ライフサイエンスコーパス: insulin secretion

1 IPF5 disruption by decreasing the demand for insulin secretion.

2 mans and rodents they produce suppression of insulin secretion.

3 islet grafts demonstrated glucose-stimulated insulin secretion.

4 acellular stores, increasing glucose-induced insulin secretion.

5 lin resistance, is associated with increased insulin secretion.

6 ounger granules occurs in glucose-stimulated insulin secretion.

7 n frequency and decreases glucose-stimulated insulin secretion.

8 h as nutrient sensing is directly coupled to insulin secretion.

9 CCK is necessary for the full stimulation of insulin secretion.

10 ired for insulin SG biogenesis and regulated insulin secretion.

11 essary for robust ex vivo glucose-stimulated insulin secretion.

12 ithout a negative impact islet viability and insulin secretion.

13 y shown that primary cilia directly regulate insulin secretion.

14 wild-type islets reduces glucose-stimulated insulin secretion.

15 nisms including increased beta-cell mass and insulin secretion.

16 embrane hyperpolarization and suppression of insulin secretion.

17 ose tissue for storage and triggered greater insulin secretion.

18 ) and stimulated (45 mM KCl + 14 mM glucose) insulin secretion.

19 lin content, and enhanced glucose-stimulated insulin secretion.

20 effect of SPARC on oxotremorine-M-stimulated insulin secretion.

21 L and this process is inversely regulated to insulin secretion.

22 howed that knockdown of FICD and TPX2 alters insulin secretion.

23 tion of the Delta/Notch pathway in beta-cell insulin secretion.

24 tion, triggering enhanced Rap1 signaling and insulin secretion.

25 by enhancing fetal beta-cell development and insulin secretion.

26 esponses in pancreatic beta cells to control insulin secretion.

27 nin CD63 prevent SINGD, leading to increased insulin secretion.

28 h insulin resistance but also with decreased insulin secretion.

29 haperone crucial for proinsulin handling and insulin secretion.

30 non-beta-cells could underlie persistent T1D insulin secretion.

31 d leading to reduced cell mass and decreased insulin secretion.

32 ose intolerance, hyperglycemia, and impaired insulin secretion.

33 oint of glucose-stimulated Ca(2+) influx and insulin secretion.

34 nnels, increased [Ca(2+)](i), which triggers insulin secretion.

35 e peripheral clock in the pancreas regulates insulin secretion.

36 ation, a prominent ROS-producing pathway, to insulin secretion.

37 o reach high local concentrations and affect insulin secretion.

38 nhibited by cellular mechanisms that promote insulin secretion.

39 g programs ranging from protein synthesis to insulin secretion.

40 endoplasmic reticulum, ultimately decreasing insulin secretion.

41 2 in mouse islets impairs glucose-stimulated insulin secretion.

42 ral role in coupling glucose metabolism with insulin secretion.

43 he generation of SC-beta cells with improved insulin secretion.

44 letion of insulin SG content and a defect in insulin secretion.

45 ative role for C1ql3 in regulating beta-cell insulin secretion.

46 betes via potentiation of glucose-stimulated insulin secretion.

47 llele may be caused by decreased early-phase insulin secretion.

48 )-mediated suppression of glucose-stimulated insulin secretion.

49 G protein subunit beta 5 (Gnb5) knockout on insulin secretion.

50 mmune disease resulting in severely impaired insulin secretion.

51 esicles away from the plasma membrane limits insulin secretion.

52 and second-phase dynamic glucose-stimulated insulin secretion.

53 thin the pancreatic islet drives oscillatory insulin secretion.

54 ically preproglucagon peptides in regulating insulin secretion.

55 in GLP-1R protein levels or GLP-1R-mediated insulin secretion.

56 e GLP-1 receptor, in paracrine regulation of insulin secretion.

57 itochondrial oxidation that is necessary for insulin secretion.

58 LCS) islets, two major processes involved in insulin secretion.

59 TrkB.T1 show impaired glucose tolerance and insulin secretion.

60 reased cell viability and glucose-stimulated insulin secretion.

61 (P(i)) accompanied the events of stimulated insulin secretion.

62 First-phase insulin secretion (0-10 min) increased by 70%, while sec

63 mponent C3a, which acts to augment beta cell insulin secretion(5).

