ライフサイエンスコーパス: GIP

1 GIP also reportedly increased glucose uptake and inhibit

2 GIP amplified GSIS in all groups.

3 GIP and GIP receptor mRNA were both detected in the embr

4 GIP and GLP-1 levels increased both at fast and after OG

5 GIP concentrations after pasta consumption were lower th

6 GIP depletion in the gip1gip2 knockdown mutant leads to

7 GIP induces a downregulation of plasma membrane GIPR by

8 GIP induces the expression of the proatherogenic cytokin

9 GIP infusion decreased pancreatic but increased small in

10 GIP is an incretin, known to modulate glucose-induced in

11 GIP lowered circulating FFAs compared with saline contro

12 GIP plays pivotal roles in cellular signaling, protein s

13 GIP receptor (GIPR) and OPN mRNA levels are higher in ca

14 GIP receptor (GIPR) protein and mRNA were decreased in R

15 GIP reduced activity of 11beta-HSD1 promoter constructs

16 GIP signaling may play a role in early embryonic pancrea

17 GIP signaling was inhibited in cultured embryonic pancre

18 GIP signals through activation of the GIP receptor (GIPR

19 GIP stimulated OPN protein expression in a dose-dependen

20 GIP was generally coexpressed with glucagon by immunosta

21 GIP(1-42) was modified C-terminally, and the truncated p

22 GIP, but not GLP-1, promotes beta cell Tcf7 expression v

23 GIP, CCK and OXM molecules appear to offer promising new

24 ental areas under the curve for total GLP-1, GIP, and cholecystokinin (CCK) in plasma.

25 hase, LQT2 patients display increased GLP-1, GIP, and insulin secretion and defective glucagon secret

26 , but neither dose affected glucagon, GLP-1, GIP, cholecystokinin, gastric emptying, or energy intake

27 nal pressures; stimulated plasma CCK, GLP-1, GIP, insulin, and glucagon (all r > 0.57, P < 0.01); and

28 ma concentrations of the gut hormones GLP-1, GIP, PYY, CCK and insulin did not offer an explanation o

29 show that lipid conjugated forms of a GLP-1/GIP/glucagon hybrid peptides stay in circulation for hou

30 (IC50) was determined using [(125)I-Tyr(10)]GIP(1-30) as radioligand and GIP(1-30) as control peptid

31 Notably, [d-Ala(2)]GIP also reduced the numbers of circulating neutrophils

32 GIP receptor (GIPR) signaling with [d-Ala(2)]GIP in mice and in Y1 adrenocortical cells.

33 [d-Ala(2)]GIP increased cAMP levels, activated extracellular signa

34 [d-Ala(2)]GIP increased murine corticosterone levels in a GIPR-dep

35 In addition, [d-Ala(2)]GIP reduced adipose tissue infiltration of IFN-gamma-pro

36 Administration of [d-Ala(2)]GIP resulted in adipocytes of increased size, increased

37 Furthermore, [d-Ala(2)]GIP treatment induced a favorable adipose tissue adipoki

38 ) using the long-acting GIP analog [d-Ala(2)]GIP.

39 p plasma glucose above 2 mmol/L (155 +/- 36 [GIP] vs. 232 +/- 40 [GLP-1] vs. 212 +/- 56 [saline] mg k

40 cited larger glucagon responses (164 +/- 50 [GIP] vs. 23 +/- 25 [GLP-1] vs. 17 +/- 46 [saline] min pm

41 hibition of 11beta-HSD1 completely abolished GIP-induced effects on FFA release.

42 -induced obesity (DIO) using the long-acting GIP analog [d-Ala(2)]GIP.

43 Accurate detection of the most active GIP is desirable to assess the potential celiac toxicity

44 eata using morpholine-ring antisense against GIP ligand and receptor, or small interfering RNA (siRNA

45 se concentrations, along with vehicle alone, GIP, xenin-25, or GIP plus xenin-25.

46 This study determines if xenin-25 amplifies GIP-mediated GSIS in humans with normal glucose toleranc

47 d neurotensin-related peptide that amplifies GIP-mediated GSIS in hyperglycemic mice.

