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1 lates fat deposition and is a potent insulin secretagogue.
2 activity of osteocalcin, which is an insulin secretagogue.
3 g cells of secretory cargo in the absence of secretagogue.
4 omosyn similar to that of application of the secretagogue.
5 eins were stored and released in response to secretagogue.
6 ide that acts as a glucose-dependent insulin secretagogue.
7  of the cells with ATP, an established mucin secretagogue.
8 d in the cells after the addition of a mucin secretagogue.
9                We find that 23G3 is a potent secretagogue.
10  monooxygenase release is more responsive to secretagogue.
11 f T2DM demonstrate that P5 is a weak insulin secretagogue.
12 ry granule exocytosis was more responsive to secretagogue.
13 ng urinary oxalate excretion, via an unknown secretagogue.
14 and specific for muscarinic receptor, as the secretagogue.
15  the entire length of tropomyosin, were weak secretagogues.
16 s very poorly responsive to Ca(2+)-elevating secretagogues.
17 sponse to glucose (15 mm) and other nutrient secretagogues.
18 retion stimulated by noncarbohydrate insulin secretagogues.
19 onfirmed that they were increased by insulin secretagogues.
20  glucose, KCl, and a combination of multiple secretagogues.
21 ch was not possible from studying individual secretagogues.
22 ynthesis, resulting in a reduced response to secretagogues.
23 l insulin responses to glucose and beta-cell secretagogues.
24  with physiological or supramaximal doses of secretagogues.
25 e a step toward developing therapeutic GLP-1 secretagogues.
26  the cells and later released in response to secretagogues.
27 hibited surfactant secretion, independent of secretagogues.
28 ges in AMPK activity in the actions of other secretagogues.
29 phorylation was not observed with other fuel secretagogues.
30 rtant differences from conventional chloride secretagogues.
31 ct mitochondrial metabolism as novel insulin secretagogues.
32 decrease in the level of HMG-CoA produced by secretagogues.
33 n in islet cells was not affected by insulin secretagogues.
34 inar cells stimulated with calcium-releasing secretagogues.
35 ere hyper-responsive to in vivo injection of secretagogues.
36 th compounds were similar for several common secretagogues.
37 refore secrete less chloride when exposed to secretagogues.
38 not corticosterone, in response to different secretagogues.
39 esters, and analogs of cAMP, all key insulin secretagogues.
40 d secretion during stimulation with nutrient secretagogues.
41 n secretion in response to glucose and other secretagogues.
42 parable to that from beta-cells treated with secretagogues.
43 not abrogated by inhibiting degranulation to secretagogues.
44 ecretion of gut peptide by other gut peptide secretagogues.
45 glucagon secretion even after treatment with secretagogues.
46          The ghrelin receptor growth hormone secretagogue 1 receptor (GHSR) is present in hypothalami
47                          Some growth hormone secretagogues act as agonists at the ghrelin receptor an
48                       We show that these PRL secretagogues act on primary pituitary cells and thus ar
49 de-binding proteins that mediate the insulin secretagogue action of cAMP, the possible contributions
50 l homeobox 1 gene expression and the insulin secretagogue action of pancreatic beta-cells.
51 ivation of the CaSR on neuronal and hormonal secretagogue actions.
52                    Here we report that basic secretagogues activate mouse mast cells in vitro and in
53 mosyn-syntaxin 1A interaction in response to secretagogue activation is an important mechanism allowi
54                                      Insulin secretagogues acutely stimulated 1.5-5-fold increases in
55  for dual oral agent therapy with an insulin secretagogue and sensitizer.
56 de generated by adipsin, as a potent insulin secretagogue and show that the C3a receptor is required
57 role of irisin as a new pancreatic beta-cell secretagogue and survival factor and its potential role
58  be induced by physiologic concentrations of secretagogues and by in vivo stimulation of the pancreas
59 of human islet cells was affected by insulin secretagogues and explore the role of cadherins in the s
60 model to study mast cell activation by basic secretagogues and identify MRGPRX2 as a potential therap
61                                          New secretagogues and mechanisms continue to be identified a
62  Islets showed good physiologic responses to secretagogues and restored normoglycemia in streptozotoc
63 beta-cells, release C-peptide in response to secretagogues and survive in vivo following transplantat
64 o E- and N-cadherins is regulated by insulin secretagogues and that E- and N-cadherin engagement prom
65  secretion occurred in response to different secretagogues and was mediated by alterations in KATP ch
66 nts include sulfonylureas, which are insulin secretagogues, and thiazolidinediones, which are insulin
67 (-/-) mice demonstrate increased severity of secretagogue- and diet-induced pancreatitis in compariso
68 imental models of rodent acute pancreatitis, secretagogue- and duct injection-induced pancreatitis.
