ライフサイエンスコーパス: beta cell

1 insulin secretory granules of the pancreatic beta cell.

2 rough reduction in STARD10 expression in the beta cell.

3 nly a single cell type-the insulin-producing beta-cell.

4 e transcription factors Pdx-1 and NKX-6.1 in beta cells.

5 by the autoimmune destruction of pancreatic beta cells.

6 t is expressed in human and mouse pancreatic beta cells.

7 nophagy) of insulin-containing DCVs in INS-1 beta cells.

8 isease that causes severe loss of pancreatic beta cells.

9 of cells, such as adipocytes and pancreatic beta cells.

10 rgeting and destruction of insulin-producing beta cells.

11 landscape of insulinomas relative to normal beta cells.

12 n secretion by both juvenile and adult human beta cells.

13 of novel heterogeneity markers in mammalian beta cells.

14 ndicated a similar function of PAX6 in human beta cells.

15 ated PLIN2 expression and ER stress in their beta cells.

16 o be directly controlled by Ca(2+) influx in beta-cells.

17 Ca(2+) fluxes in rodent as well as in human beta-cells.

18 stimulated insulin secretion from pancreatic beta-cells.

19 of KCNB1 does not inhibit Kv current in T2D beta-cells.

20 was recently found to be expressed in islet beta-cells.

21 OR mutant (KD-mTOR) transgene exclusively in beta-cells.

22 deleterious downstream effects in pancreatic beta-cells.

23 n C2C12 myotubes and INS-1 832/13 pancreatic beta-cells.

24 intaining the function and survival of human beta-cells.

25 ecretion from isolated mouse islets or INS-1 beta-cells.

26 novel approaches to regenerating pancreatic beta-cells.

27 2 is essential for proper CAMKII function in beta-cells.

28 sion to autoimmune destruction of pancreatic beta-cells.

29 etween EphA4/7 on alpha-cells and ephrins on beta-cells.

30 cy in mitochondrial extracts from APTX-/-Pol beta-/- cells.

31 ated with cytokine-mediated killing of human beta-cells, a process partially prevented by MCL-1 overe

32 a complex but not sustainable integration of beta cell-adaptive responses to nutrient overabundance,

33 agonist for activated Stat3, specifically in beta-cells ameliorated beta-cell EMT and beta-cell loss

34 licing regulators that are expressed in both beta cells and brain.

35 11.1 is also present in pancreatic alpha and beta cells and intestinal L and K cells, secreting gluca

36 tains the terminally differentiated state of beta cells and is a component of active enhancers in bot

37 of insulin-containing granules in pancreatic beta cells and is required for the postprandial spike in

38 /db-PI3Kgamma(-/-) mice have more pancreatic beta cells and larger islets than db/db mice, despite di

39 a subset of docked insulin granules in human beta cells and rat-derived clonal insulin 1 (INS1) cells

40 with respective tissue specificity for islet beta cells and renal epithelial cells were reliably char

41 arbidopa on (18)F-FDOPA uptake in insulinoma beta-cells and an insulinoma xenograft model in mice.

42 Siglec-7 was expressed on beta-cells and down-regulated in type 1 and type 2 diabe

43 tly proposed to involve dedifferentiation of beta-cells and ectopic expression of other islet hormone

44 318, rescues the exocytotic phenotype in T2D beta-cells and increases insulin secretion from T2D isle

45 gm for induction of isletokine expression in beta-cells and reveal IP-10 as a primary therapeutic tar

46 GLP1R is highly expressed on pancreatic beta-cells, and activation by endogenous incretin or GLP

47 ceptor signaling inhibits insulin release in beta-cells, and show that this can be pharmacologically

48 insulitis), and autoantibodies specific for beta-cell antigens.

49 ulating autophagy, ER stress resolution, and beta cell apoptosis and survival.

50 ads to mitigation of ER stress, forestalling beta cell apoptosis, partially restoring beta cell mass,

51 ith type 2 diabetes, where it contributes to beta-cell apoptosis and insufficient insulin secretion.

52 Pancreatic beta-cell apoptosis and proliferation were also evaluate

53 This phenotype could be explained by reduced beta-cell apoptosis in db/db-PI3Kgamma(-/-) mice compare

54 dening our understanding of cytokine-induced beta-cell apoptosis in early T1D.

