptidase 4 [DPP-4] inhibitors, glucagon-like peptide 1 [GLP-1] receptor agonists, and s

117 ite-related hormones (active ghrelin, active glucagon-like peptide 1 [GLP-1], total peptide YY [PYY],

118 ulation of cells expressing the precursor of glucagon-like peptide 1 and are glutamatergic; able to m

119 Glucagon-like peptide 1 and glucose-dependent insulinotr

120 ocrine cells (EECs) produce hormones such as glucagon-like peptide 1 and peptide YY that regulate foo

121 of 14.6% +/- 2.6% and elevated postprandial glucagon-like peptide 1 compared with controls (49.2 +/-

122 Strikingly, when P-NT was combined with the glucagon-like peptide 1 mimetic liraglutide, the two pep

123 These include biguanides, glucagon-like peptide 1 receptor (GLP-1) agonists, dipep

124 icacy and ability to reduce the body weight, glucagon-like peptide 1 receptor (GLP-1R) agonism has em

125 Glucagon-like peptide 1 receptor (GLP-1R) agonists effec

126 This appeared to be mediated in part by glucagon-like peptide 1 receptor (GLP-1R) and not the G

127 Glucagon-like peptide 1 receptor (GLP-1R) imaging with r

128 The insulinotropic actions of glucagon-like peptide 1 receptor (GLP-1R) in beta-cells

129 gh vagal afferents that require an activated glucagon-like peptide 1 receptor (GLP-1r).

130 DT) with exendin-4-IRDye700DX, targeting the glucagon-like peptide 1 receptor (GLP-1R).

131 ering glucose, incretin drugs, which include glucagon-like peptide 1 receptor (GLP1R) agonists and di

132 treatment with thiazolidinedione therapy or glucagon-like peptide 1 receptor agonism alone or in com

133 [(68)Ga]DO3A-VS-Cys(40)-Exendin-4, a glucagon-like peptide 1 receptor agonist, was evaluated

134 odium glucose cotransporter 2 inhibitors and glucagon-like peptide 1 receptor agonists have consisten

135 ntragastric infusion test sessions), whereas glucagon-like peptide 1 responses to milkshake intake we

136 onists, including ADP, arginine vasopressin, glucagon-like peptide 1, and forskolin, and, surprisingl

137 Based on the success of glucagon-like peptide 1-based therapies for type 2 diabe

138 eased gastric volume capacity and release of glucagon-like peptide 1.

139 d improved glucose tolerance, dependent upon glucagon-like peptide 1.

140 Glucagon-like peptide 1 (GLP-1) and glucagon-like peptide 2 (GLP-2) are proglucagon derived

141 The application of glucagon-like peptide one receptor agonists, specific PD

142 o-express several molecules including Glp1r (glucagon-like peptide one receptor) and manipulations of

143 Several glucagon-like peptide receptor agonists (GLP-1RA) and so

144 (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

145 Semaglutide is a once-weekly glucagon-like peptide-1 (GLP-1) analogue for type 2 diab

146 Glucagon-like peptide-1 (GLP-1) and glucose-dependent in

147 d plasma cholecystokinin (CCK), ghrelin, and glucagon-like peptide-1 (GLP-1) concentrations, appetite

148 The interaction between serotonin (5-HT) and glucagon-like peptide-1 (GLP-1) could play a role as ups

149 Glucagon-like peptide-1 (GLP-1) is an incretin hormone w

150 Exendin-4 is a glucagon-like peptide-1 (GLP-1) receptor agonist and pot

151 maglutide is the first oral formulation of a glucagon-like peptide-1 (GLP-1) receptor agonist develop

152 d to investigate the association between the glucagon-like peptide-1 (GLP-1) receptor agonist dulaglu

153 Oral semaglutide is the first oral glucagon-like peptide-1 (GLP-1) receptor agonist for gly

154 exposed to thiazolidinediones (glitazones), glucagon-like peptide-1 (GLP-1) receptor agonists and di

155 Although glucagon-like peptide-1 (GLP-1) receptor agonists and so

156 Glucagon-like peptide-1 (GLP-1) receptor agonists differ

157 body of preclinical evidence indicates that glucagon-like peptide-1 (GLP-1) receptor agonists reduce

158 Two glucagon-like peptide-1 (GLP-1) receptor agonists reduce

159 rlap between signaling and regulation of the glucagon-like peptide-1 (GLP-1) receptor by the non-pept

160 a non-peptide agonist, TT-OAD2, bound to the glucagon-like peptide-1 (GLP-1) receptor.

