ライフサイエンスコーパス: GIP

1 GIP also reportedly increased glucose uptake and inhibit

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

3 GIP concentrations after pasta consumption were lower th

4 GIP depletion in the gip1gip2 knockdown mutant leads to

5 GIP did not significantly change (Hedge g -0.213, 95% CI

6 GIP induces a downregulation of plasma membrane GIPR by

7 GIP induces the expression of the proatherogenic cytokin

8 GIP infusion decreased pancreatic but increased small in

9 GIP plays pivotal roles in cellular signaling, protein s

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

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

12 GIP signals through activation of the GIP receptor (GIPR

13 GIP stimulated OPN protein expression in a dose-dependen

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

33 le-blinded order intravenous infusions of A) GIP(3-30)NH(2) (800 pmol/kg/min) plus exendin(9-39)NH(2)

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

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

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

37 GIP-mediated insulin secretion and adipocyte GIP-R expression in subjects with well-controlled T2DM.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 consequence of rapid glucose appearance and GIP hypersecretion.

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

54 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

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

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

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

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

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

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

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

62 ones using the novel GIP receptor antagonist GIP(3-30)NH(2) and the well-established GLP-1 receptor a

63 Kaneko and colleagues show that antagonizing GIP signaling in the CNS enhances the weight-reducing ef

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

65 mol/kg/min; 20-240 min: 450 pmol/kg/min), B) GIP(3-30)NH(2), C) exendin(9-39)NH(2), and D) saline, re

66 Because GIP has antilipolytic and lipogenic effects in adipocyte

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

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

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

70 sulinemia, 2) insulinotropic effects of both GIP and GLP-1, 3) additive to supra-additive effects on

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

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

73 besogenic consequences of antagonizing brain GIP action.

74 etion and beta-cell exocytosis stimulated by GIP.

75 Distal (GLP-1/PYY/NT), but not proximal (CCK/GIP), enteroendocrine responses were generally greater i

76 sensitization or downregulation of beta-cell GIP receptors (GIP-R).

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

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

79 increase in circulating intestinally derived GIP, as a consequence of overnutrition, acts in the brai

80 ts without duodenal damage had no detectable GIP.

81 Determining GIP concentrations in several urine samples may be an es

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

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

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

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

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

87 In conclusion, endogenous GIP affects postprandial plasma glucose excursions and i

88 ual and combined contributions of endogenous GIP and GLP-1 to the postprandial changes in glucose and

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

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

91 Fasting GIP concentrations are higher in individuals with a hist

92 Fasting GIP levels remained unchanged.

93 randial GLP-1, postprandial PYY, and fasting GIP levels were included.

94 Immunohistochemistry (IHC) for GIP and GLP-1 was also done on intestinal biopsies of al

95 IHC positivity for GIP, but not GLP-1, staining cells in duodenum and colon

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

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

98 o measure indices of IS, beta-cell function, GIP, GLP-1 and glucagon response.

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

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

101 10(-8)), including variants near the GLP2R, GIP, and HLA-DQA1 genes.

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

103 a-cell function despite significantly higher GIP levels.

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

105 However, GIP also enhances glucocorticoid secretion and promotes

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

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

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

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

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

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

112 After surgery, indices of IS improved, GIP and glucagon levels decreased significantly in both

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

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

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

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

117 In parallel, we observed increased GIP-R mRNA expression in subcutaneous abdominal adipocyt

118 pogenic effects in adipocytes, the increased GIP-R expression may mediate accretion of fat in patient

119 ed, but the insulinotropic effect of infused GIP was unchanged following 12 weeks of pioglitazone tre

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

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

122 13 antagonizes the GIP receptor and inhibits GIP-induced insulin secretion in vitro and in vivo.

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

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

125 ings to the whole Bowland Shale, the maximum GIP equate to potentially economically recoverable reser

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

127 his research advances the idea that multiple GIP signaling pathways and mechanisms exist in the obese

128 ins why GLP-1, which signals via Gq, but not GIP, which signals preferentially via Gs, can effectivel

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

130 and glucoregulatory hormones using the novel GIP receptor antagonist GIP(3-30)NH(2) and the well-esta

131 (94%) and negative predictive value (97%) of GIP measurements in relation to duodenal biopsy findings

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

133 s beneficial to boost or block the action of GIP to promote weight loss remains an unresolved questio

134 2 to antagonize the physiological actions of GIP in glucose metabolism, subcutaneous abdominal adipos

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

136 of 22) of patients had measurable amounts of GIP in the urine.