48 udies unmasked a neural relay that amplifies GIP-mediated insulin secretion in a pattern reciprocal t

49 DPP-4 inhibition but reduced total GLP-1 and GIP (feedback inhibition) without affecting the numerica

50 humans, SGLT1 substrates stimulate GLP-1 and GIP and slow gastric emptying, regardless of whether the

51 GLP-1 and GIP exert their actions predominantly through unique G p

52 GLP-1 and GIP promote beta-cell proliferation and survival in rode

53 We found that GLP-1 and GIP recruit a highly coordinated subnetwork of beta cell

54 Both glucose and 3OMG stimulated GLP-1 and GIP release in advance of the meal (each P < 0.05), wher

55 ists AM-1638 and AM-6226 stimulate GLP-1 and GIP secretion from intestinal enteroendocrine cells and

56 sion, sitagliptin increased intact GLP-1 and GIP through DPP-4 inhibition but reduced total GLP-1 and

57 In GLP-1 and GIP, a single thioamide near the scissile bond renders t

58 Blood glucose, plasma total GLP-1 and GIP, serum insulin, and gastric emptying were determined

59 ncretins glucagon-like peptide-1 (GLP-1) and GIP (glucose-dependent insulinotropic polypeptide), resp

60 se, insulin, C-peptide, glucagon, GLP-1, and GIP.

61 consequence of rapid glucose appearance and GIP hypersecretion.

62 oric intake and improve glucose control, and GIP action to potentiate the incretin effect and buffer

63 GIP and GIP receptor mRNA were both detected in the embryonic pa

64 usions of GIP, GIP(3-30)NH2, or both GIP and GIP(3-30)NH2 During infusion of GIP(3-30)NH2 alone and i

65 Insulin release was greater, and GIP release less, in obese than in lean subjects (both P

66 can result in lower postprandial insulin and GIP concentrations, but not necessarily in a lower glyce

67 however, the observed changes in insulin and GIP suggest early disturbances in the insulin-incretin a

68 ter increase in plasma glucose, insulin, and GIP concentrations after surgery, which was accompanied

69 The ontogeny of the GIP ligand and GIP receptor in the embryonic pancreas was investigated

70 [(125)I-Tyr(10)]GIP(1-30) as radioligand and GIP(1-30) as control peptide.

71 The interactions of GLP-1 receptor and GIP receptor were characterized with BRET donor saturati

72 somatostatin receptors, GLP-1 receptors, and GIP receptors would allow detecting virtually all NETs a

73 ew drugs based on other gut hormones such as GIP, ghrelin, oxyntomodulin and peptide YY.

74 ification of this unprecedented link between GIP and OPN in adipose tissue might open new avenues for

75 and further elucidated the relation between GIP, 11beta-HSD1, and fatty acid metabolism.

76 Blunted GIP responsiveness in Retn(+/-) and Retn(-/-) adipocytes

77 Both GIP genes are ubiquitously expressed in all tissues anal

78 brane and intracellular compartments of both GIP-stimulated and unstimulated adipocytes.

79 tant infusions of GIP, GIP(3-30)NH2, or both GIP and GIP(3-30)NH2 During infusion of GIP(3-30)NH2 alo

80 novel internal motifs that are recognized by GIP through combinatorial phage library screening.

81 etion and beta-cell exocytosis stimulated by GIP.

82 athway may account for the lowered beta-cell GIP-R expression and resulting GIP resistance in type 2

83 tions of insulin, glucagon, cholecystokinin, GIP, GLP-1, and PYY, and an increase in total energy int

84 n delayed GLP-1 secretion but not in delayed GIP release.

85 onoclonal antibody for selectively depleting GIP in samples from two different gluteomes.

