ライフサイエンスコーパス: insulin secretion

1 on in cultured pancreatic beta cells altered insulin secretion.

2 distinct roles aside from glucose-stimulated insulin secretion.

3 ells, where it is involved in the control of insulin secretion.

4 ial bioenergetics control glucose-stimulated insulin secretion.

5 are thus instrumental in mediating pulsatile insulin secretion.

6 ne protein HID-1 in neuropeptide sorting and insulin secretion.

7 adjacent gene Sec22a, and a 39% reduction in insulin secretion.

8 d in cell signaling and pancreatic beta-cell insulin secretion.

9 cell markers and improved glucose stimulated insulin secretion.

10 beta mice in accordance with their decreased insulin secretion.

11 reduction and inhibition of glucose-induced insulin secretion.

12 ta-cells where it modulates Ca(2+)-dependent insulin secretion.

13 betic patients due to its ability to enhance insulin secretion.

14 LP) diet are normoglycemic despite collapsed insulin secretion.

15 splay decreased insulin content and impaired insulin secretion.

16 s, barr2 knockdown abolished glucose-induced insulin secretion.

17 ng ERAD of Akita proinsulin and restoring WT insulin secretion.

18 lts in reduced ADCY5 expression and impaired insulin secretion.

19 ucose homeostasis resulting from an enhanced insulin secretion.

20 and plays a critical role in the control of insulin secretion.

21 P in beta-cells with light thereby enhancing insulin secretion.

22 correlating with improved glucose-stimulated insulin secretion.

23 beta-cell mitophagy, oxygen consumption, and insulin secretion.

24 In addition, it has recently been linked to insulin secretion.

25 active oxygen species and glucose-stimulated insulin secretion.

26 se fluxes, thereby minimizing the demand for insulin secretion.

27 S: (1/GlyRa x fasting insulin) x first-phase insulin secretion.

28 an trigger pulses of electrical activity and insulin secretion.

29 ochondrial activity--which promote increased insulin secretion.

30 cal morphology with restoration of regulated insulin secretion.

31 w the overexpression of TCF7L2 may attenuate insulin secretion.

32 ce through effects on glucagon as well as on insulin secretion.

33 egulation of the miR-212/miR-132 cluster and insulin secretion.

34 tal DES or DEX treatment had no effects upon insulin secretion.

35 ding to reduced beta-cell mass and decreased insulin secretion.

36 rum concentrations of C-peptide, a marker of insulin secretion.

37 tivator of muscarinic M3 receptor-stimulated insulin secretion.

38 pression of which has been shown to increase insulin secretion.

39 ses which led to enhanced glucose-stimulated insulin secretion.

40 ayed marked glucose intolerance with reduced insulin secretion.

41 from defects in both insulin sensitivity and insulin secretion.

42 cates that PFAS alter glucose metabolism and insulin secretion.

43 utes to beta-cell apoptosis and insufficient insulin secretion.

44 lin content and increased glucose-stimulated insulin secretion.

45 s in pancreatic beta-cells that impair fetal insulin secretion.

46 imarily due to defects in glucose-stimulated insulin secretion.

47 s not expected to produce adverse effects on insulin secretion.

48 ytokine signaling in adipocytes may regulate insulin secretion.

49 ed beta-cell function and glucose-stimulated insulin secretion.

50 ) axis activation, aversive conditioning, or insulin secretion.

51 nd is required for the postprandial spike in insulin secretion.

52 can be pharmacologically exploited to boost insulin secretion.

53 xygen species (ROS) production and decreased insulin secretion.

54 Gbeta5-RGS7 strongly promotes M3R-stimulated insulin secretion.

55 y a key role in regulating glucose-dependent insulin secretion.

56 mp), lipid oxidation (indirect calorimetry), insulin secretion (2-h hyperglycemic clamp), and body co

57 n(-1), respectively; P = 0.9) or first-phase insulin secretion (-21 +/- 212 compared with 24 +/- 184

58 between the ER and the PM in the control of insulin secretion, a process impaired in patients with t

59 ease of the incretin hormone GLP-1 and hence insulin secretion after a meal.

60 ble of regulating the blood glucose level by insulin secretion after administration of oral glucose.

61 channels formed by SUR1 and Kir6.2 regulate insulin secretion and are the targets of antidiabetic su

62 ied models of compensatory increases in both insulin secretion and beta cell mass.

