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1 and specific for muscarinic receptor, as the secretagogue.
2 lates fat deposition and is a potent insulin secretagogue.
3 activity of osteocalcin, which is an insulin secretagogue.
4 g cells of secretory cargo in the absence of secretagogue.
5 omosyn similar to that of application of the secretagogue.
6 eins were stored and released in response to secretagogue.
7 ide that acts as a glucose-dependent insulin secretagogue.
8 cited by an increase in plasma ghrelin, a GH secretagogue.
9  of the cells with ATP, an established mucin secretagogue.
10 d in the cells after the addition of a mucin secretagogue.
11                We find that 23G3 is a potent secretagogue.
12 ng urinary oxalate excretion, via an unknown secretagogue.
13 f T2DM demonstrate that P5 is a weak insulin secretagogue.
14  longa plant was found to be the most potent secretagogue.
15 ry granule exocytosis was more responsive to secretagogue.
16 ecretion of gut peptide by other gut peptide secretagogues.
17 glucagon secretion even after treatment with secretagogues.
18 s very poorly responsive to Ca(2+)-elevating secretagogues.
19 nsulin secretion in response to a variety of secretagogues.
20 sponse to glucose (15 mm) and other nutrient secretagogues.
21 retion stimulated by noncarbohydrate insulin secretagogues.
22 onfirmed that they were increased by insulin secretagogues.
23  glucose, KCl, and a combination of multiple secretagogues.
24 ch was not possible from studying individual secretagogues.
25 ynthesis, resulting in a reduced response to secretagogues.
26  with physiological or supramaximal doses of secretagogues.
27 e a step toward developing therapeutic GLP-1 secretagogues.
28  the cells and later released in response to secretagogues.
29 hibited surfactant secretion, independent of secretagogues.
30  the entire length of tropomyosin, were weak secretagogues.
31 ges in AMPK activity in the actions of other secretagogues.
32 phorylation was not observed with other fuel secretagogues.
33 rtant differences from conventional chloride secretagogues.
34 ct mitochondrial metabolism as novel insulin secretagogues.
35 decrease in the level of HMG-CoA produced by secretagogues.
36 inar cells stimulated with calcium-releasing secretagogues.
37 parable to that from beta-cells treated with secretagogues.
38 ere hyper-responsive to in vivo injection of secretagogues.
39 l insulin responses to glucose and beta-cell secretagogues.
40 n in islet cells was not affected by insulin secretagogues.
41 not corticosterone, in response to different secretagogues.
42 esters, and analogs of cAMP, all key insulin secretagogues.
43 d secretion during stimulation with nutrient secretagogues.
44 n secretion in response to glucose and other secretagogues.
45 not abrogated by inhibiting degranulation to secretagogues.
46          The ghrelin receptor growth hormone secretagogue 1 receptor (GHSR) is present in hypothalami
47 cts through its receptor, the growth hormone secretagogue 1a (GHSR1a), to promote food intake and pre
48                          Some growth hormone secretagogues act as agonists at the ghrelin receptor an
49                       We show that these PRL secretagogues act on primary pituitary cells and thus ar
50 de-binding proteins that mediate the insulin secretagogue action of cAMP, the possible contributions
51 l homeobox 1 gene expression and the insulin secretagogue action of pancreatic beta-cells.
52 ivation of the CaSR on neuronal and hormonal secretagogue actions.
53                    Here we report that basic secretagogues activate mouse mast cells in vitro and in
54 mosyn-syntaxin 1A interaction in response to secretagogue activation is an important mechanism allowi
55                                      Insulin secretagogues acutely stimulated 1.5-5-fold increases in
56  for dual oral agent therapy with an insulin secretagogue and sensitizer.