86 DOTA)]GIP(1-30)NH2 (EG1), [Lys(16)(Ahx-DOTA)]GIP(1-30)NH2 (EG2), and [Nle(14), Lys(30)(Ahx-DOTA)]GIP(

87 0)NH2 (EG2), and [Nle(14), Lys(30)(Ahx-DOTA)]GIP(1-30)NH2 (EG4) were conjugated with Ahx-DOTA via the

88 ides [Lys(30)(aminohexanoic acid [Ahx]-DOTA)]GIP(1-30)NH2 (EG1), [Lys(16)(Ahx-DOTA)]GIP(1-30)NH2 (EG2

89 th GIP, whereas it increased fivefold during GIP alone.

90 to maintain the clamp were lower than during GIP alone.

91 oline-ring antisense or siRNA against either GIP ligand or GIP receptor both inhibited the differenti

92 pe 2 diabetes, 1) the capacity of endogenous GIP to lower blood glucose is impaired; 2) the effect of

93 ypoglycemia in patients with T1DM, exogenous GIP increases glucagon responses during the recovery pha

94 Fasting GIP concentrations are higher in individuals with a hist

95 uminal membranes of cells immunopositive for GIP and GLP-1, and Sglt1(-/-) mice exhibited reduced glu

96 y beneficial immunoregulatory properties for GIP in DIO and reveal that its augmentation ameliorates

97 g activity points to a more central role for GIP in intestinal regulation of peripheral tissue metabo

98 Together, these data suggest a role for GIP not only as an incretin hormone but also as a trigge

99 ceptor, or small interfering RNA (siRNA) for GIP ligand and receptor.

100 s insulin-sensitizing effect is specific for GIP because isoproterenol, which elevates adipocyte cAMP

101 -dependent insulinotropic polypeptide (GIP), GIP(3-30)NH2, was recently identified as an antagonist o

102 ic clamps with concomitant infusions of GIP, GIP(3-30)NH2, or both GIP and GIP(3-30)NH2 During infusi

103 10(-8)), including variants near the GLP2R, GIP, and HLA-DQA1 genes.

104 In both groups, GIP, GLP-1, and the magnitude of incretin effect were gr

105 induced secretion of insulinotropic hormone (GIP) and glucagon-like peptide 1 (GLP-1) in wild-type an

106 However, GIP also enhances glucocorticoid secretion and promotes

107 high potencies to mouse, rat, dog, and human GIP receptors with a Ki of 7 nm for the human GIPr.

108 cell line INR1G9 transfected with the human GIP receptor (INR1G9-hGIPr).

109 tly identified as an antagonist of the human GIP receptor.

110 treotide, (125)I-GLP-1(7-36)amide, or (125)I-GIP(1-30), with the binding using a cocktail of all 3 ra

111 Our data identify GIP-regulated metabolic pathways that are targeted by fe

112 oligand indicated the feasibility of imaging GIP receptor-positive tumors.

113 y increased plasma GIP levels, no changes in GIP or GLP-1 were observed after DJB and jejunectomy.

114 retory response and reduced hyperglycemia in GIP/DT mice.

115 The noncanonical ILGF loop in GIP moves in for the C-terminal motif but moves out for

116 (2)]GLP-1/GcG, stimulated cAMP production in GIP, GLP-1, and glucagon receptor-transfected cells.

117 ine whether resistin has additional roles in GIP-regulated adipocyte functions.

118 (2)]GLP-1/GcG via multiple targets including GIP, GLP-1, and glucagon receptors.

119 In addition, the antagonist inhibited GIP-induced increase in ATBF and decreased the adipose t

120 (SGLT1) with phloridzin partially inhibited GIP, GLP-1 and PYY secretion by 45%, suggesting another

121 13 antagonizes the GIP receptor and inhibits GIP-induced insulin secretion in vitro and in vivo.

122 xpected, sitagliptin augmented plasma-intact GIP substantially and intact GLP-1 modestly.

123 n secretion to 16.7 mmol/l glucose/10 nmol/l GIP.

124 -expressing (DT) mice that specifically lack GIP-producing cells were backcrossed five to eight times

125 We developed mice lacking GIP-producing K cells.

126 ltogether, our data show that during mitosis GIPs play a role in gamma-tubulin complex localization,

127 cal actions and therapeutic utility of novel GIP/glucagon/GLP-1 hybrid peptides.

