ライフサイエンスコーパス: alpha cell

1 y 50% were ZnT8-negative (14 +/- 1.8% of all alpha-cells).

2 than those presynaptic to the OFF sustained alpha cell.

3 a direct effect of leptin on the pancreatic alpha cell.

4 ch multiple a-cells compete to mate with one alpha-cell.

5 loss of beta cell function and expansion of alpha cells.

6 anglion cells of which 3.4% (8,300) comprise alpha cells.

7 cells in the presence of a normal number of alpha cells.

8 ich can selectively stain glucagon secreting alpha cells.

9 ak, inconsistent connections with ON and OFF alpha cells.

10 ric acid A receptor activation in pancreatic alpha cells.

11 omotes maturation of pre-alpha cells into SC-alpha cells.

12 ansient RGC type that co-stratifies with OFF Alpha cells.

13 h-2 is required for LIN-12 expression in the alpha cells.

14 ion through IL-6-induced GLP-1 production in alpha-cells.

15 beta-cells, whereas JAGGED1 is expressed in alpha-cells.

16 articular inhibiting glucagon secretion from alpha-cells.

17 nown about ATP and its relation to Ca(2+) in alpha-cells.

18 duce the proliferation of glucagon-secreting alpha-cells.

19 less dense F-actin networks than EphA4(+/+) alpha-cells.

20 al generated via beta-cell GDH that inhibits alpha-cells.

21 ease via blockade of NaChs in the pancreatic alpha-cells.

22 gulating messengers Ca(2+) and cAMP in mouse alpha-cells.

23 ion of glucagon release via GHB receptors on alpha-cells.

24 logs and quantified their incorporation into alpha-cells.

25 r EGFP resulted in an 86% pure population of alpha-cells.

26 ein (AAV GCG-EGFP), to specifically identify alpha-cells.

27 +)IL-5(+) and CD4(+)IL-2(+)IL-4(+)IL-5(+)TNF-alpha(+)) cells.

28 The cells clustered into populations of alpha-cells (5%), beta-cells (92%), delta-cells (1%), an

29 reting microarray data from MATa cells, MATa/alpha cells, a starving MATalpha/alpha control, and a me

30 riments, PC2 immunoreactivity in neighboring alpha-cells acted as a positive control.

31 her this pathway is important for regulating alpha-cell activity and glucagon secretion in human isle

32 ion channel in beta-cells to understand how alpha-cell activity is regulated by beta-cells.

33 ion of beta-cells triggered a suppression of alpha-cell activity via gap junction-dependent activatio

34 l activity in delta-cells but suppression of alpha-cell activity.

35 c deletion of the mTORC1 regulator Raptor in alpha cells (alphaRaptorKO), we showed that mTORC1 signa

36 l deletion of the mTORC1 inhibitor, TSC2, in alpha-cells (alphaTSC2(KO)).

37 n hormone glucagon-like peptide 1 (GLP-1) by alpha cells and acts directly on beta cells to stimulate

38 a transcriptional profile similar to mature alpha cells and although they produce proinsulin protein

39 l gap junction coupling was observed between alpha cells and beta cells in the islet.

40 islets and isolated islets from mice; human alpha cells and beta cells were sorted by flow cytometry

41 Glucagon released from pancreatic alpha cells and glucagon-like peptide 1 (GLP-1) released

42 peptide hormones as follows: glucagon in the alpha cells and glucagon-like peptides (GLP)-1 and -2 in

43 ble hyperglucagonemia from insulin-resistant alpha cells and is prevented by glucagon suppression or

44 INT-777 augmented PC1 expression in alpha cells and stimulated GLP-1 release from islets of

45 ial entrainment characteristics of circadian alpha-cell and beta-cell clocks are an important feature

46 ts and did not explore the interplay between alpha-cell and beta-cell clocks.