57 de generated by adipsin, as a potent insulin secretagogue and show that the C3a receptor is required
58 role of irisin as a new pancreatic beta-cell secretagogue and survival factor and its potential role
59  be induced by physiologic concentrations of secretagogues and by in vivo stimulation of the pancreas
60 of human islet cells was affected by insulin secretagogues and explore the role of cadherins in the s
61 model to study mast cell activation by basic secretagogues and identify MRGPRX2 as a potential therap
62                                          New secretagogues and mechanisms continue to be identified a
63  Islets showed good physiologic responses to secretagogues and restored normoglycemia in streptozotoc
64 beta-cells, release C-peptide in response to secretagogues and survive in vivo following transplantat
65 o E- and N-cadherins is regulated by insulin secretagogues and that E- and N-cadherin engagement prom
66  secretion occurred in response to different secretagogues and was mediated by alterations in KATP ch
67 riate, followed, if necessary, by intestinal secretagogues and/or prokinetic agents.
68 gon in response to glucose and some glucagon secretagogues, and elevate blood glucose upon transplant
69  increased calcium signalling in response to secretagogues, and improved mitochondrial energization.
70 , junctional protein regulators, analgesics, secretagogues, and serotonin antagonists have a therapeu
71 nts include sulfonylureas, which are insulin secretagogues, and thiazolidinediones, which are insulin
72 (-/-) mice demonstrate increased severity of secretagogue- and diet-induced pancreatitis in compariso
73 imental models of rodent acute pancreatitis, secretagogue- and duct injection-induced pancreatitis.
74 cell depends on anaplerosis in which insulin secretagogues are metabolized by mitochondria into molec
75 ated islets in response to glucose and other secretagogues are not well understood.
76                                        These secretagogues are released from the intestinal epithelia
77 f suggests a dual role for metabolic insulin secretagogues, as an initial sharp increase in insulin s
78 increased adrenocorticotropic hormone (ACTH) secretagogue biosynthesis in the paraventricular nucleus
79   The recognition that gastrin is not only a secretagogue but also a trophic hormone has led to new r
80 , neither MMS nor KIC (10 mm) was an insulin secretagogue, but when added together KIC (2 mm) and MMS
81 odel of pancreatitis induced by supramaximal secretagogue (caerulein) stimulation.
82                                        Other secretagogues can increase production of succinyl-CoA se
83                                     Nutrient secretagogues can increase the production of succinyl-Co
84                                     Although secretagogues can increase the production of succinyl-Co
85           The amino acid leucine is a potent secretagogue, capable of inducing insulin secretion.
86 secretory responses to the calcium-dependent secretagogue carbachol or cAMP analog 8-bromo-cAMP, indi
87 ther citrate, for the synthesis SC-CoAs from secretagogue carbon in mitochondria and the transfer of
88                                              Secretagogues (cerulein, carbachol, and bombesin) can in
89                      Interestingly, a single secretagogue challenge failed to consistently elicit an
90 ement of antioxidants in response to a mixed secretagogue challenge is an early correlate of future b
91 irs the rapid replenishment of SGs following secretagogue challenge.
92      Stimulation of cells for 5 min with the secretagogue cholecystokinin enhanced the colocalization
93 d upon stimulation with the nutrient insulin secretagogue combination of leucine plus glutamine, indi
94 d are activated by anaphylatoxin C5a and the secretagogue compound 48/80.
95 e ion flux in rabbit ileum after exposure to secretagogues correlates inversely and highly significan
96 lls that receive input from two hypothalamic secretagogues, corticotrophin-releasing hormone (CRH) an
97 lls that receive input from two hypothalamic secretagogues, corticotrophin-releasing hormone (CRH) an
98                                  The insulin secretagogue D-glucose also stimulates beta-cell p38 MAP
99 his is consistent with the fact that insulin secretagogues decrease the level of the mevalonate precu
100 cay slope; all of these characteristics were secretagogue dependent.
101 cad/Fc and E-cad/Fc acquired, in a time- and secretagogue-dependent manner, a spreading form that was
102  include central neuromodulators, intestinal secretagogues, drugs acting on opioid or 5-HT receptors,
103 henylated bovine serum albumin (DNP-BSA) and secretagogues (e.g., poly-L-lysine) was investigated by
104  not free amino acids, showed a potent GLP-1 secretagogue effect, while proteins only had a modest ef
105 ry process, because addition of an exogenous secretagogue elicited peroxidase secretion from 18-week-
106                                       In the secretagogue-elicited model, the DT-induced decrease in
107    These studies showed that pyruvate, a non-secretagogue, enters beta-cells and causes a transient r
108 siologic techniques were used to measure the secretagogue-evoked increase in [Ca2+]i and consequent a
109 cs and responded to Weibel-Palade body (WPB) secretagogues except desmopressin.
