ライフサイエンスコーパス: alpha cell

1 tion of islet architecture (ratio of beta to alpha cells).

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

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

4 than those presynaptic to the OFF sustained alpha cell.

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

6 ich can selectively stain glucagon secreting alpha cells.

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

8 ric acid A receptor activation in pancreatic alpha cells.

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

10 Z treatment sensitizes release mechanisms of alpha cells.

11 nd ROBO2 receptors were detected in beta and alpha cells.

12 resence of a separate population of Ucn 3(+) alpha cells.

13 ineage in primates, but is also expressed in alpha cells.

14 e antagonistically acting glucagon-producing alpha cells.

15 vel observation that they concomitantly gain alpha cells.

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

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

18 cells in the presence of a normal number of 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 ion through IL-6-induced GLP-1 production in alpha-cells.

23 articular inhibiting glucagon secretion from alpha-cells.

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

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

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

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

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

29 reporter was selectively activated in islet alpha-cells, a process mediated by Isl-1 in overexpressi

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

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

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

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

34 RNAs, of which only 7 were expressed more in alpha-cells (alpha-miRNAs) and 134 were expressed more i

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

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

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

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

39 a cells, and hypomethylated and expressed in alpha cells and Dnmt1-deficient beta cells.

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

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

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

43 ncreatic beta-cells with apparent sparing of alpha cells and leads to the disruption of pancreatic is

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

45 sive beta cells normally regulate juxtaposed alpha cells and that without intraislet insulin, unregul

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

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

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

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

50 n by two mechanisms, a direct stimulation of alpha-cells and an indirect inhibition via somatostatin

51 s our hypothesis that non-beta-cells such as alpha-cells and delta-cells in adults can regenerate, an

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

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 ed subplasmalemmal translocation of STIM1 in alpha-cells and retranslocation in beta-cells involving

56 a endocrine cells such as glucagon-producing alpha-cells and somatostatin producing delta-cells.

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 ion into triglycerides as compared with p110-alpha(+/+) cells, and hepatic expression of liver fatty

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

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

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

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

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

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

69 of alpha-cell proliferation and expansion of alpha-cell area, consistent with changes exhibited by en

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

71 s, with a predominance of glucagon-producing alpha cells at the expense of insulin-producing beta cel

72 rted cells are indistinguishable from native alpha-cells based on ultrastructural morphology and main

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

74 ie beta-cell dysfunction in T2D, its role in alpha-cell biology remains unclear.

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

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

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

78 ogues reveals a positive correlation between alpha-cell [Ca(2+)](i) and secretion at low glucose leve

79 d by K(ATP) channel activity or reduction in alpha-cell [Ca(2+)](i).

80 ltage-gated calcium channels is critical for alpha-cell calcium oscillations and glucagon secretion a

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

82 Interestingly, alpha cells can undergo alpha-alpha unisexual reproducti

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

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

85 Previous studies have noted the increase of alpha-cell composition in diabetes patients and in anima

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

87 nt decrease in beta-cells and an increase in alpha-cells containing glucagon and glucagon-like peptid

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

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

90 erglucagonemia, possibly due to an intrinsic alpha-cell defect.

91 ression of Ucn 3 in primary and hESC-derived alpha cells demonstrates that human Ucn 3 is not exclusi

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

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

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

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

96 s development, including islet beta-cell and alpha-cell differentiation, from single fetal progenitor

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

98 Ucn 3(+) hESC-derived alpha cells do not express Nkx6.1, Pdx1 or PC1/3 in agre

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

100 cifies the formation of the pancreatic islet alpha-cell during development.

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

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

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

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

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

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

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

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

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

110 tissue slices enabled in situ examination of alpha-cell electrophysiology.

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

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 uman alpha, beta, and acinar cells and found alpha cells exhibit intrinsic phenotypic plasticity asso

116 with exocrine and beta cells, differentiated alpha cells exhibited many more genes bivalently marked

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

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

119 Human alpha cells express the vesicular acetylcholine transpor

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

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

122 et of FoxO1-deficient beta cells adopted the alpha cell fate, resulting in hyperglucagonemia.

123 fferentiate as beta cells instead take on an alpha cell fate.

124 Mnx1 functions to promote beta and suppress alpha cell fates.

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

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

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

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

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

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

131 r, mechanisms regulating glucagon action and alpha-cell function and number are incompletely understo

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

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

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

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

139 stinfection were elevated, indicating normal alpha-cell function.

140 despite hyperglycemia, implicating defective alpha-cell function.

141 mation on whether these variants also affect alpha-cell function.

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

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

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

145 uring glucose stimulation and interacts with alpha-cell GHB receptors, thus mediating the suppressive

146 (SST) suppression of hypoglycemia-stimulated alpha-cell glucagon release plays an important role.

147 -cell secretion is not the only regulator of alpha-cell glucagon secretion.

148 and shows that UCP2 is necessary for normal alpha-cell glucose sensing and the maintenance of euglyc

149 We also identified glycine, acting via alpha-cell glycine receptors, as the predominant amino a

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

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

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

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

154 ling between pancreatic islet beta-cells and alpha-cells has been proposed to play a role in regulati

155 UCP2-deleted alpha-cells have higher levels of intracellular reactive

156 eated with incretin therapy were notable for alpha-cell hyperplasia and glucagon-expressing microaden

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

158 roliferation and dysplasia and the latter by alpha-cell hyperplasia with the potential for evolution

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

160 p)(-/-) mice developed hyperglucagonemia and alpha-cell hyperplasia.