63 ociated with small differences in markers of insulin secretion and beta-cell function.

64 cells increases basal and glucose-stimulated insulin secretion and Ca(2+) uptake in the presence of g

65 Both glucose and KCl-induced insulin secretion and calcium responses were profoundly

66 erent genes can lead to the dysregulation of insulin secretion and cause this disorder.

67 Kcne2 deletion impairs insulin secretion and causes type 2 diabetes mellitus.

68 tiple disease-relevant phenotypes, including insulin secretion and cellular proliferation.

69 2 patients display increased GLP-1, GIP, and insulin secretion and defective glucagon secretion, caus

70 e also reverses glucolipotoxic inhibition of insulin secretion and enhances glucose uptake into skele

71 neurons and the central effect of glucose on insulin secretion and food intake.

72 In addition, mutant mice displayed defective insulin secretion and GLP-1 action on islets in vivo and

73 FMD cycles restore insulin secretion and glucose homeostasis in both type 2

74 lation of LDB1 in mature beta cells impaired insulin secretion and glucose homeostasis.

75 t GLP1R expression and GLP1R agonist-induced insulin secretion and glucose tolerance.

76 , which stimulates glucose-induced beta-cell insulin secretion and helps maintain glucose homeostasis

77 associated with enhanced glucose-stimulated insulin secretion and hyperglucagonemia, in addition to

78 N2 maintains glucose homeostasis by inducing insulin secretion and improves glucose tolerance and ins

79 creatic islet enhancers for loci influencing insulin secretion and in adipocytes, monocytes, and hepa

80 -like cells show enhanced glucose stimulated insulin secretion and increased capacity to maintain glu

81 ighly coordinated, and reciprocal changes of insulin secretion and insulin sensitivity that preserve

82 will potentially create an imbalance between insulin secretion and insulin-stimulated glucose utiliza

83 le of circadian oscillators in orchestrating insulin secretion and islet gene transcription has been

84 , yet there was a dose-dependent increase in insulin secretion and plasma insulin levels.

85 aired glucose-stimulated Ca(2+) dynamics and insulin secretion and recapitulated the pattern of impro

86 grafted onto immunocompetent hosts increased insulin secretion and reversed high-fat-diet-induced wei

87 These potent effects on insulin secretion and sensitivity were fully reversed by

88 ires large studies with detailed measures of insulin secretion and sensitivity.

89 ism for glucolipotoxicity-induced defects in insulin secretion and stigmasterol treatment as a potent

90 prove glycemic control in T2DM by increasing insulin secretion and suppressing glucagon levels.

91 dispensable for the physiological control of insulin secretion and the pharmacological response to GP

92 and hepatocytes, and that glucose stimulated insulin secretion and the response to metabolic stress,

93 of adipose tissue lipolysis due to decreased insulin secretion and to a reduced response of adipose t

94 Pilocarpine also fails to stimulate insulin secretion and, instead, antagonizes the insulino

95 The risk alleles impair glucose-induced insulin secretion and, paradoxically but characteristica

96 cose tolerance, insulin tolerance, GLP-1 and insulin secretion), and decreased blood lipids and infla

97 estatin and ghrelin have opposing effects on insulin secretion, and both are mediated through ghrelin

98 f genes involved in cell survival and death, insulin secretion, and c-Jun N-terminal kinase (JNK) sig

99 orsening of glucose tolerance, impairment of insulin secretion, and diabetes by 30 weeks of age.

100 leading to beta-cell apoptosis, insufficient insulin secretion, and glucose intolerance in female rat

101 a-/-) mice develop hypoinsulinemia, impaired insulin secretion, and glucose intolerance that rapidly

102 ses energy expenditure, insulin sensitivity, insulin secretion, and glucose tolerance.

103 mass, impaired glucose tolerance, defective insulin secretion, and increased apoptosis when a combin

104 for normal beta-cell electrical activity and insulin secretion, and that Kcne2 deletion causes T2DM.

105 1 and its RGD domain on insulin sensitivity, insulin secretion, and whole-body glucose regulation.