69 cell depends on anaplerosis in which insulin secretagogues are metabolized by mitochondria into molec
70 ated islets in response to glucose and other secretagogues are not well understood.
71                                        These secretagogues are released from the intestinal epithelia
72 nknown protein kinase in response to various secretagogues as well as reductions in [Cl]i and cell vo
73 f suggests a dual role for metabolic insulin secretagogues, as an initial sharp increase in insulin s
74 increased adrenocorticotropic hormone (ACTH) secretagogue biosynthesis in the paraventricular nucleus
75   The recognition that gastrin is not only a secretagogue but also a trophic hormone has led to new r
76 , neither MMS nor KIC (10 mm) was an insulin secretagogue, but when added together KIC (2 mm) and MMS
77 odel of pancreatitis induced by supramaximal secretagogue (caerulein) stimulation.
78                                        Other secretagogues can increase production of succinyl-CoA se
79                                     Nutrient secretagogues can increase the production of succinyl-Co
80                                     Although secretagogues can increase the production of succinyl-Co
81           The amino acid leucine is a potent secretagogue, capable of inducing insulin secretion.
82 secretory responses to the calcium-dependent secretagogue carbachol or cAMP analog 8-bromo-cAMP, indi
83 r cell preparations were challenged with the secretagogue carbamylcholine, a subpopulation of zymogen
84 ther citrate, for the synthesis SC-CoAs from secretagogue carbon in mitochondria and the transfer of
85                                              Secretagogues (cerulein, carbachol, and bombesin) can in
86                      Interestingly, a single secretagogue challenge failed to consistently elicit an
87 ement of antioxidants in response to a mixed secretagogue challenge is an early correlate of future b
88 irs the rapid replenishment of SGs following secretagogue challenge.
89      Stimulation of cells for 5 min with the secretagogue cholecystokinin enhanced the colocalization
90 d upon stimulation with the nutrient insulin secretagogue combination of leucine plus glutamine, indi
91 d are activated by anaphylatoxin C5a and the secretagogue compound 48/80.
92 e ion flux in rabbit ileum after exposure to secretagogues correlates inversely and highly significan
93 lls that receive input from two hypothalamic secretagogues, corticotrophin-releasing hormone (CRH) an
94 lls that receive input from two hypothalamic secretagogues, corticotrophin-releasing hormone (CRH) an
95           Upon application of common insulin secretagogues, current spikes resulting from detection o
96                                  The insulin secretagogue D-glucose also stimulates beta-cell p38 MAP
97 his is consistent with the fact that insulin secretagogues decrease the level of the mevalonate precu
98   Release of dopamine was evoked by chemical secretagogues delivered from micropipets that were calib
99 cay slope; all of these characteristics were secretagogue dependent.
100 cad/Fc and E-cad/Fc acquired, in a time- and secretagogue-dependent manner, a spreading form that was
101 henylated bovine serum albumin (DNP-BSA) and secretagogues (e.g., poly-L-lysine) was investigated by
102 ry process, because addition of an exogenous secretagogue elicited peroxidase secretion from 18-week-
103                                       In the secretagogue-elicited model, the DT-induced decrease in
104    These studies showed that pyruvate, a non-secretagogue, enters beta-cells and causes a transient r
105 r containing Zinquin, application of insulin secretagogues evoked an increase in fluorescence around
106 siologic techniques were used to measure the secretagogue-evoked increase in [Ca2+]i and consequent a
107 cs and responded to Weibel-Palade body (WPB) secretagogues except desmopressin.
108 liferation and all caseins were potent GLP-1 secretagogues (except kappa casein).