47 ne expression, and functional outputs of the alpha-cell and beta-cell clockworks could be assessed in

48 llel analysis of the molecular properties of alpha-cell and beta-cell oscillators using a mouse model

49 forward regarding the paracrine role of the alpha-cell and specifically preproglucagon peptides in r

50 seemingly counterintuitive local actions of alpha-cells and describes how they impact islet biology

51 n, and juxtacrine signals between EphA4/7 on alpha-cells and ephrins on beta-cells.

52 may be useful for studying purified primary alpha-cells and for the in vivo delivery of other genes

53 However, Grg3 is expressed in fewer nascent alpha-cells and is progressively lost from alpha-cells a

54 xpression, and Grg3(+/-) pancreata have more alpha-cells and more polyhormonal cells, indicating that

55 re we show that islet non-beta-cells, namely alpha-cells and pancreatic polypeptide (PPY)-producing g

56 In mice, some glucagon-producing pancreatic alpha-cells and somatostatin-producing delta-cells becom

57 n increased STAT3 phosphorylation in primary alpha-cells and stimulated glucagon secretion.

58 oundary method for modeling both a-cells and alpha-cells and their cell shape changes, the extracellu

59 is widely expressed in beta-cells, absent in alpha-cells, and expressed at the mRNA, but not protein,

60 ely restricted to pancreatic islet beta- and alpha-cells, and responsible for zinc accumulation into

61 subtypes: insulin(+) beta-cells, glucagon(+) alpha-cells, and somatostatin(+) delta-cells.

62 all, this study supports the hypothesis that alpha cells are an endogenous reservoir of potential new

63 e evidence indicates that glucagon secreting alpha cells are critically involved in disease progressi

64 c beta cells via apoptosis while neighboring alpha cells are preserved.

65 The alpha-cells are also equipped with K(ATP) channels but t

66 ic inhibition at low glucose, explaining why alpha-cells are electrically active under hypoglycaemic

67 Mouse pancreatic beta- and alpha-cells are equipped with voltage-gated Na(+) curren

68 from duct cells and transdifferentiation of alpha-cells are potential contributors to the beta-cell

69 anisms that regulate glucagon secretion from alpha-cells are still unclear.

70 y explain why pancreatic beta cells, but not alpha cells, are targeted by an autoimmune response duri

71 lls that resulted in an altered beta-cell-to-alpha-cell area in the insulin- resistant group.

72 beyond glycemia and supports a new role for alpha-cells as amino acid sensors.

73 t alpha-cells and is progressively lost from alpha-cells as endocrine cells mature into adulthood.

74 led to the description of a conserved liver-alpha-cell axis where glucagon is a critical regulator o

75 linked in a mutual feedback cycle, the liver-alpha-cell axis.

76 beta-cells; specifically, glucagon-producing alpha-cells begin producing insulin by a process of repr

77 vidence that the relative birth order of the alpha cells biases their fates suggested other factors m

78 ncreatic islet, including glucagon secreting alpha-cells, but particularly in insulin-secreting beta-

79 to GLP-1 synthesis in human and mouse islet alpha cells by GS/cAMP/PKA/cAMP-response element-binding

80 tion, Slc30a8 was inactivated selectively in alpha-cells by crossing mice with alleles floxed at exon

81 The recent demonstration that pancreatic alpha cells can be continuously regenerated and converte

82 scence does not alter alpha-cell plasticity: alpha-cells can reprogram to produce insulin from pubert

83 duced [ATP]pm generation was left shifted in alpha-cells compared to beta-cells.

84 t abnormal glucagon dynamics, and EphA4(-/-) alpha-cells contain less dense F-actin networks than Eph

85 trast, before puberty there is no detectable alpha-cell conversion, although beta-cell reconstitution

86 gher numbers found in male fetuses), whereas alpha cell counts were unaffected, precipitating decreas

87 In vitro experiments in transgene positive alpha-cells demonstrated that EGFP expression did not al

88 human endocrine pancreas, demonstrating that alpha cells derived from adult human pancreatic islets c

89 ants of renin-expressing cells as pancreatic alpha cells despite a lack of active renin expression in

90 riptional and epigenetic derepression of the alpha-cell-determining Arx gene in endocrine progenitors

91 wed that mTORC1 signaling is dispensable for alpha cell development, but essential for alpha cell mat

92 e downregulating arxa, a master regulator of alpha-cell development and function.