110 liferation and all caseins were potent GLP-1 secretagogues (except kappa casein).
111  behavioral stressor implicate enhanced ACTH secretagogue expression in the increased HPA response to
112 us, GPBAR1 agonists and other powerful GLP-1 secretagogues facilitate L-cell differentiation through
113            Glucose is the main physiological secretagogue for insulin secretion by pancreatic beta-ce
114                       Kisspeptins are potent secretagogues for GnRH, and the Kiss1 gene is a target f
115 etagogue, or histamine, a Weibel-Palade body secretagogue from MCs, potentiated DVT in wild-type mice
116 lycemia occurred in mice deficient in the GH secretagogue ghrelin as a result of knockout of the gene
117 y active agonist of the human growth hormone secretagogue (GHS) receptor.
118 pression of ghrelin mRNAs and growth hormone secretagogue (GHS) receptors could be detected in human
119 etermined the effects of an orally active GH secretagogue (GHS) treatment that causes a release of en
120 ntly a nonpeptidyl small m.w. compound, a GH secretagogue (GHS), was found to induce the production o
121 80) was discovered as a human growth hormone secretagogue (GHS).
122 in novel chemical entities as growth hormone secretagogues (GHSs), a small database of peptides and n
123 by approximately one-half in response to the secretagogues glucose, glutamine plus leucine, or pyruva
124              In addition to being an insulin secretagogue, glucose regulates proliferation and surviv
125      Distinct from its role as an intestinal secretagogue, guanylin may also have a role in intestina
126       The insulin secretory response to each secretagogue had a unique genetic architecture; some of
127 ic patients who had taken insulin or insulin secretagogues had a significantly higher risk of pancrea
128                    Its potency as an insulin secretagogue has led to pharmaceutical interest in devel
129    Among them, compound 24 is a potent GLP-1 secretagogue, has low effect on gallbladder volume, and
130                                              Secretagogues have also been shown to enhance the transl
131 apy and the administration of growth hormone secretagogues, have been encouraging.
132 vent beta cell loss and some, namely insulin secretagogues, have been linked to accelerated beta cell
133                                      The WPB secretagogue histamine evoked exocytosis of these fluore
134                                 However, the secretagogue hyperstimulation model of pancreatitis is t
135 napproved drug, including the growth hormone secretagogue ibutamoren, the peroxisome proliferator-act
136                 Activation of trypsinogen by secretagogues in acinar cells was prevented by pharmacol
137 in the GLP-1 secretory response to different secretagogues in murine GLUTag L cells, as well as in th
138    Isolated acini were stimulated by various secretagogues in the presence or absence of cell-permean
139 imately 40% reduction in response to insulin secretagogues in vivo.
140 t not that of insulin, is activated by these secretagogues in vivo.
141 retion (IS) in response to glucose and other secretagogues including nonfuel stimuli.
142 cretory actions of cAMP- and cGMP-generating secretagogues, including cholera toxin and heat stable E
143 tionic substances, collectively called basic secretagogues, including inflammatory peptides and drugs
144   Stimulation of these cells with a range of secretagogues, including K(+), BaCl(2), and forskolin, d
145 nase complex and would, in part, account for secretagogues increasing the islet level of succinyl-CoA
146 bition of endogenous GEF1 activity decreases secretagogue-independent release of hormone precursors,
147 in the KO beta-cells in response to the same secretagogues, indicating reduced insulin secretion.
148             In the present study we measured secretagogue-induced acid secretion from wild-type and D
149                                              Secretagogue-induced acid secretion in wild-type mouse g
150 ved in Kcnn4(-/-) mice results from enhanced secretagogue-induced ACTH output from anterior pituitary
151 esult consistent with findings demonstrating secretagogue-induced activation of RhoA.
152 d potassium (BK) channels in spontaneous and secretagogue-induced activity.