128 This study examined the ability of GIP(3-30)NH2 to antagonize the physiological actions of

129 2 to antagonize the physiological actions of GIP in glucose metabolism, subcutaneous abdominal adipos

130 rticoids using pharmacological activation of GIP receptor (GIPR) signaling with [d-Ala(2)]GIP in mice

131 ry of GIP sensitivity following cessation of GIP stimulation.

132 asma glucagon levels, but the combination of GIP plus xenin-25 transiently increased ISR and plasma g

133 HV resulted in lower plasma concentration of GIP (P<0.001), higher plasma concentration of glucose (P

134 ith an increase of ghrelin and a decrease of GIP-labeled cells.

135 netic approaches, we show that the effect of GIP on adipocyte insulin sensitivity requires activation

136 of the antagonist on the incretin effect of GIP.

137 We studied the effects of GIP and GLP-1 on glucagon responses to insulin-induced h

138 To investigate the acute effects of GIP in humans, a randomized clinical trial was performed

139 ependent, we examined whether the effects of GIP on energy balance and glycemia are regulated by gluc

140 Extra-pancreatic effects of GIP primarily occur in adipose tissues.

141 Here we demonstrate unexpected effects of GIP signaling in the vasculature.

142 lates with desensitization to the effects of GIP.

143 bition of PI3Kgamma blocked these effects of GIP.

144 tion studies combined with the expression of GIP-green fluorescent protein fusions have shown that GI

145 The best known function of GIP is to enhance glucose-dependent insulin secretion fr

146 mouse islets caused a threefold increase of GIP-R protein and a doubling of insulin secretion to 16.

147 Infusion of GIP increases plasma OPN concentrations in healthy indiv

148 both GIP and GIP(3-30)NH2 During infusion of GIP(3-30)NH2 alone and in combination with GIP, insulin

149 linemic clamps with concomitant infusions of GIP, GIP(3-30)NH2, or both GIP and GIP(3-30)NH2 During i

150 Inhibition of GIP or its receptor also led to a decrease in the number

151 6, compared with db/+ mice, but injection of GIP did not lead to production of GLP1 or reduce glycemi

152 a inhibition, demonstrating that the loss of GIP-induced actin depolymerization was indeed limiting i

153 tin was demonstrated to be a key mediator of GIP stimulation of lipoprotein lipase (LPL) activity, in

154 Structure-based models of GIP bound to two different surrogate peptides determined

155 n release from in situ perfused pancreata of GIP/DT mice.

156 he plasma membrane and a delayed recovery of GIP sensitivity following cessation of GIP stimulation.

157 physiologic and pharmacologic regulation of GIP-R expression in beta-cells by PPARgamma signaling.

158 to investigate the immunoregulatory role of GIP in a murine model of diet-induced obesity (DIO) usin

159 Here we studied the role of GIP signaling in insulin-positive differentiation in the

160 o further understand the biological roles of GIP.

161 2) triggers the glucose-induced secretion of GIP and GLP-1, and 3) triggers the upregulation of GLUT2

162 determinant of the comparative secretion of GIP and GLP-1, as well as the magnitude of the incretin

163 or presence of phloridzin), the secretion of GIP, GLP-1 and PYY was sensitive to K+(ATP)-sensitive ch

164 tial to be used for the in vivo targeting of GIP receptor-positive tumors.

165 oteins and hydrolysates had little impact on GIP secretion.

166 etermined the effects of 4 sweet preloads on GIP and GLP-1 release, gastric emptying, and postprandia

167 onged in vivo exposure to support studies on GIP biology.

168 ncretin effect without reduction in GLP-1 or GIP, similar to that seen in adult dysglycemia.

169 cted insulin, C-peptide, glucagon, GLP-1, or GIP.

170 along with vehicle alone, GIP, xenin-25, or GIP plus xenin-25.