55 y as the mechanism by which mTORC1 regulates beta-cell apoptosis, size and autophagy, whereas mTORC1/

56 wn to reduce beta-cell function and increase beta-cell apoptosis.

57 s insulin sensitivity and reduces pancreatic beta-cell apoptosis.

58 ess, explaining why SRp55 depletion triggers beta-cell apoptosis.

59 2 proteins DP5 and PUMA and consequent human beta-cell apoptosis.

60 ifests when the insulin-producing pancreatic beta cells are destroyed as a consequence of an inflamma

61 Pancreatic beta cells are functionally programmed to release insuli

62 e methylation differences between alpha- and beta-cells are concentrated in enhancers.

63 bust glucose responsiveness, whereas younger beta-cells are more proliferative but less functional.

64 regulates insulin secretion from pancreatic beta-cells are now well described, the way glucose modul

65 ncreata of cadaveric donors, suggesting that beta-cells are prone to attract CCR2(+) Treg cells.

66 mption, glucose dyshomeostasis develops when beta-cells are unable to adapt to peripheral insulin dem

67 nduced apoptosis in human and rat pancreatic beta-cells, as well as in human and murine pancreatic is

68 carrying abnormal chromatin marking in vital beta-cell-associated genes.

69 pancreatic islets release the intracellular beta-cell autoantigens in human T1D, GAD65, IA-2, and pr

70 The introduction of beta-cell autoantigens via the gut through Lactococcus l

71 In human beta-cells, barr2 knockdown abolished glucose-induced in

72 reporter line and found that both alpha- and beta-cells become targets of endogenous TH signaling dur

73 wild-type, an effect likely related to their beta-cells being more functionally efficient.

74 functional states with increasing time since beta-cell birth, leading to functional and proliferative

75 apoptotic Bcl-2 proteins in human pancreatic beta-cells, broadening our understanding of cytokine-ind

76 ssary component of the autophagy pathway, in beta cells by pancreatic intra-ductal AAV8-shAtg7 infusi

77 s surrogate imaging biomarker for pancreatic beta-cells by targeting the protein GPR44.

78 ression and function of NMDARs in pancreatic beta-cells, by contrast, are poorly understood.

79 ur results suggest that chronically elevated beta-cell [Ca(2+)]i in Abcc8(-/-) islets contributes to

80 ll identity, revealing clues as to how adult beta cells can partially dedifferentiate or become repro

81 tage led to immature and dysfunctional islet beta cells carrying abnormal chromatin marking in vital

82 Spry2 deletion in the adult mouse beta-cell caused hyperglycemia and hypoinsulinemia.

83 and functional outputs of the alpha-cell and beta-cell clockworks could be assessed in vivo and in vi

84 thways was significantly different in KATPHI beta-cells compared with control, providing a mechanism

85 s, and more proliferative and less apoptotic beta-cells compared with the age-matched wild-type (WT)

86 significantly decreased numbers of apoptotic beta-cells compared with those treated with vehicle or l

87 Hence, factors controlling functional beta-cell compensation are potentially important targets

88 genetics to understand how subpopulations of beta-cells control the overall [Ca(2+)]i response and in

89 an mitigate cytokine- and ER stress-mediated beta cell death.

90 critical prosurvival protein for preventing beta-cell death and clarify the mechanisms behind its do

91 iabetes, but success is limited by extensive beta-cell death in the immediate posttransplant period a

92 reted to the circulation, is associated with beta-cell death in type-2 diabetes (T2D).

93 interventions tested to date failed to halt beta cell demise.

94 aired insulin secretion of fission-deficient beta-cells, demonstrating that defective mitochondrial d

95 by diabetogenic T cells and cause selective beta cell destruction in type 1 diabetes (T1D) has focus

96 alities was employed to study the pattern of beta cell destruction.

97 nical efforts capable of delaying or halting beta-cell destruction has been limited.

98 A5 genes (respectively related to autophagy, beta-cell development and function, and lipid metabolism

99 onal relevance of mTOR enzymatic activity in beta-cell development and glucose homeostasis, we genera

100 ormation of all pancreatic cell types, islet beta-cell development, and adult islet beta-cell functio

101 diabetes is thought to involve a compromised beta cell differentiation state, but the mechanisms unde

102 rmation, but it is inadequate for functional beta cell differentiation.

103 that exogenous TH precociously activates the beta-cell differentiation genes pax6b and mnx1 while dow

104 immature, a common downfall off most current beta-cell differentiation protocols.