64 CXCL12 enhanced glucose-stimulated insulin secretion activity of SC-beta cells and induced

65 R controls, among others, growth hormone and insulin secretion, adiposity, feeding, and glucose metab

66 lly due to the progressive loss of beta-cell insulin secretion against a background of insulin resist

67 Changes in fasting glucose, acute insulin secretion (AIR), and insulin sensitivity (Si) we

68 hibition of PKD exacerbates SINGD, mitigates insulin secretion and accelerates diabetes.

69 tivation of the innate immune system impairs insulin secretion and action, and inflammation also cont

70 rial of pioglitazone therapy on GIP-mediated insulin secretion and adipocyte GIP-R expression in subj

71 ugh targeting several critical regulators of insulin secretion and beta cell proliferation.

72 a (miR-26a) in beta cells not only modulates insulin secretion and beta cell replication in an autocr

73 d that sEVs from GDM women fail to stimulate insulin secretion and cause exacerbated insulin resistan

74 s on GLP-1, in the context of their roles in insulin secretion and consequently glucose metabolism.

75 -1R agonism to potentiate glucose-stimulated insulin secretion and decrease body weight in diet-induc

76 pe 2 diabetes are characterized by deficient insulin secretion and decreased beta-cell mass.

77 finding that correlates with enhanced islet insulin secretion and decreased glucagon secretion at th

78 uces platelet hyperactivation, triggers both insulin secretion and degradation, and increases insulin

79 lin injection, suggesting an altered rate of insulin secretion and degradation.

80 betes (T2D) is characterized by insufficient insulin secretion and elevated glucose levels, often in

81 enriched gene sets, including regulation of insulin secretion and endocannabinoid signaling.

82 RNF40 regulate beta-cell gene expression and insulin secretion and establish a link between Isl1 comp

83 e diabetic beta-cell alters function, limits insulin secretion and exacerbates hyperglycemia.

84 ometric test) enriched in pathways linked to insulin secretion and extracellular matrix-receptor inte

85 cell and skeletal muscle respectively impair insulin secretion and glucose uptake.

86 Spexin decreases insulin secretion and has potent anorectic, analgesic, a

87 atic steatosis on the complex integration of insulin secretion and hepatic and extrahepatic tissue ex

88 uggest no direct role for CCK in stimulating insulin secretion and highlight the critical role of int

89 hormone dysregulation contributes to reduced insulin secretion and hyperglycemia in patients with typ

90 estigate the preferential secretion model of insulin secretion and identify how granule aging is affe

91 o prevented impairment of glucose-stimulated insulin secretion and improved glucose tolerance in NOD

92 ry reduction of BCAAs decreases postprandial insulin secretion and improves white adipose tissue meta

93 characterized by impaired glucose-stimulated insulin secretion and increased peripheral insulin resis

94 diet lowered glucose excursions and reduced insulin secretion and incretin hormone responses, but en

95 Inhibition of CB1R improves insulin secretion and insulin sensitivity in pancreatic

96 The effect of 72-h glucose infusion on insulin secretion and insulin sensitivity was similar in

97 arities in key aspects of glucose-stimulated insulin secretion and insulin-stimulated glucose oxidati

98 his transporter decreases glucose-stimulated insulin secretion and intracellular insulin content, par

99 1ql3 is expressed in beta-cells, it inhibits insulin secretion and key genes that are involved in bet

100 tic beta cells play key roles in stimulating insulin secretion and maintaining physiological blood gl

101 sulin response is the result of two factors: insulin secretion and metabolic clearance rate of insuli

102 ing nutrient-dependent lysosomal function to insulin secretion and more generally to beta cell health

103 F complex is required for glucose-stimulated insulin secretion and normal mitochondrial reactive oxyg

104 iculum (ER) calcium (Ca(2+)) levels diminish insulin secretion and reduce beta-cell survival in both

105 ze their fasting glycemia by both increasing insulin secretion and regenerating beta-cells.

106 cagonemia on glucose homeostasis by inducing insulin secretion and resistance to glucagon in the live

107 s such a tight correlation between defective insulin secretion and rising glucose levels.

108 ry processes critical for glucose-stimulated insulin secretion and suggest a rationale for a therapeu

109 sible role of NAA as modulator of pancreatic insulin secretion and suggest NAA as a critical energy m

110 tions, NIPAL1 knockdown decreased both basal insulin secretion and total insulin content; in contrast

111 nd peptide YY that regulate food absorption, insulin secretion, and appetite.