93 alpha-cells did not express Glp1r mRNA and delta-cells e

94 ed for 3D imaging of live islets by staining alpha cell directly.

95 The resulting SC-alpha cells do not express insulin, share an ultrastruct

96 nd other alpha-cell markers, suggesting that alpha-cells drive much of the insulin(low) phenotype in

97 tion, we demonstrate conserved plasticity of alpha cells during islet regeneration.

98 ta-cells and concomitantly increases that of alpha-cells during early pancreatic development.

99 The cause and the underlying mechanisms of alpha cell dysfunction are unknown.

100 that postprandial lipemia induces pancreatic alpha cell dysfunction characteristic of type 2 diabetes

101 etes and, therefore, propose that pancreatic alpha cell dysfunction could be viewed, at least partly,

102 ells may contribute to beta cell failure and alpha cell dysfunction in diabetes.

103 The TGRL-induced alpha cell dysfunction was due to reduced gamma-aminobut

104 ype 2 diabetes is associated with pancreatic alpha cell dysfunction, characterized by elevated fastin

105 lipoproteins (TGRLs) might cause pancreatic alpha cell dysfunction.

106 cision during C. elegans gonadogenesis, two "alpha cells," each with equal potential to be an AC or a

107 ability of an a-cell to distinguish between alpha-cells either making or not making alpha-factor, an

108 imulation of somatostatin secretion inhibits alpha-cell electrical activity by a paracrine mechanism.

109 ting platelet-derived growth factor receptor-alpha cell endocytosis.

110 igated whether TGR5 activation in pancreatic alpha cells enhances hyperglycemia-induced PC1 expressio

111 tochastic initial difference between the two alpha cells, ensuring that the cell with higher lin-12 a

112 cagon secretion through tonic stimulation of alpha-cell EphA receptors.

113 MitoNEET-challenged alpha-cells exert potent antiapoptotic effects on beta-c

114 ntify that reduced mitochondrial function in alpha-cells exerts potently protective effects on beta-c

115 These pre-alpha cells exhibit a transcriptional profile similar to

116 Importantly, this replicating alpha-cell exhibited activated Sonic hedgehog signaling,

117 t-amplifying" cells supports a model whereby alpha-cells expand by self-renewal and not via specializ

118 g that the potential impact of GRAs to drive alpha-cell expansion in adult patients is unclear.

119 ergo elevation of plasma glucagon levels and alpha-cell expansion similar to wild-type mice.

120 Pancreatic alpha-cells express voltage-gated Na(+) channels (NaChs)

121 share an ultrastructure similar to cadaveric alpha cells, express and secrete glucagon in response to

122 y an increase and decrease, respectively, in alpha-cell F-actin density.

123 ZnT8 is thus important in a subset of alpha-cells for normal responses to hypoglycemia and act

124 y facilitate the generation and expansion of alpha-cells for transdifferentiation into beta-cells and

125 howed a negative linear correlation with the alpha-cell fraction (Pearson r = -0.76).

126 stem cell-derived human pancreatic alpha (SC-alpha) cells from pluripotent stem cells via a transient

127 We also examined a naturally proliferating alpha-cell from a healthy adult, for which pathway analy

128 a positive role of linagliptin in modulating alpha cell function to restore normoglycemia.

129 onal regulation of key genes responsible for alpha cell function.