153 e-activated (BK) channels in spontaneous and secretagogue-induced activity.
154 but only partially decreases the severity of secretagogue-induced acute pancreatitis and has no effec
155 uorescent 70 kDa dextran to demonstrate that secretagogue-induced bulk endocytosis also occurs in bov
156 in depletion causes a near-complete block in secretagogue-induced exocytosis.
157                                              Secretagogue-induced histamine release, inflammation and
158                 However, in isolated islets, secretagogue-induced insulin release (by glucose, GLP-1,
159 nhibitor exhibited reduced sulfonylurea- and secretagogue-induced insulin secretion.
160                                          The secretagogue-induced interaction was strongly reduced by
161 experimental models of acute pancreatitis (a secretagogue-induced model and a model elicited by retro
162  type and Tpl2(-/-) mice subjected to either secretagogue-induced or bile salt-induced pancreatitis.
163 f decreasing extracellular pH (pHe) in early secretagogue-induced pancreatitis (zymogen activation an
164 ation that occurs during the early stages of secretagogue-induced pancreatitis is not altered by admi
165  These data demonstrate that the severity of secretagogue-induced pancreatitis is significantly ameli
166                                              Secretagogue-induced pancreatitis was achieved by 12 hou
167 acid load might sensitize the acinar cell to secretagogue-induced pancreatitis.
168 essential early event in the pathogenesis of secretagogue-induced pancreatitis.
169 n inhibitor-I (PSTI-I) in mice could prevent secretagogue-induced pancreatitis.
170  pancreatic activation of trypsinogen during secretagogue-induced pancreatitis.
171 nge sensitizes the pancreatic acinar cell to secretagogue-induced zymogen activation and injury and m
172 acini, lowering pHe from 7.6 to 6.8 enhanced secretagogue-induced zymogen activation and injury, but
173 c beta cells are believed to convert insulin secretagogues into products that are translocated to the
174 mon to glucose, amino acid, and organic acid secretagogues, involving flux through the pyruvate/isoci
175 ked by a maximal concentration of the strong secretagogue ionomycin (1 microM), for which there was a
176 c beta-cells in response to glucose or other secretagogues is tightly coupled to membrane potential.
177 on, although its function regarding specific secretagogues is unclear.
178 s for glucose and branched-chain oxoacids as secretagogues (it does so partially for fatty acids).
179                   Secretion induced by basic secretagogues (KCl and Arg) was not affected by these dr
180 ment, and under chronic challenge by insulin secretagogues, loss of Sorcs1 leads to diabetes.
181   The frequencies of use of insulin, insulin secretagogues, metformin, and other antidiabetic medicat
182 in the regulation of pancreatic secretion by secretagogues, modulatory proteins and neural pathways a
183  aimed to assess whether glutamine, a potent secretagogue of GLP-1 in vivo, increases GLP-1 release,
184 eased responsiveness to kisspeptin, the main secretagogue of GnRH.
185 RF1 is not a typical sensitizer, mimetic, or secretagogue of insulin.
186 esponse to KCl and norepinephrine, a natural secretagogue of TRH.
187  released upon stimulation with histamine, a secretagogue of Weibel-Palade bodies, slowed down leukoc
188 Stimulation of endothelium with histamine, a secretagogue of WPBs, or injection of serotonin normaliz
189 ent, and by measuring the effects of insulin secretagogues on cPLA(2) distribution, on changes in [Ca
190 (2)beta in beta-cells incubated with insulin secretagogues or thapsigargin, that this requires prior
191 imulation either by mastoparan, a wasp venom secretagogue, or by the physiological mechanism of antig
192 Topical application of compound 48/80, an MC secretagogue, or histamine, a Weibel-Palade body secreta
193 in response to P2Y2 receptor agonists and to secretagogues, phorbol 12-myristate 13-acetate (PMA) and
194  be differentially regulated by hypothalamic secretagogues provides a mechanism for differential cont
195 on-signaling ghrelin receptor growth hormone secretagogue R1b (GHS-R1b) has been suggested to simply
196 tive, and orally bioavailable growth hormone secretagogue receptor (GHS-R) antagonists are reported.