105 ceptibility genes for diabetes contribute to beta cell dysfunction and death.

106 Since beta cell dysfunction occurs during diabetes development

107 which islet inflammation develops and causes beta cell dysfunction.

108 diabetic patients before they develop severe beta cell dysfunction.

109 Islet beta-cell dysfunction and aggressive macrophage activity

110 al role of inflammation in cytokine-mediated beta-cell dysfunction and death in type 1 diabetes melli

111 beta-Cell dysfunction and declining beta-cell mass are t

112 target 12/15-LOX can prevent progression of beta-cell dysfunction and glycemic deterioration in mode

113 The hyperglycaemia results from beta-cell dysfunction and is associated with lower fasti

114 by the loss of insulin production caused by beta-cell dysfunction and/or destruction.

115 ave interrogated the molecular mechanisms of beta-cell dysfunction at the level of mRNA translation u

116 serves as an important nexus linking primary beta-cell dysfunction to progressive beta-cell mass dete

117 n-dependent kinase 2 (CDK2), couples primary beta-cell dysfunction to the progressive deterioration o

118 oreover, chronically elevated glucose causes beta-cell dysfunction, but little is known about how cel

119 hibit glycemic dysregulations and pancreatic beta-cell dysfunctions, we evaluated islet function and

120 n mediating the effect of leptin to modulate beta-cell electrical activity by promoting AMP-activated

121 d insulin granule priming and contributes to beta-cell electrical activity.

122 the islet, and these affect the way in which beta-cells electrically interact.

123 tat3, specifically in beta-cells ameliorated beta-cell EMT and beta-cell loss and prevented the onset

124 Specifically, the older beta-cells exhibit robust glucose responsiveness, wherea

125 at insulinomas hold the "genomic recipe" for beta cell expansion, we surveyed 38 human insulinomas to

126 1 is cytoprotective to rat, mouse, and human beta-cells exposed to cytokines or thapsigargin-induced

127 nfirmed that LDB1-depleted, insulin-negative beta cells express NEUROG3 but do not adopt alternate en

128 A specific beta-cell expression of the CCR2-ligand (CCL2) was obser

129 endoplasmic reticulum (ER) stress expedites beta cell failure in this situation.

130 Progressive pancreatic beta cell failure underlies the transition of impaired g

131 beta-Cell failure in type 2 diabetes (T2D) was recently

132 ion in obese patients who are predisposed to beta-cell failure is not expected to produce adverse eff

133 potential to generate an unlimited supply of beta cells for diabetes treatment.

134 results demonstrate the suitability of NT-ES-beta-cells for cell replacement for type 1 diabetes and

135 r incomplete understanding of how pancreatic beta cells form limits the generation of beta-like cells

136 el mechanism for IL-6-mediated protection of beta cells from stress-induced apoptosis.

137 ulation of vesicles containing proinsulin in beta-cells from Ab+ donors, suggesting a defect in proin

138 istance) and homeostasis model assessment of beta cell function (HOMA-B) were measured after a mean +

139 and ketosis that were attributed to loss of beta cell function and expansion of alpha cells.

140 Inadequate pancreatic beta cell function underlies type 1 and type 2 diabetes

141 ining of the expression of genes involved in beta cell function, but also continual repression of clo

142 mpaired glucose tolerance due to compromised beta-cell function and glucose-stimulated insulin secret

143 e a novel mechanism of glucose regulation of beta-cell function and growth by repressing stress-induc

144 gulation in offspring predisposed to altered beta-cell function and hyperglycemia and place it as a c

145 ncreatic beta-cells has been shown to reduce beta-cell function and increase beta-cell apoptosis.

146 of pancreatic histopathology, impairment of beta-cell function and mass, islet inflammation (i.e., i

147 th impaired expression of genes required for beta-cell function and maturity in isolated islets.

148 Mechanisms underlying altered beta-cell function in aging are poorly understood in mou

149 We assessed the importance of GPR119 for beta-cell function in Gpr119(-/-) mice and in newly gene

150 ontributed to islet inflammation and loss of beta-cell function in islet grafts.