109  behavioral stressor implicate enhanced ACTH secretagogue expression in the increased HPA response to
110            Glucose is the main physiological secretagogue for insulin secretion by pancreatic beta-ce
111                       Kisspeptins are potent secretagogues for GnRH, and the Kiss1 gene is a target f
112 etagogue, or histamine, a Weibel-Palade body secretagogue from MCs, potentiated DVT in wild-type mice
113 lycemia occurred in mice deficient in the GH secretagogue ghrelin as a result of knockout of the gene
114       The recently discovered growth hormone secretagogue, ghrelin, is a potent agonist at the human
115  an endogenous ligand for the growth hormone secretagogue (GHS) receptor, yielded the surprising resu
116 y active agonist of the human growth hormone secretagogue (GHS) receptor.
117 pression of ghrelin mRNAs and growth hormone secretagogue (GHS) receptors could be detected in human
118 etermined the effects of an orally active GH secretagogue (GHS) treatment that causes a release of en
119 ntly a nonpeptidyl small m.w. compound, a GH secretagogue (GHS), was found to induce the production o
120 80) was discovered as a human growth hormone secretagogue (GHS).
121 in novel chemical entities as growth hormone secretagogues (GHSs), a small database of peptides and n
122 by approximately one-half in response to the secretagogues glucose, glutamine plus leucine, or pyruva
123              In addition to being an insulin secretagogue, glucose regulates proliferation and surviv
124      Distinct from its role as an intestinal secretagogue, guanylin may also have a role in intestina
125 ic patients who had taken insulin or insulin secretagogues had a significantly higher risk of pancrea
126                    Its potency as an insulin secretagogue has led to pharmaceutical interest in devel
127    Among them, compound 24 is a potent GLP-1 secretagogue, has low effect on gallbladder volume, and
128                                              Secretagogues have also been shown to enhance the transl
129 apy and the administration of growth hormone secretagogues, have been encouraging.
130                                      The WPB secretagogue histamine evoked exocytosis of these fluore
131                                 However, the secretagogue hyperstimulation model of pancreatitis is t
132 napproved drug, including the growth hormone secretagogue ibutamoren, the peroxisome proliferator-act
133                 Activation of trypsinogen by secretagogues in acinar cells was prevented by pharmacol
134 in the GLP-1 secretory response to different secretagogues in murine GLUTag L cells, as well as in th
135    Isolated acini were stimulated by various secretagogues in the presence or absence of cell-permean
136 ranted to determine the potential role of GH secretagogues in the treatment of CHF.
137 t not that of insulin, is activated by these secretagogues in vivo.
138 imately 40% reduction in response to insulin secretagogues in vivo.
139 retion (IS) in response to glucose and other secretagogues including nonfuel stimuli.
140 cretory actions of cAMP- and cGMP-generating secretagogues, including cholera toxin and heat stable E
141 tionic substances, collectively called basic secretagogues, including inflammatory peptides and drugs
142   Stimulation of these cells with a range of secretagogues, including K(+), BaCl(2), and forskolin, d
143 nase complex and would, in part, account for secretagogues increasing the islet level of succinyl-CoA
144 bition of endogenous GEF1 activity decreases secretagogue-independent release of hormone precursors,
145 in the KO beta-cells in response to the same secretagogues, indicating reduced insulin secretion.
146             In the present study we measured secretagogue-induced acid secretion from wild-type and D
147                                              Secretagogue-induced acid secretion in wild-type mouse g
148 ved in Kcnn4(-/-) mice results from enhanced secretagogue-induced ACTH output from anterior pituitary
149 esult consistent with findings demonstrating secretagogue-induced activation of RhoA.
150 d potassium (BK) channels in spontaneous and secretagogue-induced activity.
151 e-activated (BK) channels in spontaneous and secretagogue-induced activity.
152 uorescent 70 kDa dextran to demonstrate that secretagogue-induced bulk endocytosis also occurs in bov
153 in depletion causes a near-complete block in secretagogue-induced exocytosis.
154                                              Secretagogue-induced histamine release, inflammation and
155                 However, in isolated islets, secretagogue-induced insulin release (by glucose, GLP-1,
156 nhibitor exhibited reduced sulfonylurea- and secretagogue-induced insulin secretion.
157                                          The secretagogue-induced interaction was strongly reduced by
158 experimental models of acute pancreatitis (a secretagogue-induced model and a model elicited by retro
159  type and Tpl2(-/-) mice subjected to either secretagogue-induced or bile salt-induced pancreatitis.