197 vailable tetralin carboxamide growth hormone secretagogue receptor (GHS-R) antagonists were discovere
198 on, ghrelin and its receptor (growth hormone secretagogue receptor (GHS-R)) are widely expressed in a
199 t is mediated by its receptor Growth Hormone Secretagogue Receptor (GHS-R), but the physiologically r
200 f the peptide's receptor, the growth hormone secretagogue receptor (GHS-R), in the caudal brainstem.
201 bed endogenous ligand for the growth hormone secretagogue receptor (GHS-R), is produced by stomach ce
202 an endogeneous ligand for the growth hormone secretagogue receptor (GHS-R).
203 s an endogenous ligand of the growth hormone secretagogue receptor (GHS-R).
204 genous ligand for the type 1a growth hormone secretagogue receptor (GHS-R1a) and the only currently k
205 ed for the early detection of growth hormone secretagogue receptor (GHS-R1a) antagonists in urine sam
206 gnals in the hypothalamus via growth hormone secretagogue receptor (GHS-R1a).
207                           The growth hormone secretagogue receptor (GHSR) (ghrelin receptor) plays an
208                               Growth hormone secretagogue receptor (GHSR) 1a is the only molecularly
209       The ghrelin receptor or growth hormone secretagogue receptor (GHSR) is a G-protein-coupled rece
210 eased ghrelin levels, whereas growth hormone secretagogue receptor (Ghsr) null mice showed increased
211     Synthetic agonists of the growth hormone secretagogue receptor (GHSR) rejuvenate the pulsatile pa
212 at Ghrl and ghrelin receptor (growth hormone secretagogue receptor (GHSR)) are expressed in thymic st
213 relin and delta-cells express growth hormone secretagogue receptor (GHSR), suggesting the possibility
214 action with its receptor, the growth hormone secretagogue receptor (GHSR).
215 y known ghrelin receptor, the growth hormone secretagogue receptor (GHSR).
216 Endogenous ghrelin receptors [growth hormone secretagogue receptor (GHSR)] are also present in extrah
217 the endogenous ligand for the growth hormone secretagogue receptor (GHSR; ghrelin receptor).
218 elin are mediated through the growth hormone secretagogue receptor 1a (ghrelin receptor), a peptidic
219 xhibits dual affinity for the growth hormone secretagogue receptor 1a (GHS-R1a) and the cluster of di
220 n receptor, also known as the growth hormone secretagogue receptor 1a (GHS-R1a), is a G-protein-coupl
221 and acts at its receptor, the growth hormone secretagogue receptor 1a (GHSR1a), in the hypothalamus t
222   Ghrelin is an endogenous ligand for the GH secretagogue receptor 1a (GHSR1a, ie, ghrelin receptor).
223 57BL/6N mice administered the growth hormone secretagogue receptor agonist HM01 or vehicle.
224 elin acts as a ligand for the growth hormone secretagogue receptor and can stimulate the release of g
225              A novel neuronal growth hormone secretagogue receptor circuit involving urocortin 1 neur
226 ogical states and because the growth hormone secretagogue receptor has been identified in blood vesse
227 is the natural ligand for the growth hormone secretagogue receptor in the pituitary gland, thus fulfi
228 monstrate that binding to the growth hormone secretagogue receptor is accompanied by a conformational
229 ting KATP conductance via the growth hormone secretagogue receptor subtype 1a-Galphai -PI3K-Erk1/2-KA
230 s natural ligand for the growth hormone (GH) secretagogue receptor that has recently been isolated fr
231 ynaptic ghrelin receptor, the growth hormone secretagogue receptor type 1a (GHS-R1a), in VP neurons c
232 ch binds to and activates the growth hormone secretagogue receptor type 1a (GHS-R1a), is considered t
233 in, the natural ligand of the growth hormone secretagogue receptor type 1a (GHS-R1a), is mainly secre
234                           The growth hormone secretagogue receptor, GHSR1a, mediates the biological a
235 the endogenous ligand for the growth hormone secretagogue receptor, has been implicated not only in t
236 ural endogenous ligand of the growth hormone secretagogue receptor, it potently stimulates growth hor
237 ive blood-brain transport and growth hormone secretagogue receptor-1 agonist activity.