161 etate and early-phase insulin, C-peptide and glucagon-like peptide-1 (GLP-1) secretion were increased

162 lasma levels of insulin, leptin, amylin, and glucagon-like peptide-1 (GLP-1) were assessed using Lumi

163 CK in enteroendocrine cells (EECs) that were glucagon-like peptide-1 (GLP-1)(+)/Peptide YY (PYY(-)) i

164 for their production of the incretin hormone glucagon-like peptide-1 (GLP-1), also release other neur

165 Glucagon-like peptide-1 (GLP-1), an incretin secreted by

166 FAs and 2-OG, on enteroendocrine secretions [glucagon-like peptide-1 (GLP-1), glucose-dependent insul

167 on of glucose-regulating hormones, including glucagon-like peptide-1 (GLP-1), peptide YY (PYY), and i

168 ll-bowel motility, other MRI parameters, and glucagon-like peptide-1 (GLP-1), polypeptide YY (PYY), a

169 ed receptors (GPCRs) for glucagon (GluR) and glucagon-like peptide-1 (GLP-1R) are normally considered

170 .coli and purification of HepoK-incorporated glucagon-like peptide-1 (GLP1) is demonstrated.

171 visceral or cognitive threats that increase glucagon-like peptide-1 (GLP1) signaling from the caudal

172 Liraglutide, a glucagon-like peptide-1 analogue, improves glycaemic con

173 Glucagon-like peptide-1 receptor (GLP-1R) agonists, wide

174 Glucagon-like peptide-1 receptor (GLP-1R) is a class B G

175 The glucagon-like peptide-1 receptor (GLP-1R), a key pharmac

176 o acid sequence of exendin-4 and targets the glucagon-like peptide-1 receptor (GLP-1R).

177 The glucagon-like peptide-1 receptor (GLP1R) is a class B G

178 Trial evidence shows that the glucagon-like peptide-1 receptor agonist liraglutide sig

179 e available for the subcutaneous form of the glucagon-like peptide-1 receptor agonist semaglutide but

180 we evaluated the efficacy of a short-course glucagon-like peptide-1 receptor agonist therapy-specifi

181 als, including cholecystokinin, exendin-4 (a glucagon-like peptide-1 receptor agonist), amylin, and m

182 Insulin regimens and specific glucagon-like peptide-1 receptor agonists (GLP-1 RAs) ad

183 lucose-lowering medication occurred, and for glucagon-like peptide-1 receptor agonists (GLP-1 RAs; 3.

184 However, the distinction may be crucial for glucagon-like peptide-1 receptor agonists and other anti

185 es and consensus statements have recommended glucagon-like peptide-1 receptor agonists and sodium-glu

186 Glucagon-like peptide-1 receptor agonists and sodium-glu

187 Indeed, in several of the new statements, glucagon-like peptide-1 receptor agonists are suggested

188 More data regarding effects of glucagon-like peptide-1 receptor agonists in patients wi

189 to dramatic weight loss in combination with glucagon-like peptide-1 receptor agonists in preclinical

190 Although glucagon-like peptide-1 receptor agonists may be appropr

191 to micelles, and these micelles activate the glucagon-like peptide-1 receptor with a potency comparab

192 l literature suggests that targeting central glucagon-like peptide-1 receptors (GLP-1Rs) may represen

193 us of the stria terminalis (alBST) expresses glucagon-like peptide-1 receptors (GLP1Rs) and receives

194 ucose cotransporter 2) inhibitors and GLP-1 (glucagon-like peptide-1) receptor agonists, has changed

195 nt research has indicated a crucial role for glucagon-like peptide-1-producing preproglucagon (PPG) n

196 , insulin, C-peptide, and incretin hormones; glucagon-like peptide-1; and glucose-dependent insulinot

197 us of the solitary tract (cNTS) that produce glucagon-like peptide-1; published work in rodents indic

198 The FIGHT (Functional Impact of GLP-1 [glucagon-like peptide-1] for Heart Failure Treatment) tr

199 e effects of once-weekly exenatide (a GLP-1 [glucagon-like peptide-1] receptor agonist) versus placeb