106 ing an amplified biphasic glucose-stimulated insulin secretion arising from an increase in size of th

107 oved glucose tolerance, cAMP production, and insulin secretion as well as protection against diabetes

108 genome-wide association study of first-phase insulin secretion, as measured by intravenous glucose to

109 gues have been prepared and characterized in insulin secretion assays using both mouse and human isle

110 sing [Ca(2+)] imaging, static and perifusion insulin secretion assays, and gap junction permeability

111 e that fatty acids enhance both glucagon and insulin secretion at fasting glucose concentrations and

112 ere associated with a measure of first-phase insulin secretion at P < 0.05 and provided new evidence,

113 ANP augmented insulin secretion at the threshold glucose concentration

114 In hyperinsulinaemic hypoglycaemia, insulin secretion becomes dysregulated (ie, uncoupled fr

115 the temporal trends of glucose homeostasis, insulin secretion, beta cell morphometry, and islet gene

116 There was no difference in body weight or insulin secretion between diets (P = NS).

117 ow that sirolimus impairs glucose-stimulated insulin secretion both in human and murine pancreatic is

118 nation of several characteristic features of insulin secretion both in vitro and in vivo by using a m

119 was accompanied by impaired glucose-induced insulin secretion both in vivo in hyperglycemic clamps a

120 termittent translocation of PKCs and reduced insulin secretion but did not affect [Ca(2+)]pm elevatio

121 s strongly associated with lower first-phase insulin secretion but has no evidence for an effect on t

122 lucose tolerance was caused by a decrease in insulin secretion but not in insulin sensitivity.

123 We did not observe a CKD-specific deficit in insulin secretion, but the combination of insulin resist

124 acterized by insulin resistance and impaired insulin secretion, but the mechanisms underlying insulin

125 Although glucose is known to stimulate insulin secretion by beta cells, whether it directly eng

126 dult islets, since Ex-4 treatment stimulated insulin secretion by both juvenile and adult human beta

127 We aim to increase insulin secretion by developing strategies that work thr

128 Rather, PDIA6 affected insulin secretion by modulating one of the activities of

129 ) is a critical regulator of glucose-induced insulin secretion by pancreatic beta-cells.

130 tes glucagon-like peptide 1 (GLP-1)-mediated insulin secretion by upregulating interleukin-6 (IL-6).

131 s in proliferation, autophagy, apoptosis and insulin secretion by using mice with conditional (betara

132 Reduced insulin secretion can result from reduced proliferative

133 Hence, a possible deterioration of insulin secretion capacity in patients who are predispos

134 a hormone with essential roles in regulating insulin secretion, carbohydrate metabolism and appetite.

135 gnificant difference in glucose tolerance or insulin secretion compared with mice expressing the Cre

136 Postnatal insulin secretion correlated with beta cell numbers (P =

137 We found that glucose-induced insulin secretion declined by 50% in rats housed at 5 de

138 ll)) exhibit lower levels of meal-stimulated insulin secretion, decreased expansion of adipose tissue

139 developed glucose intolerance and beta-cell insulin secretion defect but showed no changes in beta-c

140 However, without further worsening of the insulin secretion defect, glucose homeostasis deteriorat

141 Persistent insulin secretion defects culminate in progressive defic

142 nsulinism (CHI) is a disorder of unregulated insulin secretion despite hypoglycaemia that can occur i

143 s physical activity, 24-h glycemia, and 24-h insulin secretion did not differ between intervention da

144 s control the overall [Ca(2+)]i response and insulin secretion dynamics of the islets of Langerhans.

145 Ca(2+)] dynamics, gap junction coupling, and insulin secretion dynamics with age.

146 Frequent insulin secretion exposes ZnT8 to the cell surface, but

147 lin secretion, but the mechanisms underlying insulin secretion failure are not completely understood.

148 in significantly improved glucose-stimulated insulin secretion for both non-diabetic and diabetic hum

149 and insulin resistance in part by promoting insulin secretion from beta cells in mice.

150 Insulin secretion from beta-cells depends on the firing

151 inal L cells, glucose dependently stimulates insulin secretion from beta-cells.

152 its selective activation by CH 275 inhibited insulin secretion from human islets, with no effect on m

153 ehydrogenase (GDH) was required to stimulate insulin secretion from INS-1 832/13 cells.