171 ocytes, suggesting that GIP signaling and/or GIP responsiveness were compromised in Retn(+/-) and Ret

172 lycerol, FFA, insulin, glucose, glucagon, or GIP related to protein type or MC-SFA content.

173 isense or siRNA against either GIP ligand or GIP receptor both inhibited the differentiation of insul

174 , may represent a novel approach to overcome GIP resistance and therefore treat humans with T2DM.

175 Paradoxically, GIP levels were also induced in these mice.

176 he insulinotropic glucose-dependant peptide (GIP) and of the beta-microseminoprotein (MSMB) were sign

177 Gastric inhibitory peptide (GIP) is an incretin hormone secreted in response to food

178 lusively for the gastric inhibitory peptide (GIP) receptor and the glucagon-like peptide 1 (GLP-1) re

179 Glucose-dependent insulinotropic peptide (GIP) induces production of interleukin 6 (IL6) by adipoc

180 nd glucose-dependent insulinotropic peptide (GIP) receptors, can be overexpressed in gut and bronchia

181 , glucose-responsive insulinotropic peptide (GIP), forskolin) that act upon glucose transporters, pot

182 e secretion of gluco-insulinotropic peptide (GIP), glucagon-like peptide-1 (GLP-1) and peptide tyrosi

183 n, glucose-dependent insulinotropic peptide (GIP), glucose and acetaminophen.

184 fication of the gluten immunogenic peptides (GIP) by using G12 mAb.

185 to the relevant gluten immunogenic peptides (GIP).

186 "recovery phase." During the recovery phase, GIP infusions elicited larger glucagon responses (164 +/

187 Since the majority of gas-in-place (GIP) is stored as an adsorbed phase in fine pores of coa

188 n, serum C-peptide, plasma GLP-1, and plasma GIP responses (P=0.03-0.001) and decreased plasma glucos

189 rointestinal glucose disposal (GIGD), plasma GIP, GLP-1, and glucagon secretion in health and type 2

190 While ileectomy increased plasma GIP levels, no changes in GIP or GLP-1 were observed aft

191 d stimulated gastric inhibitory polypeptide (GIP) levels.

192 etion of the gastric inhibitory polypeptide (GIP) receptor (GIPR) prevents high-fat diet (HFD)-induce

193 in increased gastric inhibitory polypeptide (GIP) secretion.

194 vestigation, gastric inhibitory polypeptide (GIP), as proof-of-principle peptides to demonstrate the

195 ecystokinin, gastric inhibitory polypeptide (GIP), glucagon-like peptide 1 (GLP-1), and peptide tyros

196 (GLP-1), and gastric inhibitory polypeptide (GIP).

197 lso known as gastric inhibitory polypeptide (GIP)] and its receptor (GIPR) may link overnutrition to

198 lucose-dependent insulinotropic polypeptide (GIP) account for up to 60% of postprandial insulin relea

199 lucose-dependent insulinotropic polypeptide (GIP) and GLP-1 are incretins secreted by respective K an

200 lucose-dependent insulinotropic polypeptide (GIP) and glucagon receptors.

201 lucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) secretion, on g

202 lucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) were measured.

203 lucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), is unknown.

204 lucose-dependent insulinotropic polypeptide (GIP) are altered in the disease state.

205 lucose-dependent insulinotropic polypeptide (GIP) are incretin hormones that control the secretion of

206 lucose-dependent insulinotropic polypeptide (GIP) gene transcripts were observed in the gut of Hnf1al

207 lucose-dependent insulinotropic polypeptide (GIP) has been suggested to have direct effects on nonisl

208 lucose-dependent insulinotropic polypeptide (GIP) in response to oral glucose.