130 In return, amino acids regulate alpha-cell function and proliferation.

131 rate an inhibitory role of PI3K signaling on alpha-cell function and provide experimental evidence fo

132 k regulation involving amino acids regulates alpha-cell function and secretion, while glucagon, in tu

133 nying articles show, the emerging picture of alpha-cell function is one of increased complexity that

134 ncretin and beta-cell function and decreased alpha-cell function, and thus lower glucose levels.

135 e showed no differences in glycemic control, alpha-cell function, or alpha-cell mass.

136 eceptor signaling has deleterious effects on alpha-cell function, promoting hyperglycemia.

137 ing reduced beta-cell secretory capacity and alpha-cell function.

138 PI3K) signaling is an important regulator of alpha-cell function.

139 rance, reduced fasting insulin, and improved alpha-cell function.

140 found that HNF1A is necessary to repress an alpha cell gene expression signature, maintain endocrine

141 with a phosphomutant form of Ngn3 increases alpha cell generation, the earliest endocrine cell type

142 In alpha-cells, genetically ablating Scn3a reduces the Na(+

143 onal maturation, including evidence of fetal alpha-cell GLP-1 production and signaling to beta-cells.

144 Pancreatic alpha-cell gp130 knockout (alphagp130KO) mice showed no

145 logy modeling type 2 diabetes, activation of alpha-cell gp130 receptor signaling has deleterious effe

146 Antagonism of alpha-cell gp130 receptor signaling may be useful for th

147 In this study, we elucidated the effects of alpha-cell gp130 receptor signaling on glycemic control

148 concerns that GRAs might cause uncontrolled alpha-cell growth.

149 hat TSPAN-7 is highly expressed in beta- and alpha-cells; however, the function of islet TSPAN-7 has

150 nockout mice), pancreatic swelling is due to alpha-cell hyperplasia with gross hypersecretion of gluc

151 pha-cells link glucagon receptor blockage to alpha-cell hyperplasia.

152 proved in Gcgr(-/-) mice as a consequence of alpha-cell hyperplasia.

153 glucose tolerance, insulin sensitivity, and alpha-cell hyperplasia.

154 se but also results in hyperglucagonemia and alpha-cell hyperplasia.

155 These alterations may prime alpha cells in STZ-treated mice for more glucagon releas

156 practical tool to evaluate and identify live alpha cells in terms of localization, distribution and a

157 We found higher proportions of alpha cells in the dorsal and ventral retinas.

158 omeostasis, but the developmental biology of alpha-cells in adults remains poorly understood.

159 shed in the last decade on the physiology of alpha-cells in human islets and incorporates results fro

160 alpha-cells in lean mouse islets and 70% of alpha-cells in human islets, suggesting a paracrine alph

161 exclusively produced in approximately 50% of alpha-cells in lean mouse islets and 70% of alpha-cells

162 ation may affect glucagon secretion by human alpha-cells in response to SGLT2 inhibitors.

163 ecovery of regulated glucagon secretion from alpha-cells in small pseudoislets depends upon the combi

164 eride metabolism in adipose tissue regulates alpha-cells in the endocrine pancreas.

165 asma triglyceride metabolism do not regulate alpha-cells in the pancreas.

166 indicate that XBP1 deficiency in pancreatic alpha-cells induces altered insulin signaling and dysfun

167 olazine, via blockade of NaChs in pancreatic alpha-cells, inhibits their electrical activity and redu

168 rglucagonemia has been thought to arise from alpha-cell insensitivity to suppressive effects of gluco

169 m pluripotent stem cells via a transient pre-alpha cell intermediate.

170 Proglucagon is expressed in pancreatic alpha cells, intestinal L cells, and some hypothalamic a

171 c activator that promotes maturation of pre-alpha cells into SC-alpha cells.

172 re poorly understood and likely involve both alpha-cell-intrinsic and intraislet paracrine signaling.

173 The data indicate that an alpha-cell-intrinsic mechanism controls glucagon in hypo

174 Secretion of glucagon from the pancreatic alpha-cells is conventionally seen as the first and most

175 The study of primary glucagon-secreting alpha-cells is hampered by their low abundance and scatt

176 -cells is increased, while the percentage of alpha-cells is reduced.