200 Glucagon-like peptide-2 was used in 17 patients.

201 gh-fat diet as well as wild-type C57BL/6 and glucagon-like polypeptide 1 receptor deficient (Glp-1r(-

202 Here, we investigated whether amylin- and glucagon-like-peptide-1 (GLP-1)-based combination therap

203 Glucagon-like-peptide-2 (GLP-2) is an enteroendocrine ti

204 we histologically assessed amylase, insulin, glucagon, lipase, and/or trypsinogen in 78 organ donor p

205 To tease out whether and how glucagon may influence the glucose-lowering effect of SG

206 K2 in the liver is key for allowing complete glucagon-mediated responses and efficient metabolic adap

207 limited-glucose conditions, whereas neither glucagon nor insulin altered AMPK activation.

208 steatosis causes resistance to the effect of glucagon on amino acid metabolism.

209 This review summarizes novel approaches to glucagon optimization, methods with potential applicatio

210 annot be explained by the increase in plasma glucagon or decrease in plasma insulin or glucose concen

211 hile having minimal inhibitory action versus glucagon or GLP-1 at the GLP-1R.

212 ne D(2) receptor was seen with somatostatin, glucagon, or polypeptide Y.

213 We illustrate that glucagon- or PGC1A-induced IRS2 expression was dependent

214 addition to maintaining glucose homeostasis, glucagon participates in the regulation of cholesterol m

215 n of endocrine progenitors into insulin- and glucagon-positive cells through non-cell-autonomous regu

216 ositive cells at the expense of insulin- and glucagon-producing cells during endocrine cell developme

217 In mice, some glucagon-producing pancreatic alpha-cells and somatostat

218 effectors, including antiphasic insulin and glucagon pulses.

219 processes mainly orchestrated by the insulin/glucagon ratio.

220 The glucagon receptor (GCGR) activated by the peptide hormon

221 cs simulations to access the dynamics of the glucagon receptor (GCGR) ECD in the presence of native-l

222 Despite the importance of the glucagon receptor (GCGR) in disease and in pharmaceutica

223 s characterized by reduced expression of the glucagon receptor (GCGR), PEPCK, and genes involved in a

224 e compared the structure and function of the glucagon receptor (GCGR; family B) with the beta(2) adre

225 2) the SGLT2i empagliflozin (25 mg), 3) the glucagon receptor antagonist LY2409021 (300 mg), or 4) t

226 These findings may have implications for glucagon receptor antagonist or agonist-based therapies.

227 Although glucagon receptor antagonists (GRAs) have great potentia

228 ional structures of GPCRs such as GLP-1R and glucagon receptor has helped to drive the rational desig

229 Utilizing whole-body glucagon receptor knockout (Gcgr(-/-)) mice and their wi

230 ought to determine the role of hepatic Gcgr (glucagon receptor) signaling in plasma cholesterol regul

231 ass B G-protein-coupled receptor (GPCR), the glucagon receptor.

232 t effects of GHB on alpha-cell signaling and glucagon release have not been investigated.

233 a-cells might mediate glucose suppression of glucagon release via GHB receptors on alpha-cells.

234 Glucagon resistance in alphaTSC2(KO) mice was associated

235 Liver glucagon resistance in alphaTSC2(KO) mice was characteri

236 can improve glucose homeostasis by inducing glucagon resistance in the liver.

237 es of IS, beta-cell function, GIP, GLP-1 and glucagon response.

238 and incretin hormone responses, but enhanced glucagon responses compared with the CR diet.

239 thesized that hepatic steatosis might impair glucagon's action on hepatic amino acid metabolism and l

240 ete glucagon in response to glucose and some glucagon secretagogues, and elevate blood glucose upon t

241 However, glucagon secreted from pancreatic alpha-cells may accumu

242 cells, considerable evidence indicates that glucagon secreting alpha cells are critically involved i

243 The study of primary glucagon-secreting alpha-cells is hampered by their low

244 complex 1 (mTORC1) regulation that controls glucagon secretion and alpha-cell mass.

245 and the antagonist NCS-382 had no effects on glucagon secretion and did not affect stimulation of sec

246 eated and used to investigate its effects on glucagon secretion and glucose metabolism.

247 mechanisms underlying glucose regulation of glucagon secretion are poorly understood and likely invo

248 nhibitor vigabatrin also failed to influence glucagon secretion at 1 mm glucose and did not prevent t

249 In human islets, GHB tended to stimulate glucagon secretion at 1 mm glucose, an effect mimicked b

250 us and correlated with dapagliflozin-induced glucagon secretion at 6 mmol/L glucose.