209 lucose-dependent insulinotropic polypeptide (GIP) in the splanchnic region in 10 obese patients with

210 lucose-dependent insulinotropic polypeptide (GIP) is a member of a structurally related group of horm

211 lucose-dependent insulinotropic polypeptide (GIP) is a strong stimulator of adipogenesis and may play

212 lucose-dependent insulinotropic polypeptide (GIP) is an endogenous hormonal factor (incretin) that, u

213 lucose-dependent insulinotropic polypeptide (GIP) is an incretin hormone that also plays a regulatory

214 lucose-dependent insulinotropic polypeptide (GIP) is an incretin hormone that mediates postprandial i

215 lucose-dependent insulinotropic polypeptide (GIP) is an incretin hormone with extrapancreatic effects

216 lucose-dependent insulinotropic polypeptide (GIP) is glucagonotropic, and glucagon-like peptide-1 (GL

217 lucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-stimulated insulin secretion (G

218 lucose-dependent insulinotropic polypeptide (GIP) promotes glucose-dependent insulin secretion.

219 lucose-dependent insulinotropic polypeptide (GIP) receptor transduce nutrient-stimulated signals to c

220 lucose-dependent insulinotropic polypeptide (GIP) receptor, and pyruvate carboxylase) that are import

221 lucose-dependent insulinotropic polypeptide (GIP) receptor.

222 lucose-dependent insulinotropic polypeptide (GIP) secretions are unaltered.

223 lucose-dependent insulinotropic polypeptide (GIP) were analyzed.

224 lucose-dependent insulinotropic polypeptide (GIP) were measured.

225 lucose-dependent insulinotropic polypeptide (GIP)) are secreted from enteroendocrine cells in the int

226 lucose-dependent insulinotropic polypeptide (GIP), a protein with potential therapeutic activity for

227 lucose-dependent insulinotropic polypeptide (GIP), an incretin hormone secreted from gastrointestinal

228 lucose-dependent insulinotropic polypeptide (GIP), and cholecystokinin (leucine study only) were meas

229 lucose-dependent insulinotropic polypeptide (GIP), and glucagon bind to related members of the same r

230 lucose-dependent insulinotropic polypeptide (GIP), and insulin, and improved oral glucose tolerance i

231 lucose-dependent insulinotropic polypeptide (GIP), by inhibiting their breakdown.

232 lucose-dependent insulinotropic polypeptide (GIP), GIP(3-30)NH2, was recently identified as an antago

233 lucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), cholecystokinin (

234 lucose-dependent insulinotropic polypeptide (GIP), slow gastric emptying, and reduce postprandial gly

235 lucose-dependent insulinotropic polypeptide (GIP).

236 lucose-dependent insulinotropic polypeptide (GIP, also known as gastric inhibitory polypeptide) recep

237 lucose-dependent insulinotropic polypeptide [GIP]), whereas metformin may increase GLP-1 levels.

238 Consistent with this, carbachol potentiated GIP-mediated insulin release from in situ perfused pancr

239 These data suggest that xenin-25 potentiates GIP-mediated insulin release by activating non-ganglioni

240 Human glutaminase interacting protein (GIP), also known as tax interacting protein 1, is unique

241 ulin complex protein 3-interacting proteins (GIPs) in Arabidopsis centromere regulation.

242 pendent insulinotropic polypeptide receptor (GIP-R) promoter sequence.

243 me mice were given injections of recombinant GIP, IL6, GLP, a neutralizing antibody against IL6 (anti

244 ele showed protective properties via reduced GIP effects.

245 red beta-cell GIP-R expression and resulting GIP resistance in type 2 diabetes.

246 th 2-h intravenous administration of saline, GIP, or GLP-1.

247 ne (Arg) and glutamine (Gln) also stimulated GIP, GLP-1 and PYY secretion, which was completely aboli

248 l/min], a rate that predominantly stimulates GIP but not GLP-1) after sitagliptin versus control in 1

249 may reflect defective neuronal, rather than GIP, signaling.

250 Here, we demonstrate that GIP increases insulin-dependent translocation of the Glu

251 the nucleus in adipocytes, establishing that GIP has a general effect on insulin action in adipocytes

252 Downstream, we find that GIP, much like glucose stimulation, activates the small

253 ts from human beings and mice, we found that GIP induces production of IL6 by alpha cells, leading to

254 -), Retn(+/-), and Retn(+/+) mice found that GIP stimulated the PKB/LKB1/AMPK/LPL pathway and fatty a

255 e adipose tissue TAG uptake, indicating that GIP also plays a crucial role in lipid metabolism.