154 eover, the BRD3308 treatment increased basal insulin secretion from islets cultured in vitro All meta

155 d that palmitate enhances glucose-stimulated insulin secretion from isolated human islets via free fa

156 This results in doubling of insulin secretion from isolated mouse islets or INS-1 be

157 3 agonist MRS 5698 inhibited glucose-induced insulin secretion from mouse islets, with no effect on h

158 P1], HIP14, GASP-1, and Nedd4) that decrease insulin secretion from murine insulinoma MIN6B1 cells in

159 gh the mechanisms by which glucose regulates insulin secretion from pancreatic beta-cells are now wel

160 pe 2 diabetes, culminating in the failure of insulin secretion from pancreatic beta-cells.

161 brain or directly enhance glucose-stimulated insulin secretion from pancreatic beta-cells.

162 agonist AR231453 failed to directly enhance insulin secretion from perifused islets.

163 ic phenotype in T2D beta-cells and increases insulin secretion from T2D islets.

164 In addition to affecting insulin secretion, genetic variation at the TCF7L2 locus

165 ssociated with inhibition of glucose-induced insulin secretion (GIIS), but only in the presence of in

166 robe intervention improved glucose-dependent insulin secretion, glucose metabolism and cholesterol me

167 insulin biosynthesis and glucose-stimulated insulin secretion (GSIS) in a PKA-dependent manner and p

168 plays an integral role in glucose-stimulated insulin secretion (GSIS) in beta-cells.

169 d first- and second-phase glucose-stimulated insulin secretion (GSIS) resulting from reduction in rea

170 tors best correlates with glucose-stimulated insulin secretion (GSIS), define the fate of glucose in

171 own that ghrelin inhibits glucose-stimulated insulin secretion (GSIS), the effect of obestatin on GSI

172 8 overexpression impaired glucose-stimulated insulin secretion (GSIS), which was recovered by NNAT ov

173 on the cell surface, and glucose-stimulated insulin secretion (GSIS).

174 asis, partly by enhancing glucose-stimulated insulin secretion (GSIS).

175 Glucose stimulation of insulin secretion has been extensively studied, but its

176 the relationship of structure to effects on insulin secretion have not been significantly studied.

177 to inhibit glucagon secretion and stimulate insulin secretion in a glucose-dependent manner.

178 and umami taste, and enhance glucose-induced insulin secretion in a Trpm5-dependent manner.

179 ation was not the primary cause of decreased insulin secretion in A2AAR-KO mice.

180 Glucose metabolism promotes insulin secretion in beta-cells via metabolic coupling f

181 ited significant but reversible reduction in insulin secretion in both mouse and human islets.

182 ked kinase, enhanced insulin sensitivity and insulin secretion in C2C12 myotubes and INS-1 832/13 pan

183 promoted actin reorganization, and improved insulin secretion in cells exposed to glucolipotoxicity.

184 for the channel might contribute to impaired insulin secretion in diabetes.

185 fat, impaired glucose tolerance, and reduced insulin secretion in first- (F1) and second-generation (

186 ensing are likely to contribute to defective insulin secretion in human carriers of PAX6 mutations.

187 a-cell genes and improves glucose-stimulated insulin secretion in human islets from donors with T2D.

188 Knockdown of Camta1 decreased insulin secretion in INS-1 832/13 cells and Wistar rat i

189 However, glucose homeostasis and insulin secretion in IRS2(5A)-beta mice were impaired wh

190 Unlike controls, insulin secretion in KATPHI islets increased in response

191 Intact insulin secretion in L-CC1 mice with protected hepatic i

192 Both doses of BPA significantly impaired insulin secretion in male but not female F1 and F2 offsp

193 bolism, we find decreased glucose-stimulated insulin secretion in MENX rats, while insulin sensitivit

194 mycin treatment decreases CPE expression and insulin secretion in mice and human islets.

195 CMPF inhibits insulin secretion in mouse and human islets in vitro and

196 fission is necessary for glucose-stimulated insulin secretion in mouse and human islets.

197 on and activation of bPAC increased cAMP and insulin secretion in murine islets and in beta-cell pseu

198 that wild type hSCGN overexpression promotes insulin secretion in pancreatic beta cells, while C193S-

199 calcium binding protein, plays key roles in insulin secretion in pancreatic beta-cells.

200 ing for their role in GLP-1R potentiation of insulin secretion in pancreatic beta-cells.

201 These findings suggest that insulin secretion in pancreatic cells is regulated by Ca

202 tive oxygen species (ROS) and also restoring insulin secretion in pancreatic cells.

203 e the concept that PI3Kgamma is required for insulin secretion in response to glucose in vivo, and in

204 pancreatic beta cells is required for normal insulin secretion in response to glucose.