151 sting plasma glucose (FPG) concentration and beta-cell function in subjects with impaired fasting glu

152 Thus, beta-cell function measured with the insulin secretion/i

153 We examined glucose homeostasis and beta-cell function of these mice fed a control chow or h

154 er, recent evidence shows that early loss of beta-cell function plays an important role in the pathog

155 FPG concentration and beta-cell function was measured with a nine-step hypergl

156 NO2 exposure negatively affected beta-cell function, evidenced by a faster decline in dis

157 measures of fasting insulin sensitivity and beta-cell function, for time spent in slow-wave sleep, a

158 While mitophagy is critical to pancreatic beta-cell function, the posttranslational signals govern

159 islet beta-cell development, and adult islet beta-cell function.

160 s demonstrate the essential role of GATA6 in beta-cell function.

161 ferences in markers of insulin secretion and beta-cell function.

162 cAMP Epac pathways in the effects of ANP on beta-cell function; the latter seems to prevail.

163 We report on East-Asian alpha- and beta-cell gene signatures and substantiate several genes

164 eased expression of the critically important beta-cell gene, Igf2 in whole F1 embryos.

165 Furthermore, deficiencies in beta cell glucose sensing are likely to contribute to de

166 es, but no teratomas, were observed in NT-ES-beta-cell grafts.

167 of glucose homeostasis by insulin depends on beta-cell growth and function.

168 evated cholesterol content within pancreatic beta-cells has been shown to reduce beta-cell function a

169 n islets in the context of T2D pathology and beta cell health, which may have broad translational imp

170 ymmetric pattern of organ growth, pancreatic beta cell hyperplasia, and elevated plasma insulin and l

171 either to beta-cell tumours (insulinomas) or beta-cell hyperplasia.

172 ll, indicating that acquiring and sustaining beta cell identity and function requires not only active

173 ntiated gene program, indicated by a loss of beta cell identity genes and induction of the endocrine

174 tein 1 (LDB1) serve to maintain mature adult beta cell identity, revealing clues as to how adult beta

175 cellular Ca(2+) concentration ([Ca(2+)]i) on beta-cell identity and gene expression.

176 -/-) islets contributes to the alteration of beta-cell identity, islet cell numbers and morphology, a

177 Inducible ablation of LDB1 in mature beta cells impaired insulin secretion and glucose homeos

178 progenitors, and differentiating and mature beta cells in vivo Pdx1(DeltaAREAII/-) mice exhibit a ma

179 for the functional maturation of alpha- and beta-cells in order to maintain glucose homeostasis.

180 12204657, was evaluated for visualization of beta-cells in pigs and nonhuman primates by positron emi

181 Calcium imaging shows that the beta-cells in the embryonic islet become functional duri

182 autoimmune destruction of insulin-producing beta-cells in the pancreas.

183 Here, the authors show that beta-cells in zebrafish switch from proliferative to fun

184 KCNE2 may regulate multiple K(+) channels in beta cells, including the T2DM-linked KCNQ1 potassium ch

185 Inhibition of KCC2 activity in clonal MIN6 beta-cells increases basal and glucose-stimulated insuli

186 tion and, in doing so, determine the overall beta-cell incretin responses.

187 monstrates the highly volatile nature of the beta cell, indicating that acquiring and sustaining beta

188 in rat insulinoma 832/13 cells and in human beta-cells, indicating that this pathway is conserved ac

189 0 as a primary therapeutic target to prevent beta-cell-induced inflammatory loss of graft function af

190 ed diabetes (CFRD) is thought to result from beta-cell injury due in part to pancreas exocrine damage

191 Pancreatic beta-cell insulin production is orchestrated by a comple

192 generation, which stimulates glucose-induced beta-cell insulin secretion and helps maintain glucose h

193 Insulin production by the pancreatic beta-cell is required for normal glucose homeostasis.

194 ever, the role of STIM1 in insulin-secreting beta-cells is unresolved.

195 gents, which boost the secretory capacity of beta-cells, is linked to adverse side effects.

196 At later stages, younger beta-cells join the islet following differentiation from

197 d mice lacking Abcc8, a key component of the beta-cell KATP-channel, to analyze the effects of a sust

198 containing lysates from an insulin-producing beta-cell line were implanted subcutaneously in autoimmu

199 matin conformational capture (3C) studies in beta cell lines, we localize the causal variant(s) at th

200 ere further characterized in mouse and human beta-cell lines and human islets.

201 promoter regulators and demonstrates a novel beta-cell link between Spry2 and human diabetes.

202 cologic targets to prevent cytokine-mediated beta cell loss in diabetes.