256 P within human glioma cells, indicating that GIP might be a potential target for anticancer therapeut

257 Our data suggest that GIP reduces FFA release from adipose tissue by inhibitio

258 Importantly, recent evidence suggested that GIP is a potential suppressor of inflammation in several

259 nly in Retn(+/+) adipocytes, suggesting that GIP signaling and/or GIP responsiveness were compromised

260 In general, the presented data support that GIP has direct and insulin-independent effects on adipos

261 We thus postulate that GIPs are required to ensure CENH3 deposition and/or main

262 We show that GIPs form a complex with CENH3 in cycling cells.

263 fluorescent protein fusions have shown that GIPs colocalize with gamma-tubulin, GCP3, and/or GCP4 an

264 The GIP receptor was typically coexpressed with insulin.

265 Gipg013 antagonizes the GIP receptor and inhibits GIP-induced insulin secretion

266 ed high affinity toward GIP receptor for the GIP conjugates.

267 The ontogeny of the GIP ligand and GIP receptor in the embryonic pancreas wa

268 A common variant of the GIP receptor (GIPR) (rs10423928) gene was associated wit

269 g target for diabetes, the importance of the GIP receptor (GIPR) for the function of beta cells remai

270 GIP signals through activation of the GIP receptor (GIPR), a G-protein-coupled receptor (GPCR)

271 Most of the GIP were retained by the G12-agarose and represented the

272 On the GIP days, significantly less exogenous glucose was neede

273 er peptide produced by K cells, restored the GIP-mediated insulin secretory response and reduced hype

274 both oleic acid and 2-OG contributed to the GIP response.

275 (pmol/L) x 120 min; P = 0.733], whereas the GIP response was higher for olive oil than for C8-dietar

276 The antibody epitope overlaps with the GIP binding site on the GIPr ECD, ensuring competitive a

277 ere identified to be critical for binding to GIP through site-directed mutagenesis studies.

278 cardiovascular disease in humans responds to GIP stimulation with an exaggerated downregulation from

279 he exocytotic and insulinotropic response to GIP receptor activation, whereas responses to the glucag

280 ed the exocytotic and secretory responses to GIP during PI3Kgamma inhibition, demonstrating that the

281 magnitudes of insulin secretory responses to GIP were similar in all groups, ISRs were not restored t

282 impairs the cytoprotective responsiveness to GIP and enhances the magnitude of apoptotic injury, wher

283 stin treatment rescued LPL responsiveness to GIP.

284 Altogether, we ascribe a central function to GIPs for the proper recruitment and/or stabilization of

285 and augmented total and intact GLP-1, total GIP, and glucagon in type 2 diabetic subjects, with no a

286 uration studies) showed high affinity toward GIP receptor for the GIP conjugates.

287 /-) mice exhibited reduced glucose-triggered GIP and GLP-1 levels.

288 We here analyzed whether GIP modifies lipid metabolism and further elucidated the

289 development of obesity, we explored whether GIP directly would stimulate OPN expression in adipose t

290 We investigated whether GIP regulates GLP1 and glycemia via IL6.

291 We investigated whether GIP-associated pathways may be targeted by fetal program

292 Stimulation of adipocytes with GIP alone has no effect on these processes.

293 mouse and human pancreatic alpha cells with GIP induced their production of IL6, leading to producti

294 One of the peptides colocalizes with GIP within human glioma cells, indicating that GIP might

295 f GIP(3-30)NH2 alone and in combination with GIP, insulin levels and the total glucose amount infused

296 increased only slightly in combination with GIP, whereas it increased fivefold during GIP alone.

297 the antagonist alone and in combination with GIP.

298 ndogenous glucose production was higher with GIP and lower with GLP-1 compared with saline (P < 0.02)

299 sorted by flow cytometry and incubated with GIP.

300 Injection of control mice with GIP increased plasma levels of GLP1, insulin, and glucos

301 binding of GLP-1 that could be reversed with GIP addition.