112 equired for glucose sensing, calcium influx, insulin secretion, and cross regulation of alpha- and de

113 al lumen that can modulate lipid metabolism, insulin secretion, and energy expenditure by activating

114 nelle that has been implicated in regulating insulin secretion, and found that the beta-cell cilia ar

115 portant role in fetal beta-cell development, insulin secretion, and glucose metabolism.

116 cose tolerance, increased glucose-stimulated insulin secretion, and hyperglucagonemia.

117 We studied glucose homeostasis, insulin secretion, and insulin sensitivity in male and f

118 this "phosphate flush," its association with insulin secretion, and its regulation have since then re

119 ind that in Eipr1 KO cells, there is reduced insulin secretion, and mature DCV cargoes such as insuli

120 romised survival, insulin-vesicle packaging, insulin secretion, and nutrient-induced Ca(2+) influx of

121 using IPC retained normal islet morphology, insulin secretion, and the ability to reverse diabetes a

122 Chronic exposure to stress causes impaired insulin secretion, apoptosis, and loss of cell identity,

123 gest that vesicle trafficking events such as insulin secretion are regulated by the post-translationa

124 et al. develop an elegant approach to assess insulin secretion as a function of granule age in pancre

125 re compared using dynamic glucose-stimulated insulin secretion as a measure of beta-cell function and

126 eBCs display glucose-stimulated insulin secretion as early as three days after transplan

127 sion are implicated in insulin signaling and insulin secretion, as a manifestation of pancreatic beta

128 olerance by ~60% in part because of enhanced insulin secretion, as indicated by an increase in the in

129 Insulin secretion (assessed by C-peptide/glucose ratio)

130 roRNAs (miRNAs) are associated with residual insulin secretion at diagnosis and predict the severity

131 lting in an increase in their function (i.e. insulin secretion at low-intensity: 1.15 +/- 0.17, mediu

132 ents; however, it is unknown if FGF1 targets insulin secretion at the islet level.

133 ts in impaired glucose tolerance and reduced insulin secretion, both in vitro and in vivo.

134 cell transcription factor MAFA and abolished insulin secretion, both in vitro in primary human islets

135 hyperglycemia for 72 h 1) increases absolute insulin secretion but impairs beta-cell function, 2) cau

136 ay can be widely used for examining not only insulin secretion but other secreted factors from differ

137 wn to exhibit impaired glucose tolerance and insulin secretion, but the underlying mechanism remains

138 Weight loss in people with obesity decreased insulin secretion by 35% even though insulin sensitivity

139 M) for 24 hours decreased glucose-stimulated insulin secretion by approximately 30% without affecting

140 to the still debated autocrine regulation of insulin secretion by insulin/insulin-like growth factor

141 autophagy in pancreatic beta-cells decreases insulin secretion by selectively degrading insulin granu

142 hese adipose tissue-derived factors regulate insulin secretion by silencing a pair of inhibitory neur

143 obilization in human beta-cells and supports insulin secretion by stabilizing STX1A.

144 obilization in human beta cells and supports insulin secretion by stabilizing Stx1a.

145 ngly, while GLP-1 is well known to stimulate insulin secretion by the pancreatic beta-cells, direct e

146 circadian amplitude of T2D islet clocks and insulin secretion by these islets.

147 ) promotes NGSIS, but not glucose-stimulated insulin secretion, by increasing mitochondrial proton le

148 ng target for treatment aimed at maintaining insulin secretion capacity in T2D.

149 these channels, including but not limited to insulin secretion, cardiac protection, and blood flow re

150 y reducing expression of genes important for insulin secretion, cell polarity, cell junction, cilia,

151 ted in islets with higher glucose-stimulated insulin secretion compared to islets from SCS only pancr

152 a 2-week culture and assessed viability and insulin secretion compared to noncultured islets.

153 diabetes experienced a more rapid decline in insulin secretion compared with children without suscept

154 ulin sensitivity, glucose effectiveness, and insulin secretion.CONCLUSIONThese findings indicate that

155 Importantly, defects in insulin secretion constitute a hallmark in the progressi

156 icrotubule turnover, causing increased basal insulin secretion, depleting insulin vesicles from the c

157 Current therapies that increase insulin secretion do not consider the existence of these

158 sive insulin granule release to maintain low insulin secretion during fasting.