203 in beta-cells ameliorated beta-cell EMT and beta-cell loss and prevented the onset of diabetes in mi

204 peptide 1 (GLP-1) receptor agonists prevent beta-cell loss.

205 er, a high-glucose intake alone did increase beta cell mass and insulin secretion moderately.

206 symmetric organ growth, increased pancreatic beta cell mass and proliferation, and was associated wit

207 ABSTRACT: Development of pancreatic beta cell mass before birth is essential for normal grow

208 ion may contribute to the loss of functional beta cell mass in diabetes.

209 Although beta cell mass was preserved 8 days post-injection, tota

210 ing beta cell apoptosis, partially restoring beta cell mass, and ameliorating diabetes.

211 usion in C57BL/6 mice, resulted in decreased beta cell mass, impaired glucose tolerance, defective in

212 Our data indicate that beta-cell mass (and function) is maintained until shortl

213 beta-Cell dysfunction and declining beta-cell mass are two mechanisms that contribute to thi

214 primary beta-cell dysfunction to progressive beta-cell mass deterioration in diabetes.

215 mine whether the effects of UCP2 observed on beta-cell mass have an embryonic origin.

216 function to the progressive deterioration of beta-cell mass in diabetes.

217 Immunostaining revealed a decrease in beta-cell mass in knockout mice that was caused by a 39%

218 Pancreatic beta-cell mass is a critical determinant of the progress

219 n-4 induced an increase in proliferation and beta-cell mass through EGFR.

220 duced-insulin release, larger islet size and beta-cell mass, and more proliferative and less apoptoti

221 Furthermore, beta-cell mass, but not glucose-stimulated insulin relea

222 n, promotion of satiety, and preservation of beta-cell mass.

223 a-cell oxidative stress, and preservation of beta-cell mass.

224 mmunohistochemical analysis revealed smaller beta-cell masses in betaTFG KO than in controls, likely

225 s study provides a strategy to promote human beta-cell maturation and identifies an unexpected role f

226 l findings to Pdx1 gene regulation and islet beta-cell maturation postnatally.

227 ion, the posttranslational signals governing beta-cell mitochondrial turnover are unknown.

228 In pancreatic beta-cells, mitochondrial bioenergetics control glucose-

229 strongly suggest that an early deficiency in beta-cell number in infants with CF may contribute to th

230 duction in islet density, decreased relative beta-cell number, and presence of amyloid deposits.

231 Deletion of Pax6 in beta cells of adult mice led to lethal hyperglycemia and

232 of patients with type 2 diabetes, and in the beta cells of obese diabetic rodents.

233 tophagic activity has been implicated in the beta cells of patients with type 2 diabetes, and in the

234 ation of the beta-arrestin-2 gene, barr2, in beta-cells of adult mice greatly impairs insulin release

235 otemporally perturbed electrical activity in beta-cells of channelrhodopsin2-expressing islets, mappe

236 Thus, manipulating Y1 receptor signaling in beta-cells offers a unique therapeutic opportunity for c

237 ment of nuclear Nrf2 in islet cells, reduced beta-cell oxidative stress, and preservation of beta-cel

238 were larger and contained a higher number of beta-cells per islet.

239 tiation and highlight SOX5 as a regulator of beta-cell phenotype and function.

240 insulin-positive areas, lower proportion of beta-cells positive for the proliferation marker Ki67 or

241 an survival, is that of pancreatic alpha and beta cells producing glucagon and insulin for glucose ho

242 stant conditions such as obesity, pancreatic beta-cells proliferate to prevent blood glucose elevatio

243 bachol and PACAP/VIP synergistically promote beta-cell proliferation through a FoxM1-dependent mechan

244 controls, likely attributable to diminished beta-cell proliferation.

245 ration of irisin improved GSIS and increased beta-cell proliferation.

246 t mice that was caused by a 39% reduction in beta-cell proliferation.

247 hereas mTORC1/4E-BP2-eIF4E pathway regulates beta-cell proliferation.

248 ic FoxM1 deficiency also blocks compensatory beta-cell proliferation.

249 possibly in humans, exendin-4 can stimulate beta-cell proliferation.

250 indicate that optogenetic activation of the beta-cells propagates to the delta-cells via gap junctio

251 y therefore represent a promising target for beta-cell protection in type 1 diabetes mellitus.

252 focused on peptides originating from native beta cell proteins.