205 studied in vivo by measuring food intake and insulin secretion in response to increased brain glucose

206 that might provide novel targets to enhance insulin secretion in T2D.

207 ereby glucocorticoids boost cAMP to maintain insulin secretion in the face of perturbed ionic signals

208 ation with ML351 improved glucose-stimulated insulin secretion in the presence of proinflammatory cyt

209 and acts directly on beta cells to stimulate insulin secretion in vitro Uncovering physiologic mechan

210 Kcne2 deletion impaired beta-cell insulin secretion in vitro up to 8-fold and diminished b

211 Several molecules that influence insulin secretion in vitro were identified.

212 ts expressing 6KR mutant FoxO1 have enhanced insulin secretion in vivo and ex vivo and decreased fatt

213 ), we observed defects in glucose-stimulated insulin secretion in vivo and in isolated islets.

214 rchitecture, and impaired glucose-stimulated insulin secretion in vivo.

215 activation of stress axes or stimulation of insulin secretion - in response to GCG+ neuron activatio

216 diabetic animals and has profound effects on insulin secretion, including reduced depolarization-evok

217 ta-cell cholesterol homeostasis and impaired insulin secretion increase adiposity, reduce skeletal mu

218 lin resistance, synergistically with lowered insulin secretion, increases serum glucose levels, which

219 atical simulations were used to test whether insulin secretion induced by oral glucose could cause hy

220 s regulate numerous cellular processes, like insulin secretion, inflammation, proliferation, and cell

221 Insulin secretion, insulin sensitivity, Ra, and disposit

222 Thus, beta-cell function measured with the insulin secretion/insulin sensitivity (disposition) inde

223 vidence, or the strongest evidence yet, that insulin secretion, intrinsic to the islet cells, is a ke

224 Loss of first-phase insulin secretion is an early sign of developing type 2

225 The control of insulin secretion is complex and affected by circulating

226 ng hyperglucagonemia of longer duration when insulin secretion is inhibited.

227 lycemic condition, and obestatin's effect on insulin secretion is mediated by GHS-R in pancreatic bet

228 Insulin secretion is precisely regulated so that, under

229 ssing a mutant form of Sox4, glucose-induced insulin secretion is reduced by 40% despite normal intra

230 oss of this organization underlies disturbed insulin secretion kinetics in T2D.

231 ontributing to delays in glucose sensing and insulin secretion kinetics.

232 in resistance and inadequate augmentation of insulin secretion led to a high prevalence of impaired g

233 However, insulin secretion, maximal ATP/ADP responses to glucose,

234 tification of the novel role of Gbeta5-R7 in insulin secretion may lead to a new therapeutic approach

235 can be displayed on the cell surface and how insulin secretion may regulate the level of ZnT8 exposur

236 d the computational model against [Ca2+] and insulin secretion measurements in islets expressing ATP-

237 intake alone did increase beta cell mass and insulin secretion moderately.

238 Intestinal nutrients stimulate insulin secretion more potently than intravenous (IV) gl

239 Importantly, a compensatory augmentation in insulin secretion occurs following inhibition or cessati

240 Notably, pyruvate fully rescues the impaired insulin secretion of fission-deficient beta-cells, demon

241 nt to rescue the impaired glucose-stimulated insulin secretion of transgenic mice, pointing to a pote

242 that it reads (GALR3) and galanin inhibited insulin secretion only from mouse islets.

243 s fatty acids, resulting in amplification of insulin secretion only in the presence of elevated gluco

244 tion of Arap1 in beta cells had no impact on insulin secretion or proinsulin conversion in mice.

245 Whilst some treatments work by increasing insulin secretion, over time their effectiveness decreas

246 we examined cytosolic calcium ([Ca(2+)] i ), insulin secretion, oxygen consumption, and [U-(13)C]gluc

247 , uncoupled from glucose metabolism) so that insulin secretion persists in the presence of low plasma

248 e (cGMP) analog on KATP channel activity and insulin secretion point to participation of the cGMP/PKG

249 in offers a rational approach to rectify the insulin secretion problem in MIDY.

250 e and 4-hydrpxnonenal both assayed by ELISA, insulin secretion quantified using ELISA or radioimmunoa

251 tifies the mechanisms modulating first-phase insulin secretion rate in response to basal hyperglycemi

252 eak insulin response than on C-peptide-based insulin secretion rate, suggesting a possible additional

253 brain activity during deep sleep and fasting insulin secretion rate.