238 (+) cells, while ghrelin- and growth hormone secretagogue receptor-deficient (GHS-R-deficient) mice d
239 ary cells express significant growth hormone secretagogue receptor.
240 ncrease feeding by binding at growth hormone secretagogue receptors (GHS-R), the only sites of action
241 duced in the stomach, acts on growth hormone secretagogue receptors (GHSRs) in hypothalamic neurons t
242                               Growth hormone secretagogue receptors (GHSRs) in the central nervous sy
243         Much information is available on how secretagogue receptors acutely couple through heterotrim
244                                              Secretagogue receptors and their intracellular signaling
245                                    The major secretagogue receptors on acinar cells include those bin
246                                          The secretagogue receptors present on acinar cells, especial
247  interaction with endothelial growth hormone secretagogue receptors.
248 y of these pseudogranules, which we show are secretagogue responsive, to recruit membrane proteins.
249 n of immature content proteins and producing secretagogue-responsive mature granules.
250                          The use of glucagon secretagogues reveals a positive correlation between alp
251                                    Different secretagogues selectively release vesicles from the RRP
252                                          Our secretagogue-siRNA conjugate prevented cytokine-induced
253 l line was used to test the efficacy of this secretagogue-siRNA conjugate.
254    The purpose of this study was to create a secretagogue-small interfering RNA (siRNA) conjugate to
255    The absence of AC6 reduced cAMP-dependent secretagogue-stimulated amylase secretion, and abolished
256 es approximately 180-220 nm in diameter, and secretagogue-stimulated exocytosis of CgA from A35C cell
257 sually distinguished two sequential steps of secretagogue-stimulated exocytosis: fusion of individual
258 eta catalytic activity and that BEL inhibits secretagogue-stimulated insulin secretion from these cel
259 deconvolution and electron microscopy and by secretagogue-stimulated release assays.
260 TPase by bafilomycin A1 markedly reduced the secretagogue-stimulated release of CgA-EAP by perturbing
261 al deconvolution fluorescence microscopy and secretagogue-stimulated release studies demonstrate that
262 n microscopy, subcellular fractionation, and secretagogue-stimulated release, examining a series of f
263 bioactive peptides that feed back to inhibit secretagogue-stimulated release.
264 rescent protein localization in the basal or secretagogue-stimulated state.
265 dent beta-cells causes a rapid inhibition of secretagogue-stimulated subcellular Ca(2+) signaling and
266 KS) is a central regulatory molecule linking secretagogue stimulation at the cell surface to mucin gr
267       In PC-12 cells overexpressing tomosyn, secretagogue stimulation in the presence of lysophosphat
268                                              Secretagogue stimulation leads to an enlargement of the
269 et-induced insulin resistance, pharmacologic secretagogue stimulation of beta-cells with an incretin
270  in a Ca(2+)-sensitive manner in response to secretagogue stimulation of pancreatic beta-cells.
271                Downstream events involved in secretagogue stimulation of pancreatic secretion have be
272                          We demonstrate that secretagogue stimulation results in the rapid translocat
273 olecystokinin for 40 min, demonstrating that secretagogue stimulation transiently alters the associat
274 d WPB exocytosis and is present on WPBs, and secretagogue stimulation triggers an increased recruitme
275 cholic acid-3-sulfate (TLCS) or supramaximal secretagogue stimulation with caerulein.
276  pancreatic acini appropriately responded to secretagogue stimulation with the secretion of digestive
277 ure can sensitize pancreatic acinar cells to secretagogue stimulation, resulting in dysregulation of
278                When succinate esters are the secretagogue, succinyl-CoA can be generated via the succ
279                This effect was not seen with secretagogues such as glucose that stimulate secretion v
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                               By using these secretagogues, we developed a paradigm in which phorbol
297                     Among various endogenous secretagogues, we found that PGE2 had the lowest EC50 va
298                 In contrast to other insulin secretagogues, we show that chronic replenishment of adi
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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