160 f decreasing extracellular pH (pHe) in early secretagogue-induced pancreatitis (zymogen activation an
161 ation that occurs during the early stages of secretagogue-induced pancreatitis is not altered by admi
162  These data demonstrate that the severity of secretagogue-induced pancreatitis is significantly ameli
163                                              Secretagogue-induced pancreatitis was achieved by 12 hou
164                                           In secretagogue-induced pancreatitis, large amounts of tryp
165 acid load might sensitize the acinar cell to secretagogue-induced pancreatitis.
166 essential early event in the pathogenesis of secretagogue-induced pancreatitis.
167 n inhibitor-I (PSTI-I) in mice could prevent secretagogue-induced pancreatitis.
168 nge sensitizes the pancreatic acinar cell to secretagogue-induced zymogen activation and injury and m
169 acini, lowering pHe from 7.6 to 6.8 enhanced secretagogue-induced zymogen activation and injury, but
170 c beta cells are believed to convert insulin secretagogues into products that are translocated to the
171 mon to glucose, amino acid, and organic acid secretagogues, involving flux through the pyruvate/isoci
172 ked by a maximal concentration of the strong secretagogue ionomycin (1 microM), for which there was a
173 c beta-cells in response to glucose or other secretagogues is tightly coupled to membrane potential.
174 on, although its function regarding specific secretagogues is unclear.
175                   Secretion induced by basic secretagogues (KCl and Arg) was not affected by these dr
176 ment, and under chronic challenge by insulin secretagogues, loss of Sorcs1 leads to diabetes.
177 n contrast with the ability of IL-3 to alter secretagogue-mediated cytosolic calcium responses follow
178   The frequencies of use of insulin, insulin secretagogues, metformin, and other antidiabetic medicat
179 in the regulation of pancreatic secretion by secretagogues, modulatory proteins and neural pathways a
180  aimed to assess whether glutamine, a potent secretagogue of GLP-1 in vivo, increases GLP-1 release,
181 eased responsiveness to kisspeptin, the main secretagogue of GnRH.
182 RF1 is not a typical sensitizer, mimetic, or secretagogue of insulin.
183 esponse to KCl and norepinephrine, a natural secretagogue of TRH.
184 ssels with calcium ionophore A23187, a known secretagogue of Weibel-Palade bodies, induced immediate
185  released upon stimulation with histamine, a secretagogue of Weibel-Palade bodies, slowed down leukoc
186 Stimulation of endothelium with histamine, a secretagogue of WPBs, or injection of serotonin normaliz
187 ent, and by measuring the effects of insulin secretagogues on cPLA(2) distribution, on changes in [Ca
188 (2)beta in beta-cells incubated with insulin secretagogues or thapsigargin, that this requires prior
189 imulation either by mastoparan, a wasp venom secretagogue, or by the physiological mechanism of antig
190 Topical application of compound 48/80, an MC secretagogue, or histamine, a Weibel-Palade body secreta
191 in response to P2Y2 receptor agonists and to secretagogues, phorbol 12-myristate 13-acetate (PMA) and
192  be differentially regulated by hypothalamic secretagogues provides a mechanism for differential cont
193  be differentially regulated by hypothalamic secretagogues provides a mechanism for differential cont
194 on-signaling ghrelin receptor growth hormone secretagogue R1b (GHS-R1b) has been suggested to simply
195 tive, and orally bioavailable growth hormone secretagogue receptor (GHS-R) antagonists are reported.
196 vailable tetralin carboxamide growth hormone secretagogue receptor (GHS-R) antagonists were discovere
197 on, ghrelin and its receptor (growth hormone secretagogue receptor (GHS-R)) are widely expressed in a
198 t is mediated by its receptor Growth Hormone Secretagogue Receptor (GHS-R), but the physiologically r
199 f the peptide's receptor, the growth hormone secretagogue receptor (GHS-R), in the caudal brainstem.
200 bed endogenous ligand for the growth hormone secretagogue receptor (GHS-R), is produced by stomach ce
201 an endogeneous ligand for the growth hormone secretagogue receptor (GHS-R).
202 s an endogenous ligand of the growth hormone secretagogue receptor (GHS-R).
203 genous ligand for the type 1a growth hormone secretagogue receptor (GHS-R1a) and the only currently k
204                           The growth hormone secretagogue receptor (GHSR) (ghrelin receptor) plays an
205                               Growth hormone secretagogue receptor (GHSR) 1a is the only molecularly
206 eased ghrelin levels, whereas growth hormone secretagogue receptor (Ghsr) null mice showed increased
207     Synthetic agonists of the growth hormone secretagogue receptor (GHSR) rejuvenate the pulsatile pa
208 at Ghrl and ghrelin receptor (growth hormone secretagogue receptor (GHSR)) are expressed in thymic st
209 action with its receptor, the growth hormone secretagogue receptor (GHSR).