177 ever, the mechanism of glucagon secretion in alpha-cells is still not well established.

178 Exocytosis in alpha-cells is tightly linked to the opening of voltage-

179 Sorted alpha-cells lack endogenous stimulation of EphA forward

180 e replication of beta cells, but not that of alpha cells, leading to enlarged beta cell area and hype

181 found that GIP induces production of IL6 by alpha cells, leading to islet production of GLP1 and ins

182 glucagon-like peptide (GLP)-1 by L cells and alpha cells, leading to secretion of insulin from beta c

183 Induction of mitoNEET in alpha-cells leads to fasting-induced hypoglycemia and hy

184 O] mice) and in vitro (stable XBP1 knockdown alpha-cell line [alphaXBPKD]) models.

185 in alpha-TC6 glucagonoma cells (a pancreatic alpha-cell line) were similar to the observations in Min

186 plasma amino acids and their transport into alpha-cells link glucagon receptor blockage to alpha-cel

187 egulators of beta-cell (Pdx1 and Nkx6.1) and alpha-cell (MafB and Arx) formation and function are dow

188 Notably, insulin-producing alpha-cells maintain expression of alpha-cell markers, a

189 , urocortin-3, or appeared to co-express the alpha-cell marker, glucagon.

190 producing alpha-cells maintain expression of alpha-cell markers, as seen by deep transcriptomic and p

191 The alpha-cell markers, Sst and Hhex, are upregulated in Sno

192 cells contained abundant glucagon and other alpha-cell markers, suggesting that alpha-cells drive mu

193 responsible for the regulation of pancreatic alpha cell mass and function are not completely understo

194 R complex 1 (mTORC1) as a major regulator of alpha cell mass and glucagon secretion.

195 GCGR antibody blockage expanded alpha-cell mass 5.7-fold, and S961 had no additional eff

196 the maintenance of pancreatic beta-cell and alpha-cell mass and for glucose-stimulated insulin secre

197 Elevation of glucagon levels and increase in alpha-cell mass are associated with states of hyperglyce

198 mechanisms regulating glucagon secretion and alpha-cell mass are not well understood.

199 tween pancreatic tracer uptake and beta- and alpha-cell mass in a rat model for beta-cell loss.

200 rating leukocyte subtypes, and beta-cell and alpha-cell mass in pancreata recovered from organ donors

201 butions, decreased beta-cell mass, increased alpha-cell mass, and hyperglucagonemia.

202 mpensatory hyperglucagonemia or expansion of alpha-cell mass, and that it cannot be given to induce s

203 rsecretion involving expansion of pancreatic alpha-cell mass.

204 but did not alter plasma glucagon levels or alpha-cell mass.

205 in glycemic control, alpha-cell function, or alpha-cell mass.

206 ulation that controls glucagon secretion and alpha-cell mass.

207 nd identify a role for mTORC1 in controlling alpha cell-mass maintenance.

208 or alpha cell development, but essential for alpha cell maturation during the transition from a milk-

209 However, glucagon secreted from pancreatic alpha-cells may accumulate at high concentrations to exe

210 se differences in intracellular Zn(2+) among alpha-cells may contribute to the inhibition in glucagon

211 r: beta-cells principally express Nav1.7 and alpha-cells Nav1.3.

212 In OFF Alpha cells, NMDAR-mediated responses followed stimuli a

213 ontrols, whereas STZ-associated increases in alpha-cell number and serum glucagon were significantly

214 acrine cells presynaptic to the ON sustained alpha cell of mouse retina provide currents with a highe

215 acellular Ca(2+) increases were unchanged in alpha-cells of alphaZnT8KO KO mice.

216 ls, with high expression in the hyperplastic alpha-cells of Gcgr(-/-) mice.