137 ry of GIP sensitivity following cessation of GIP stimulation.

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

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

140 r regulation of the insulinotropic effect of GIP in subjects with T2DM.

141 of the antagonist on the incretin effect of GIP.

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

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

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

145 lates with desensitization to the effects of GIP.

146 bition of PI3Kgamma blocked these effects of GIP.

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

148 Infusion of GIP increases plasma OPN concentrations in healthy indiv

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

150 g) or placebo, combined with 2) infusions of GIP (1.5 pmol/kg/min), GLP-1 (0.5 pmol/kg/min), or salin

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

152 6, compared with db/+ mice, but injection of GIP did not lead to production of GLP1 or reduce glycemi

153 The introduction of GIP testing as an assessment technique for GFD adherence

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

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

156 and substantially enhanced SL(predicted) of GIP over control, irrespective of storage conditions.

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

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

159 o further understand the biological roles of GIP.

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

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

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

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

164 -2.9%, 13%; P = 0.22), whereas the effect on GIP again differed between groups (+78% in controls, P <

165 d NT (+71%, P < 0.01), whereas the effect on GIP differed between groups (+90% in controls, P < 0.01;

166 oteins and hydrolysates had little impact on GIP secretion.

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

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

169 -controlled trial of pioglitazone therapy on GIP-mediated insulin secretion and adipocyte GIP-R expre

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

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

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

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

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

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

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

177 es glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide 1 (GLP-1) is characterize

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

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

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

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

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

183 ulness of urine gluten immunogenic peptides (GIP) as a biomarker monitoring GFD adherence in celiac p

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 es used to predict the maximum gas in place (GIP) in the absence of production data.

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

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

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

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

192 d stimulated gastric inhibitory polypeptide (GIP) levels.

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

194 in increased gastric inhibitory polypeptide (GIP) secretion.

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

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

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

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

199 lucose-dependent insulinotropic polypeptide (GIP) action may occur through desensitization or downreg

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

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

202 lucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are secreted po

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

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

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

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

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

208 lucose-dependent insulinotropic polypeptide (GIP) are two incretins secreted from gastrointestinal ce

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

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

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

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

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

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

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

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

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

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

219 lucose-dependent insulinotropic polypeptide (GIP) receptor (GIPR) prevents weight gain and leads to d

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

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

222 lucose-dependent insulinotropic polypeptide (GIP) receptor.

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), cholecystokinin (CCK), peptide YY (PYY), and neuro

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

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

235 lucose-dependent insulinotropic polypeptide (GIP), has garnered much attention as a potential target:

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

237 lucose-dependent insulinotropic polypeptide (GIP).

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

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

240 Gingerols infused product (GIP), with 3.67 mg gingerols/100 g and non-infused produ

241 ch is based on Gaussian Interaction Profile (GIP) kernel on the drug-drug interaction profiles and th

242 se and circRNA Gaussian Interaction Profile (GIP) kernel similarity information based on known circRN

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

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

245 r downregulation of beta-cell GIP receptors (GIP-R).

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

247 ele showed protective properties via reduced GIP effects.

248 ese results show PPARgamma agonists regulate GIP-R expression through PPREs in human adipocytes, but

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

250 Studies in rodents and cell lines show GIP-R expression can be regulated through peroxisome pro

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

252 fects on insulin secretion when combining SU+GIP and SU+GLP-1, respectively, and 4) increased fasting

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

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

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

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

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

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

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

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

263 e week, urine samples were collected and the GIP concentrations were tested.

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

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

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

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

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

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

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

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

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

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

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

275 troglitazone increased PPARgamma binding to GIP-R PPREs.

276 tcome of beta-cell dysfunction consequent to GIP resistance and hyperglucagonemia.

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

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

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

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

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

282 stin treatment rescued LPL responsiveness to GIP.

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

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

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

286 ulation, 94% (17 of 18) had detectable urine GIP; however, between 60% and 80% were asymptomatic and

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

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

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

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

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

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

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

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

295 the antagonist alone and in combination with GIP.

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

297 sorted by flow cytometry and incubated with GIP.

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

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

300 The effect of SUs together with GIP or GLP-1, respectively, on insulin and glucagon secr