253 ously in autoimmune diabetes-prone NOD mice, beta-cell-reactive T cells homed to these scaffolds and

254 s are thought to contain functionally mature beta cells, recent analyses of transgenic rodent and hum

255 btain insights into therapeutic pathways for beta cell regeneration.

256 The role of alternative splicing in beta cells remains unclear, but recent data indicate tha

257 Ngn3-driven generation of insulin-producing beta cells, resembling that observed during pancreatic d

258 ranscriptome analysis in separated alpha and beta cells revealed that a high number of genes with key

259 Transcriptomic analysis of LDB1-depleted beta cells revealed the collapse of the terminally diffe

260 ole-methylome comparison of human alpha- and beta-cells revealed generality of the genes active in on

261 ession has recently been described as highly beta-cell selective in the human pancreas and constitute

262 Correspondingly, beta-cell-selective deletion of StarD10 in mice led to i

263 Here, using a beta-cell specific epidermal growth factor receptor (EGF

264 To examine this possibility, beta-cell specific TFG knockout mice (betaTFG KO) were g

265 ve characterized the pathogenic potential of beta cell-specific T cells, we have limited mechanistic

266 Inducible beta-cell-specific FoxM1 deficiency also blocks compensa

267 We generated beta-cell-specific Syn-1A-KO (Syn-1A-betaKO) mice to mim

268 The pathways regulating pancreatic beta cell survival in diabetes are poorly understood.

269 lators play key roles in insulin release and beta cell survival, and their dysfunction may contribute

270 ood glucose levels and increases concomitant beta-cell survival and number in a streptozotocin-induce

271 ndin 1 (THBS1) was recently shown to promote beta-cell survival during lipotoxic stress.

272 Whether GLP-1 mediates beta-cell survival via the key lysosomal-mediated proces

273 ific Syn-1A-KO (Syn-1A-betaKO) mice to mimic beta-cell Syn-1A deficiency in T2D.

274 s mature state, heterogeneity diminishes and beta-cells synchronize function and proliferation.

275 lucagon and insulin co-expressing cells, and beta cells that were incapable of maturation.

276 duce developmental adaptations in pancreatic beta-cells that impair fetal insulin secretion.

277 stem cells, and insulin-releasing pancreatic beta cells through a signaling pathway involving the sec

278 in conjunction with insulin from pancreatic beta cells to regulate glucose metabolism.

279 tion, likely enhancing the susceptibility of beta cells to stress-induced apoptosis.

280 ce labeling enabled sorting of heterogeneous beta cells to subpopulations that exhibited marked diffe

281 insulin mimicking the function of pancreatic beta-cells to achieve meticulous control of blood glucos

282 ssion is rapidly eliminated upon exposure of beta-cells to normal glucose levels.

283 ved glucose metabolism and the adaptation of beta-cells to obesity-induced insulin resistance.

284 Although treatment with the pancreatic beta-cell toxin streptozotocin induced hyperglycemia and

285 The pancreatic beta-cell transcriptome is highly sensitive to external

286 es (such as human islet or stem cell-derived beta cell transplantation) without immunosuppression.

287 Light activation of beta-cells triggered a suppression of alpha-cell activit

288 es of hypoglycaemia and can be due either to beta-cell tumours (insulinomas) or beta-cell hyperplasia

289 served sequences that control pancreatic and beta-cell type-specific transcription, which are found w

290 ose metabolism promotes insulin secretion in beta-cells via metabolic coupling factors that are incom

291 The preservation of beta-cells was because of a significant decrease in isle

292 Extracts from single alpha and beta cells were analyzed with CE-ESI-MS to obtain qualit

293 lly expressed transcripts between alpha- and beta-cells were detected using ANOVA and in silico repli

294 cells, but particularly in insulin-secreting beta-cells, where we provide evidence for its role in th

295 ofore unappreciated effect of chronic HFD on beta-cells, wherein continued DNA damage owing to persis

296 e is known to stimulate insulin secretion by beta cells, whether it directly engages nutrient signali

297 entify individual pancreatic islet alpha and beta cells, which were then targeted for liquid microjun

298 upregulates miR-155-5p in murine pancreatic beta-cells, which improved glucose metabolism and the ad

299 city treatment increased free cholesterol in beta-cells, which was accompanied by increased reactive

300 Under a high-fat diet, deletion of PKD1 in beta-cells worsened hyperglycemia, hyperinsulinemia, and