210 y known ghrelin receptor, the growth hormone secretagogue receptor (GHSR).
211 Endogenous ghrelin receptors [growth hormone secretagogue receptor (GHSR)] are also present in extrah
212 the endogenous ligand for the growth hormone secretagogue receptor (GHSR; ghrelin receptor).
213 elin are mediated through the growth hormone secretagogue receptor 1a (ghrelin receptor), a peptidic
214 xhibits dual affinity for the growth hormone secretagogue receptor 1a (GHS-R1a) and the cluster of di
215 n receptor, also known as the growth hormone secretagogue receptor 1a (GHS-R1a), is a G-protein-coupl
216 and acts at its receptor, the growth hormone secretagogue receptor 1a (GHSR1a), in the hypothalamus t
217   Ghrelin is an endogenous ligand for the GH secretagogue receptor 1a (GHSR1a, ie, ghrelin receptor).
218 a potent agonist at the human growth hormone secretagogue receptor 1a (hGHSR1a).
219 elin acts as a ligand for the growth hormone secretagogue receptor and can stimulate the release of g
220              A novel neuronal growth hormone secretagogue receptor circuit involving urocortin 1 neur
221 ogical states and because the growth hormone secretagogue receptor has been identified in blood vesse
222 is the natural ligand for the growth hormone secretagogue receptor in the pituitary gland, thus fulfi
223 ting KATP conductance via the growth hormone secretagogue receptor subtype 1a-Galphai -PI3K-Erk1/2-KA
224 s natural ligand for the growth hormone (GH) secretagogue receptor that has recently been isolated fr
225 ynaptic ghrelin receptor, the growth hormone secretagogue receptor type 1a (GHS-R1a), in VP neurons c
226 ch binds to and activates the growth hormone secretagogue receptor type 1a (GHS-R1a), is considered t
227 in, the natural ligand of the growth hormone secretagogue receptor type 1a (GHS-R1a), is mainly secre
228                           The growth hormone secretagogue receptor, GHSR1a, mediates the biological a
229 the endogenous ligand for the growth hormone secretagogue receptor, has been implicated not only in t
230 ural endogenous ligand of the growth hormone secretagogue receptor, it potently stimulates growth hor
231 ive blood-brain transport and growth hormone secretagogue receptor-1 agonist activity.
232 (+) cells, while ghrelin- and growth hormone secretagogue receptor-deficient (GHS-R-deficient) mice d
233 ary cells express significant growth hormone secretagogue receptor.
234 ncrease feeding by binding at growth hormone secretagogue receptors (GHS-R), the only sites of action
235 duced in the stomach, acts on growth hormone secretagogue receptors (GHSRs) in hypothalamic neurons t
236                               Growth hormone secretagogue receptors (GHSRs) in the central nervous sy
237         Much information is available on how secretagogue receptors acutely couple through heterotrim
238                                              Secretagogue receptors and their intracellular signaling
239                                    The major secretagogue receptors on acinar cells include those bin
240                                          The secretagogue receptors present on acinar cells, especial
241  interaction with endothelial growth hormone secretagogue receptors.
242 s structurally related to the growth hormone secretagogue receptors.
243 sms by which cholecystokinin (CCK) and other secretagogues regulate pancreatic acinar function are mo
244  secretion by the parietal cell involves the secretagogue-regulated re-cycling of the H+-K+-ATPase at
245 y of these pseudogranules, which we show are secretagogue responsive, to recruit membrane proteins.
246 n of immature content proteins and producing secretagogue-responsive mature granules.
247                          The use of glucagon secretagogues reveals a positive correlation between alp
248                                    Different secretagogues selectively release vesicles from the RRP
249                                          Our secretagogue-siRNA conjugate prevented cytokine-induced
250 l line was used to test the efficacy of this secretagogue-siRNA conjugate.