251 hanced islet insulin secretion and decreased glucagon secretion at the study end.

252 herapeutic concentrations of insulin inhibit glucagon secretion by an indirect (paracrine) mechanism

253 n SGLT2 expression and regulation may affect glucagon secretion by human alpha-cells in response to S

254 Moreover, glucagon secretion by islets from 31 donors at low gluco

255 lucose cotransporter 2 (SGLT2) inhibitors in glucagon secretion by pancreatic alpha-cells reported co

256 l role, either stimulatory or inhibitory, in glucagon secretion depending on glucose levels.

257 Glucagon secretion from perifused mouse islets was also

258 orchestrate temporal profiles of insulin and glucagon secretion in a physiological context.

259 in Min6-K8 cells, no effect was observed on glucagon secretion in alpha-TC6 cells under the conditio

260 e, and stimulates GPR119-dependent GLP-1 and glucagon secretion in mice.

261 h GIP or GLP-1, respectively, on insulin and glucagon secretion in patients with HNF1A diabetes is cu

262 glucose administration and showed increased glucagon secretion in response to a glucose injection co

263 Moreover, failure of alpha-cells to increase glucagon secretion in response to falling blood glucose

264 Insulin secretion was reduced, and glucagon secretion increased on the CRHP diet after both

265 Glucagon secretion is regulated by circulating glucose,

266 P measurement with inhibition of insulin and glucagon secretion with somatostatin infusion and replac

267 -like peptide 1 (GLP-1) is known to suppress glucagon secretion, but the mechanism by which GLP-1 exe

268 ased amino acid concentrations and increased glucagon secretion, providing a likely explanation for f

269 and to increase both glucose production and glucagon secretion.

270 comitantly stimulates euglycemic insulin and glucagon secretion.

271 an increase in glucagon content and enhanced glucagon secretion.

272 mediate the inhibitory effect of glucose on glucagon secretion.

273 with inhibition rather than acceleration of glucagon secretion.

274 ffects of SGLT2i on alpha-cells to stimulate glucagon secretion.

275 pression of SGLT2 protein and variability in glucagon secretory responses contribute to interindividu

276 a are increased during pregnancy; therefore, glucagon should be available to the patient and close co

277 Loss of glucagon signaling alters white adipose tissue browning.

278 into the molecular interplay between hepatic glucagon signaling and lipid metabolism and describe a n

279 Glucagon signaling increases hepatic glucose output, and

280 Interrupting glucagon signaling lowers blood glucose but also results

281 A drove the expression of IRS2 downstream of glucagon signaling while simultaneously reducing IRS1 ex

282 nduced ketosis is altered by interruption of glucagon signaling.

283 be important, as PAHSAs inhibited basal and glucagon-stimulated EGP directly in isolated hepatocytes

284 P2 isoform induction occurs in response to glucagon-stimulated upregulation of TET3, not previously

285 Here we show that glucagon stimulates hepatic gluconeogenesis by increasin

286 Glucagon stimulation not only promoted GCGR endocytic tr

287 al-hormone therapy and enhances postprandial glucagon suppression in diabetic pigs.

288 nes important but often overlooked roles for glucagon that extend beyond glycemia and supports a new

289 By secreting insulin and glucagon, the beta- and alpha-cells of the pancreatic is

290 uding metabolic hormones such as insulin and glucagon, the cellular master switches 5' AMP-activated

291 as been a resurgence of interest in improved glucagon therapy, including nonconventional liquid formu

292 for example, by switching from secretion of glucagon to secretion of insulin and back (transdifferen

293 Moreover, any effect of glucagon to stimulate ketogenesis is severely limited by

294 s enhanced responses in LAdrKO mice during a glucagon tolerance test (250 ug/kg intraperitoneally).

295 Glucagon treatment increased the expression of thermogen

296 However, these effects of chronic glucagon treatment-reversing hepatic steatosis and gluco

297 patic glucose and amino acid metabolism when glucagon was at basal levels and at high physiological l

298 he current investigation was to determine if glucagon was required for the effects of cold on WAT bro

299 Baseline values of serum glucagon were not different between the 2 trials; howeve

300 h after intraperitoneal (i.p.) injection of glucagon, which is known to rapidly deplete hepatic glyc