159 -linked polymorphisms, resulting in impaired insulin secretion during glucose tolerance tests as well

160 s in glucose-, alanine-, or GLP-1-stimulated insulin secretion during perifusion.

161 10 min) increased by 70%, while second-phase insulin secretion during the first (10-80 min) and secon

162 homeostasis through insulin secretion, where insulin secretion dynamics are regulated by intracellula

163 t cytokine-mediated beta-cell dysfunction to insulin secretion dynamics during the development of dia

164 mediated beta-cell death as well as preserve insulin secretion dynamics during the development of dia

165 eta-cells, regulating calcium signalling and insulin secretion dynamics.

166 ng cyclic synthesis of energy metabolism and insulin secretion effectors, including antiphasic insuli

167 e important modulators of glucose-stimulated insulin secretion, essential for maintaining energy home

168 with previous work, Gnb5 knockout diminished insulin secretion evoked by the muscarinic cholinergic a

169 Kisspeptin modulates glucose-stimulated insulin secretion, food intake and/or energy expenditure

170 ed receptor that controls growth hormone and insulin secretion, food intake, and reward-seeking behav

171 ic pathways necessary for glucose stimulated insulin secretion for protection from viral lysis.

172 Insulin secretion from beta-cells is reduced at the onse

173 glucose in vivo and increased ex vivo islet insulin secretion from diabetic, but not control, mice.

174 Insulin secretion from DO islets ranged >1,000-fold even

175 Insulin secretion from islet beta-cells is driven by glu

176 le (MT) network is an essential regulator of insulin secretion from pancreatic beta cells, which is c

177 channel) couples blood levels of glucose to insulin secretion from pancreatic beta-cells.

178 m was tested by measuring glucose-stimulated insulin secretion from single and groups of murine and h

179 ever, show that alpha-cell signals stimulate insulin secretion from the neighboring beta-cell.

180 Impaired insulin secretion from the pancreatic beta-cells is cent

181 These functions, which include insulin secretion, gastric emptying, satiety, and the he

182 related to pancreatic acinar cells (GP2) and insulin secretion (GLP1R).

183 onse to glucose-potentiated arginine-induced insulin secretion (GPAIS) challenge in rat insulin promo

184 n of TBK1, PIAA augmented glucose-stimulated insulin secretion (GSIS) and expression of beta-cell dif

185 Growth, glucose-stimulated insulin secretion (GSIS) and glucose utilization rates (

186 GL pseudoislets, biphasic glucose-stimulated insulin secretion (GSIS) and insulin secretion to IBMX a

187 P2Y14 by UDP-G suppressed glucose-stimulated insulin secretion (GSIS) and knockdown of P2Y14 abolishe

188 gnant women promote islet glucose-stimulated insulin secretion (GSIS) and peripheral insulin resistan

189 release and insufficient glucose-stimulated insulin secretion (GSIS) are hallmarks of diabetes.

190 Two key prerequisites for glucose-stimulated insulin secretion (GSIS) in beta cells are the proximity

191 NADPH facilitates glucose-stimulated insulin secretion (GSIS) in pancreatic islets (PIs) of b

192 Glucose-stimulated insulin secretion (GSIS) is regulated by calcium (Ca(2+)

193 heir ability to carry out glucose stimulated insulin secretion (GSIS) upon damage.

194 GL pseudoislets, biphasic glucose-stimulated insulin secretion (GSIS), and insulin secretion to 3-iso

195 s a negative regulator of glucose-stimulated insulin secretion (GSIS), which is mediated by DA D(2)-l

196 slet beta-cells regulates glucose-stimulated insulin secretion (GSIS).

197 n as a result of impaired glucose-stimulated insulin secretion (GSIS).

198 ng is not required during glucose-stimulated insulin secretion (GSIS).

199 entration [Ca(2+)](c) and glucose-stimulated insulin secretion (GSIS).

200 isruption of MAMs altered glucose-stimulated insulin secretion (GSIS).

201 of kisspeptin in impaired glucose-stimulated insulin secretion (GSIS).

202 s, without alterations in glucose-stimulated insulin secretion (GSIS).

203 female islets, T enhanced glucose-stimulated insulin secretion (GSIS).

204 correlated with decreased glucose-stimulated insulin secretion (GSIS).

205 al role of pancreatic GLP-1 in regulation of insulin secretion has been proposed.