217 is a 29-amino-acid peptide released from the alpha-cells of the islet of Langerhans, which has a key

218 pal hyperglycaemic hormone, is released from alpha-cells of the pancreatic islet.

219 ecreting insulin and glucagon, the beta- and alpha-cells of the pancreatic islets play a central role

220 vealed recombination in approximately 30% of alpha-cells, of which approximately 50% were ZnT8-negati

221 The effect of TGR5-mediated GLP-1 from alpha cells on insulin release from islets could be bloc

222 for beta-cells and that the influence of the alpha-cells on (111)In-exendin uptake is negligible.

223 promising initial results, the influence of alpha-cells on the uptake of the radiotracer remains a m

224 xpressing three reporter genes: one labeling alpha cells, one specific for beta cells, and a third mo

225 Similar to previous studies of beta-cells, alpha-cells only divided once in both basal and stimulat

226 xample, other pancreatic islet cells such as alpha-cells, or other cells derived from endoderm); the

227 n in platelet-derived growth factor receptor alpha(+) cells (PDGFRalpha(+) cells) in murine colonic m

228 pathways, can drive pancreatic cells with an alpha-cell phenotype toward a beta-cell-like phenotype.

229 provide experimental evidence for enhancing alpha-cell PI3K signaling for diabetes treatment.

230 We found that senescence does not alter alpha-cell plasticity: alpha-cells can reprogram to prod

231 diabetogenic role of glucagon released from alpha-cells plays a major role in the etiology of both t

232 study demonstrates that GLP-1 (via GLP-1R in alpha-cells) plays a bidirectional role, either stimulat

233 on led to EGFP expression selectively in the alpha-cell population.

234 Glucagon-containing alpha-cells potently regulate glucose homeostasis, but t

235 cle addresses these new findings surrounding alpha-cell preproglucagon products, with a particular fo

236 Here, we show that alpha cells produce the endocannabinoid 2-arachidonoylgl

237 Identification of novel factors regulating alpha-cell proliferation and mass may facilitate the gen

238 GRA drove a 2.4-fold increase in alpha-cell proliferation in young mice.

239 Investigation of the mechanism for alpha-cell proliferation led to the description of a con

240 Basal alpha-cell proliferation rapidly declined soon after bir

241 angptl4 and Angptl4 supplementation promote alpha-cell proliferation specifically.

242 In contrast, GRA-induced alpha-cell proliferation was severely reduced in aged mi

243 uce chronic hyperglucagonemia as a result of alpha-cell proliferation, cell size, and mass expansion.

244 t mice without increasing glucagon levels or alpha-cell proliferation, underscoring the importance of

245 receptor inhibition to hyperglucagonemia and alpha-cell proliferation.

246 not previously known to contribute to human alpha-cell proliferation.

247 ormal islet size distributions, beta-cell to alpha-cell ratios, endocrine hormone profiles, and RARbe

248 toration of EphA forward signaling in sorted alpha-cells recapitulates both normal basal glucagon sec

249 hibitors in glucagon secretion by pancreatic alpha-cells reported controversial results.

250 Ectopic expression of Grg3 in alpha-cells represses glucagon and Arx, and the addition

251 eta-cell regeneration therapies relying upon alpha-cell reprogramming.

252 tion in transient Off mini and transient Off alpha cells, respectively.

253 on (V0.5) at -100 mV and -50 mV in beta- and alpha-cells, respectively).

254 was fixed at basal, mimicking the diminished alpha-cell response to hypoglycemia seen in T1DM.