251    The purpose of this study was to create a secretagogue-small interfering RNA (siRNA) conjugate to
252    The absence of AC6 reduced cAMP-dependent secretagogue-stimulated amylase secretion, and abolished
253 es approximately 180-220 nm in diameter, and secretagogue-stimulated exocytosis of CgA from A35C cell
254 sually distinguished two sequential steps of secretagogue-stimulated exocytosis: fusion of individual
255 eta catalytic activity and that BEL inhibits secretagogue-stimulated insulin secretion from these cel
256 entration, distribution, and modification in secretagogue-stimulated rat pancreatic acinar cells.
257 deconvolution and electron microscopy and by secretagogue-stimulated release assays.
258 TPase by bafilomycin A1 markedly reduced the secretagogue-stimulated release of CgA-EAP by perturbing
259 al deconvolution fluorescence microscopy and secretagogue-stimulated release studies demonstrate that
260 n microscopy, subcellular fractionation, and secretagogue-stimulated release, examining a series of f
261 bioactive peptides that feed back to inhibit secretagogue-stimulated release.
262 rescent protein localization in the basal or secretagogue-stimulated state.
263 dent beta-cells causes a rapid inhibition of secretagogue-stimulated subcellular Ca(2+) signaling and
264 KS) is a central regulatory molecule linking secretagogue stimulation at the cell surface to mucin gr
265       In PC-12 cells overexpressing tomosyn, secretagogue stimulation in the presence of lysophosphat
266                                              Secretagogue stimulation leads to an enlargement of the
267 et-induced insulin resistance, pharmacologic secretagogue stimulation of beta-cells with an incretin
268  in a Ca(2+)-sensitive manner in response to secretagogue stimulation of pancreatic beta-cells.
269                Downstream events involved in secretagogue stimulation of pancreatic secretion have be
270                          We demonstrate that secretagogue stimulation results in the rapid translocat
271 olecystokinin for 40 min, demonstrating that secretagogue stimulation transiently alters the associat
272 d WPB exocytosis and is present on WPBs, and secretagogue stimulation triggers an increased recruitme
273 cholic acid-3-sulfate (TLCS) or supramaximal secretagogue stimulation with caerulein.
274  pancreatic acini appropriately responded to secretagogue stimulation with the secretion of digestive
275 ure can sensitize pancreatic acinar cells to secretagogue stimulation, resulting in dysregulation of
276 th the apical plasma membrane in response to secretagogue stimulation.
277                When succinate esters are the secretagogue, succinyl-CoA can be generated via the succ
278                This effect was not seen with secretagogues such as glucose that stimulate secretion v
279 inophils are activated by various classes of secretagogues, such as cytokines (e.g., IL-5), lipid med
280 a simple mathematical model of a hormone and secretagogue system with concentration dependent secreti
281 secretion, tomosyn-2, in response to insulin secretagogues targets it to degradation by the Hrd-1 E3-
282 teral region and blocks secretion induced by secretagogues that act via calcium.
283                                              Secretagogues that stimulate gastric acid secretion indu
284 ors blocked amylase secretion in response to secretagogues that use calcium as a second messenger (e.
285  Na-K-Cl cotransporter NKCC1 is activated by secretagogues through a phosphorylation-dependent mechan
286    Current therapeutic strategies for SS use secretagogues to induce secretion via muscarinic recepto
287  vascular or diffusion delivery of beta-cell secretagogues to islets, we showed that reduced insulin
288                               The binding of secretagogues to parietal cells generates changes in sec
289 n one of the latter occasions, the beta-cell secretagogue tolbutamide was infused in a dose of 1.0 g/
290 -2-chloroethylamide effectively counteracted secretagogue-triggered excessive hMMC degranulation.
291 ssion of the ghrelin receptor growth hormone secretagogue type 1a (GHS-R1a) in the hypothalamus and p
292 monstrate that obestatin is a potent insulin secretagogue under hyperglycemic condition, and obestati
293 ed with reduced risk, and insulin or insulin secretagogue use was associated with increased risk of p
294 n secretion in response to arginine or other secretagogues was identical to that in cells from health
295 experiments in response to glucose and other secretagogues was similar in islets isolated from Pdx1(+
296  and because neutrophil elastase is a potent secretagogue, we examined the hypothesis that LTB(4) cau
297                               By using these secretagogues, we developed a paradigm in which phorbol
298                     Among various endogenous secretagogues, we found that PGE2 had the lowest EC50 va
299                 ALA is a highly potent GLP-1 secretagogue which also increases the intracellular leve
300 a antagonist, namely, the role as an insulin secretagogue with potential value for diabetes treatment

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