206 agon-like peptide 1 (GLP-1) in regulation of insulin secretion has been questioned, and a physiologic

207 timulated glucose uptake, glucose-stimulated insulin secretion, hepatic glucose metabolism, and both

208 (s)-mediated signaling pathways that promote insulin secretion, improved beta-cell function and proli

209 ave investigated the association of AAs with insulin secretion in a longitudinal setting.

210 e investigate the role of Hhip in modulating insulin secretion in adult Hhip mice (Hhip +/- vs. Hhip+

211 Galanin signalling suppresses insulin secretion in animal models (but not in humans),

212 aling pathways involved in the regulation of insulin secretion in beta-cells and studied their link t

213 nstrate that SLC19A2 deficit causes impaired insulin secretion in conjunction with mitochondrial dysf

214 uscarinic receptor agonist oxotremorine-M on insulin secretion in cultured mouse islets.

215 for the first time that FGF1 increases islet insulin secretion in diabetic mouse models.

216 ifferentiated human muscle cells and induces insulin secretion in human islets via TrkB.T1 identifies

217 atic islets participate in the regulation of insulin secretion in humans and, if compromised, in the

218 tive CFTR function in PDECs directly reduced insulin secretion in islet cells significantly.

219 sion of C1ql3 is correlated with the reduced insulin secretion in islets of obese mice.

220 dominantly impairs the central regulation of insulin secretion in males.

221 n to result in truncated RIMS2 and decreased insulin secretion in mammalian cells.

222 associated with beta-cell recovery of acute insulin secretion in many individuals, possibly by redif

223 ghtly blunted first-phase glucose-stimulated insulin secretion in MIN6m9 cells, but had no significan

224 ~50 mg/dL in plasma glucose concentration on insulin secretion in normal glucose-tolerant (NGT) subje

225 d C1ql3 as a putative contributor to reduced insulin secretion in obesity, linking C1ql3 to an increa

226 rter sulfonylurea receptor 1 (SUR1) regulate insulin secretion in pancreatic beta-cells to maintain g

227 estrogen metabolites, catechol estrogens, on insulin secretion in pancreatic beta-cells.

228 high levels of glucose or fatty acids impair insulin secretion in pancreatic islets, which could part

229 These results demonstrate that increased insulin secretion in people with obesity is associated w

230 ed the effect of diet-induced weight loss on insulin secretion in people with obesity who did not imp

231 Exogenous ghrelin decreased insulin secretion in perifused isolated islets in a GHSR

232 Kindlin-2 loss impairs insulin secretion in primary human and mouse islets in v

233 omising ligands not only exerts an effect on insulin secretion in rat pancreatic islets but also affe

234 tained on a Western-style diet, and measured insulin secretion in response to a variety of secretagog

235 d Ca(2+) current in mediating Ca(2+)-induced insulin secretion in response to ER stress.

236 mice are glucose intolerant and have reduced insulin secretion in response to glucose challenge, and

237 dose-dependent glucose disposal capacity and insulin secretion in response to glucose-potentiated arg

238 ranb3 in MIN6 beta-cells results in impaired insulin secretion in response to high glucose, implicati

239 Knocking down the ABO gene led to decreased insulin secretion in the murine pancreatic beta-cell lin

240 ntrols phosphate reabsorption in the kidney, insulin secretion in the pancreas, and skeletal muscle f

241 insulin transcription and glucose-stimulated insulin secretion in vitro.

242 es coordinated electrical activity (and thus insulin secretion) in the rest of the islet.

243 y human beta cells, including robust dynamic insulin secretion, increased calcium signalling in respo

244 ithelium, has important functions: promoting insulin secretion, insulin sensitivity, and beta-cell ma

245 Primary outcome was 6-month change in insulin secretion, insulin sensitivity, and disposition

246 Insulin secretion/insulin resistance (disposition) index

247 Early-phase insulin secretion is a determinant of postprandial gluco

248 Here, we report that insulin secretion is regulated by a circular RNA contain

249 Glucose-stimulated insulin secretion is the hallmark of the pancreatic beta

250 We find that when glucose metabolism induces insulin secretion, it also increases formation of Golgi-

251 r INS-1E, a beta-cell line, to repurpose the insulin secretion machinery, which enables the glucose-d

252 iated with any change in glucose metabolism; insulin secretion (mean difference -446 [95% CI -3184 to

253 iated with any change in glucose metabolism: insulin secretion (mean difference, -446; 95% confidence

254 s postprandial plasma glucose excursions and insulin secretion more than endogenous GLP-1, but the ho

255 pecifically regulates non-glucose-stimulated insulin secretion (NGSIS) in pancreatic islets that is a

256 omycin A1 and Atg5 siRNAs only rescues basal insulin secretion, not kisspeptin-impaired GSIS.