255 eta cell responsiveness to hyperglycemia and alpha cell responsiveness to hypoglycemia are observed o

256 e topographic distribution of both total and alpha cells reveal a dual topographic organization of a

257 splanted into diabetic mice, converted human alpha-cells reverse diabetes and continue to produce ins

258 ortant paracrine regulators of beta cell and alpha cell secretory activity, however the structural ba

259 EN, a negative regulator of this pathway, in alpha-cells show reduced circulating glucagon levels and

260 ucagon-like peptide 1 (GLP-1) secretion from alpha-cells, shown by experiments with MIN6 cells, and a

261 However, the direct effects of GHB on alpha-cell signaling and glucagon release have not been

262 Recent findings, however, show that alpha-cell signals stimulate insulin secretion from the

263 Additionally, alpha-cell-specific EphA4(-/-) mice exhibit abnormal glu

264 A novel alpha-cell-specific GLP-1R knockout (alphaGLP-1R(-/-)) m

265 pha-cells, we created complementary in vivo (alpha-cell-specific XBP1 knockout [alphaXBPKO] mice) and

266 ing Dnmts in pancreatic progenitors promoted alpha cell specification, while Dnmt1 overexpression or

267 s thus enabled throughout life via delta- or alpha-cell spontaneous reprogramming.

268 Hypersecretion of glucagon from pancreatic alpha-cells strongly contributes to diabetic hyperglycem

269 sly been shown to downregulate IL-4R subunit alpha cell surface expression and promote Th1 responses.

270 ptide, and glucagon to examine beta-cell and alpha-cell survival and function in a group of 10 chroni

271 ion show heterogeneous uptake of Zn(2+) into alpha-cells that correlates to the known heterogeneities

272 let size and an elevated number of beta- and alpha-cells that resulted in an altered beta-cell-to-alp

273 alpha cells, the first to develop, constitute the penins

274 Given the presumed role of alpha cells to detect brisk transient stimuli, their sim

275 while inhibition of TGFbeta signaling led to alpha-cell to beta-cell transdifferentiation.

276 vivo delivery of other genes selectively to alpha-cells to further probe their function or to manipu

277 Moreover, failure of alpha-cells to increase glucagon secretion in response t

278 iency did not impair the natural capacity of alpha-cells to reprogram into insulin production after e

279 s have described direct effects of SGLT2i on alpha-cells to stimulate glucagon secretion.

280 racellular proteostasis network may regulate alphaS cell-to-cell transmission not only by reducing th

281 urine models of diabetes, glucagon-secreting alpha cells transdifferentiate into insulin-secreting be

282 lls to infection by CVB5 and 4 indicate that alpha cells trigger a more efficient antiviral response

283 We assessed adaptive alpha-cell turnover and adaptive proliferation, administ

284 trated GLP-1 receptor (GLP-1R) expression in alpha-cells using both antibody-dependent and antibody-i

285 Zn(2+) levels were significantly lower in KO alpha-cells versus control cells.

286 Here we characterized alpha-cell voltage-gated ion channels in a streptozotoci

287 requency distributions for beta cells versus alpha cells was observed, thereby establishing both the

288 The initial difference between the alpha cells was originally envisaged as a random imbalan

289 Furthermore, TGR5-induced GLP-1 release from alpha cells was via an Epac-mediated PKA-independent mec

290 whereas the effect on electrical activity in alpha-cells was blocked by CYN 154806, an antagonist of

291 To evaluate the role of XBP1 in alpha-cells, we created complementary in vivo (alpha-cel

292 FFAR1 is also present on glucagon-secreting alpha-cells, we hypothesized that palmitate simultaneous

293 in highly purified adult glucagon-expressing alpha-cells, we observed surprisingly high insulin mRNA

294 To interrogate the lineage of GRA-induced alpha-cells, we sequentially administered thymidine anal

295 the other types, dendrites of transient Off alpha cells were spatially independent, with little rece

296 and platelet-derived growth factor receptor alpha(+) cells were unchanged.

297 and onset of HLH-2 expression, such that the alpha cell whose parent expressed HLH-2 first is biased

298 Incubation of mouse and human pancreatic alpha cells with GIP induced their production of IL6, le

299 stituted from dispersed islet cells to study alpha-cells with and without various indirect effects fr

300 ound to be expressed in pancreatic beta- and alpha-cells, with high expression in the hyperplastic al