254 s elucidated key mechanisms that control the insulin secretion rate.

255 Thus, rapid insulin secretion requires Munc13-mediated recruitment o

256 EACAM1 levels provides in vivo evidence that insulin secretion responds to changes in insulin clearan

257 tated Ins2 allele that dominantly suppresses insulin secretion, resulting in lifelong diabetes.

258 beta-Cell function (Insulin Secretion Sensitivity Index-2) was 2-fold higher

259 or glucose homeostasis, insulin sensitivity, insulin secretion, steatosis, metabolic inflammation, pa

260 xylase KO mice and exhibited in vitro normal insulin secretion stimulated by glucose and theophylline

261 As the glucose concentration fell, insulin secretion subsided, demonstrating a functional f

262 hyperglycemia and correlated negatively with insulin secretion, suggesting a potential pathogenic rol

263 hyperglycemia and correlated positively with insulin secretion, suggesting a protective role, whereas

264 tion and could form the basis for defects in insulin secretion that occur early in the pathogenesis o

265 ance, phosphate sensing, cell migration, and insulin secretion), the majority of their protein target

266 This resulted in impaired insulin secretion, thereby connecting differential methy

267 induces intestinal GLP-1 release to enhance insulin secretion, thereby counteracting insulin resista

268 g that ApoA-IV treatment enhanced pancreatic insulin secretion, these results suggests that ApoA-IV a

269 n weight loss and (b) reduce fluctuations in insulin secretion through avoidance of rapidly absorbabl

270 vivo, and tested whether obestatin regulates insulin secretion through GHS-R.

271 -fold weaker reduction in glucose-stimulated insulin secretion through the EP3 receptor as compared w

272 rea therapy and is associated with increased insulin secretion, thus mimicking the effects of sulfony

273 stinal L-cells, and augments glucose-induced insulin secretion, thus playing an important role in glu

274 These beta-cells adapt insulin secretion to ambient metabolite status and show

275 Dynamic adjustment of insulin secretion to compensate for changes of insulin s

276 f body composition, insulin sensitivity, and insulin secretion.To address existing knowledge gaps, we

277 Insulin secretion together with reciprocal inhibition of

278 glucose intolerance attributable to impaired insulin secretion, together with reduced alpha- and beta

279 nergetics reveals that Drp1 does not control insulin secretion via its effect on proton leak but inst

280 e pancreatic interleukin-33 (IL-33) promotes insulin secretion via the activity of islet-associated g

281 via hyperinsulinemic-euglycemic clamps), and insulin secretion [via intravenous-glucose-tolerance tes

282 Obestatin-induced insulin secretion was abolished in the circulation of Gh

283 dation, O2 consumption, and ATP production), insulin secretion was almost completely restored at elev

284 Insulin secretion was also diminished, with ischemic bet

285 Furthermore, glucose-induced insulin secretion was also markedly impaired in islets i

286 es to 262 proteins ex vivo The impairment of insulin secretion was associated with greater overall ch

287 The concomitant augmented insulin secretion was comparable to that from beta-cells

288 by approximately 60%, and glucose-stimulated insulin secretion was eliminated.

289 In the first 30 min of the MMTT, insulin secretion was lower in PI-CF compared with PS-CF

290 Insulin secretion was measured using the area under the

291 In contrast, glucose- and GLP-1-stimulated insulin secretion was not affected in islets of knockout

292 Insulin secretion was reduced (0.5 vs. 0.1 ng/ml; P < 0.

293 In adolescence basal insulin secretion was significantly higher in female off

294 s in leukocytes as well as 24-h glycemia and insulin secretion were analyzed.When compared with the 3

295 Basal [Ca(2+)] i and insulin secretion were higher in KATPHI islets compared

296 particularly those that also correlated with insulin secretion, were considered the strongest candida

297 diabetes of youth (MIDY), there is decreased insulin secretion when mutant proinsulin expression prev

298 on-like peptide 1 (GLP-1) on glucose-induced insulin secretion, which could be caused by a cGMP-media

299 uating insulin demands and adjusted rates of insulin secretion, which is the function of pancreatic b

300 tional islet mass and associated early-phase insulin secretion, which with decreased incretin respons