257 olved in the control of intestinal function, insulin secretion, nutrient assimilation and food intake

258 sulin and insulin ((pro)insulin) content and insulin secretion of NIT-1 cells, autophagy inhibition u

259 , it has no effect on either glucose-induced insulin secretion or insulin sensitivity.

260 ated by antihyperglycemic drugs that enhance insulin secretion or signaling.

261 stemic glucose concentration, independent of insulin secretion or utilization.

262 We uncovered deficits in insulin secretion, partly due to reduced mitochondrial o

263 We uncovered deficits in insulin secretion, partly due to reduced mitochondrial o

264 on of purported BMAL1-target genes mediating insulin secretion, processing, and lipid metabolism.

265 ulin sensitivity progressively decreased and insulin secretion progressively increased from the lean-

266 oncentrations (+21.5 +/- 13.4 ng/mL) but not insulin secretion rates (primary outcome of the parent s

267 Basal and postprandial insulin secretion rates were >50% greater in people with

268 Weight loss increased beta-cell function (insulin secretion relative to insulin sensitivity) by 1.

269 glucose-stimulated and incretin-potentiated insulin secretion response of islets from HFD-fed beta c

270 The Restoring Insulin Secretion (RISE) Adult Medication Study and the

271 n without induction of cell death or loss of insulin secretion, suggesting that appropriate levels of

272 eria for transplantation (glucose-stimulated insulin secretion tests, islet numbers, and purity).

273 abolite, was more efficacious in stimulating insulin secretion than any other tested catechol estroge

274 esults demonstrate that genetic variation in insulin secretion that can lead to type 2 diabetes is di

275 esion on Oxo-M-stimulated glucose-stimulated insulin secretion; this effect likely involved the adhes

276 ose-stimulated insulin secretion (GSIS), and insulin secretion to 3-isobutyl-1-methylxanthine and KCl

277 cells integrate external signals to modulate insulin secretion to better regulate blood glucose level

278 cose-stimulated insulin secretion (GSIS) and insulin secretion to IBMX and KCl were all reduced witho

279 BMI, and measures of insulin resistance and insulin secretion) to cluster adult-onset diabetes patie

280 roles in numerous beta-cell pathways such as insulin secretion, transcription, metabolism, endoplasmi

281 ations responding to CDC with an increase in insulin secretion under control conditions were less imp

282 g, which either controlled GSIS or prevented insulin secretion under fasting conditions.

283 A ring, rapidly potentiated glucose-induced insulin secretion via a nongenomic mechanism.

284 et-wide free-calcium activity ([Ca(2+)]) and insulin secretion via gap-junction electrical coupling.

285 chenodeoxycholic acid (CDC) acutely enhance insulin secretion via the farnesoid X receptor (FXR).

286 21% higher (P < 0.05), whereas meal-derived insulin secretion was 28% lower (P < 0.05).

287 Unlike GSIS, such insulin secretion was blocked with mitochondrial antioxi

288 as diminished and the potentiating effect on insulin secretion was completely lost.

289 islets was alleviated and glucose-stimulated insulin secretion was increased ~2.5-fold compared to a

290 days from diagnosis), during which residual insulin secretion was measured with a mixed meal toleran

291 Insulin secretion was reduced, and glucagon secretion in

292 lvement of autophagy in kisspeptin-regulated insulin secretion, we overexpressed Kiss1 in NIT-1 cells

293 Plasma glucose, insulin sensitivity and insulin secretion were also comparable between condition

294 -1, 3) additive to supra-additive effects on insulin secretion when combining SU+GIP and SU+GLP-1, re

295 ted from gastrointestinal cells that amplify insulin secretion when glucose is high.

296 gerhans maintain glucose homeostasis through insulin secretion, where insulin secretion dynamics are

297 insulin content and impaired glucose-induced insulin secretion, which was more severe in males.

298 endocrine pancreas as a key control point of insulin secretion, with additional roles in regulating b

299 Consequently, the source of persistent insulin secretion within T1D remains unclear.

300 -NL and obese-NAFLD is due to an increase in insulin secretion, without a decrease in total hepatic o