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

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

163 that without intraislet insulin, unregulated alpha cells hypersecrete glucagon, which directly causes

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

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

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

167 Acetylcholine secretion by alpha cells in turn sensitizes the beta cell response to

168 e effects of anti-TNF-alpha treatment on TNF-alpha(+) cells in the skin and blood of patients with ps

169 Our data showed the number of alpha-cells in each islet increased following STZ-mediat

170 sistent with changes exhibited by endogenous alpha-cells in Gcgr(-/-) and Gcgr(Hep)(-/-) pancreata.

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

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

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

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

175 sing and insulin secretion, as well as islet alpha-cell infiltration, which contribute to reduced glu

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

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

178 dult islet, including the glucagon-producing alpha cells, insulin-producing beta cells, somatostatin-

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

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

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

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

183 Sorted alpha-cells lack endogenous stimulation of EphA forward

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

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

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

187 Infection of the pancreatic alpha cell line alpha-TC6 with 7B2-encoding adenovirus e

188 f miR-200c, miR-125b or miR-182 in the mouse alpha cell line alphaTC6 decreases the level of cMAF mRN

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

190 iated knockdown of Arx, a determinant of the alpha-cell lineage, inhibits the conversion.

191 -expressed in either pituitary or pancreatic alpha cell lines, proglucagon processing was preferentia

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

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

194 -secreting beta cells and glucagon-secreting alpha cells maintain physiological blood glucose levels,

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

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

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

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

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

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

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

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

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

204 Although alpha-cell mass of STZ-treated mice remained unchanged,

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

206 P-4 inhibitors expand beta-cell mass, reduce alpha-cell mass, and inhibit glucagon secretion in precl

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

208 y which signaling through the Gcgr regulates alpha-cell mass, wild-type islets were transplanted into

209 rsecretion involving expansion of pancreatic alpha-cell mass.

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

211 taless related homeobox, result in decreased alpha-cell mass.

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

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

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

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

216 g of Adora1 and loss of Adora1 expression on alpha-cells may explain the hyperglucagonemia observed i

217 Thus, diploid a and alpha cells must undergo a developmental transition to t

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

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

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

221 ta-cell allocation with accompanying reduced alpha-cell numbers.

222 Transition of beta-cells into alpha-cells occurs after beta-cell degranulation and is

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

224 M4 cells apparently correspond to ON alpha cells of earlier reports, and are easily distingui

225 Instead, we find that the alpha cells of human islets provide paracrine cholinergi

226 alpha cells of STZ-treated mice exhibited the following:

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

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

229 eceptor (Adora1), is gradually diminished in alpha-cells of NOD mice, autoantibody-positive (AA(+)) a

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

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

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

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

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

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

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

237 countered no overt changes in numbers of TNF-alpha(+) cells or signs of apoptosis in lesional psoriat

238 ltrastructural morphology and maintain their alpha-cell phenotype after transplantation in vivo.

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

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

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

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

243 have suggested that, under some conditions, alpha cells possess the capacity to transdifferentiate i

244 es replication of beta cells but not that of alpha cells, PP cells, or fibroblasts.

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

246 ep)(-/-) mice exhibited an increased rate of alpha-cell proliferation and expansion of alpha-cell are

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

248 ption of hepatic Gcgr signaling can increase alpha-cell proliferation independent of direct pancreati

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

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

251 receptor inhibition to hyperglucagonemia and alpha-cell proliferation.

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

253 Furthermore, beta/alpha cell ratios were increased by approximately 18% an

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

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

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

257 so sufficient to cause Arx-dependent beta-to-alpha-cell reprogramming.

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

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

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

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

262 basal Glp1r signalling in the suppression of alpha cell secretion during exercise.

263 ing receptor-based mechanism for controlling alpha-cell secretory responses to metabolic fuels.

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

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

266 Further to this, we created alpha-cell-specific UCP2 knockout (UCP2AKO) mice, which

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

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

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 glucagon expression expressed selectively in alpha-cells (TFalpha) is targeted by beta-miRNAs; miR-20

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

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

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

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

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

277 ession of Arx in beta cells, causing beta-to-alpha-cell transdifferentiation.

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

279 Therefore, alpha-cell UCP2 deletion perturbs the fasting/hypoglycem

280 ow that glucagon, secreted by the pancreatic alpha cell, up-regulates the expression of its own gene

281 , Arx mRNA levels were up-regulated in islet alpha-cells upon Isl-1 overexpression in vivo.

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

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

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

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

286 Direct effects of SSTR2a on alpha-cells was assessed by resecting the pancreas, whic

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

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

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

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

291 sing enhanced yellow fluorescence protein in alpha cells were used to identify alpha cells within pan

292 Glucagon-secreting alpha-cells were unambiguously identified by cell specif

293 found SLIT1 and SLIT3 in both beta cells and alpha cells, whereas SLIT2 was predominantly expressed i

294 by SST receptor type 2 (SSTR2) antagonism of alpha-cells, which relieve SSTR2 inhibition, thereby inc

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

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

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

298 protein in alpha cells were used to identify alpha cells within pancreas slices.

299 -releasing beta-cells and glucagon-secreting alpha-cells within intact mouse and human pancreatic isl

300 undergo a conversion into glucagon-producing alpha-cells without introduction of any genetic modifica