ライフサイエンスコーパス: metformin

1 patients treated with antidiabetic doses of metformin.

2 oduction in primary hepatocytes treated with metformin.

3 atient populations, typically in addition to metformin.

4 e, but this association was not observed for metformin.

5 d sensitivity to the mitochondrial inhibitor metformin.

6 se patients and improve the effectiveness of metformin.

7 h type 2 diabetes inadequately controlled by metformin.

8 were estimated to be effective when added to metformin.

9 the benefits of lifestyle-based programs and metformin.

10 oline transport, which was also inhibited by metformin.

11 c expression of Igf2, which were reversed by metformin.

12 r anti-aging compounds, such as curcumin and metformin.

13 ide diuretics, calcium channel blockers, and metformin.

14 there was no increase in hypoglycaemia with metformin.

15 suggesting these proteins as new targets for metformin.

16 lls at 2-25 mm glucose, with or without 5 mm metformin.

17 mean cIMT was not significantly reduced with metformin (-0.005 mm per year, 95% CI -0.012 to 0.002; p

18 line) was reduced on average over 3 years by metformin (-0.13%, 95% CI -0.22 to -0.037; p=0.0060), bu

19 as well as of gadolinium-enhancing lesions (metformin, 1.8 at study entry to 0.1 at month 24; piogli

20 n interactive voice response system) to oral metformin 1000 mg twice daily or placebo.

21 ron emission tomography with [(11)C]-labeled metformin ([(11)C]-metformin) in mice to investigate the

22 insulin (39.5%), sulfonylureas (32.4%), and metformin (17%) being the most commonly used AHMs.

23 n the number of new or enlarging T2 lesions (metformin, 2.5 at study entry to 0.5 at month 24; piogli

24 Metformin (200 mg/kg/d) was used to treat wild-type and

25 + regulatory T cells compared with controls (metformin, 6.7 [1.5] vs 2.1 [1.0], P = .001; pioglitazon

26 Use of metformin (8 studies, n = 616) and orlistat (3 studies,

27 also investigated the metabolic footprint of metformin, a drug associated with improved post-MI LV fu

28 Metformin, a drug prescribed to treat type-2 diabetes, e

29 underlying the antineoplastic properties of metformin, a first-line drug for type 2 diabetes, remain

30 estigate the anti-cervical cancer effects of metformin, a first-line therapeutic drug for type 2 diab

31 Metformin, a first-line therapy for type 2 diabetes, is

32 Metformin, a widely implemented anti-diabetic drug, exhi

33 ) based drug-screening platform we show that Metformin, a widely used anti-diabetic drug, reduces lev

34 Here, we show that metformin abated the progression of diabetes-accelerated

35 teins (MATE), are essential for transport of metformin across membranes, but tissue-specific activity

36 key role for hepatic GLUT2 in regulation of metformin action.

37 Metformin acts by upregulating microRNA let-7 through AM

38 The present results indicate that T4 and metformin, administered during the neonatal period that

39 Importantly, early postnatal metformin administration decreased serotonin concentrati

40 Both T4 and metformin alleviated contextual fear memory deficit indu

41 Interestingly, metformin along with diet reversal restored the levels o

42 ed that treatment with the FDA-approved drug metformin also rescued memory.

43 tropic), chlorogenic acid (a polyphenol) and metformin (an antidiabetic and possible longevity promot

44 Metformin, an anti-diabetic drug commonly used for type

45 p63 transcriptional activity, but induced by metformin, an anti-diabetic drug that activates p63.

46 CI, -1.44 to -0.29; 6 studies; I2 = 0%) for metformin and -0.50 to -0.94 for orlistat.

47 t, 20 patients with MS who were treated with metformin and 10 who received pioglitazone showed a sign

48 tion substrates: the commonly used drugs: 1) metformin and 2) cimetidine; and two prototypic cationic

49 mly assigned patients, 219 were allocated to metformin and 209 to placebo.

50 enrolled in this Phase II clinical trial, 18 metformin and 26 insulin patients.

51 HbA1c (mean 8.1% [SD 0.9] for metformin and 8.0% [0.8] for placebo at baseline) was re

52 (AMPK) activation, which can be induced with metformin and AICAR inhibited proliferation, TGF-beta ex

53 ointestinal adverse events were highest with metformin and GLP-1 receptor agonists.

54 , LPH-PolyMet nanoparticles act similarly to Metformin and induce antitumour efficacy through activat

55 1 year of follow-up in the DPP intervention (metformin and lifestyle) and control (placebo) arms.

56 Anti-TNF treatment, as well as metformin and methotrexate, which are associated with de

57 These results suggest that clinical use of metformin and nelfinavir in combination is expected to h

58 We found that both metformin and nelfinavir, when used alone, were moderate

59 loss and lifestyle interventions, as well as metformin and other obesity-targeted therapies, are prom

60 tion transporters (OCTs), uptake carriers of metformin and oxaliplatin, were inhibited by several cli

61 OCT1/2(-/-) mice when evaluated with [(11)C]-Metformin and PET/MRI, we found that the protective effe

62 iguanides, such as the diabetes therapeutics metformin and phenformin, have shown antitumor activity

63 Treatment with metformin and pioglitazone has beneficial anti-inflammat

64 Both metformin and pioglitazone resulted in a significant inc

65 modulated by common disease risk modifiers (metformin and pravastatin).

66 1450 patients with type 2 diabetes receiving metformin and randomly assigned to either once-daily can

67 e patch can be thermally actuated to deliver Metformin and reduce blood glucose levels in diabetic mi

68 Both metformin and resveratrol protected against spontaneous

69 9 trials (10,598 patients) of drugs added to metformin and sulfonylurea (triple therapy).

70 In all treatment groups, previous background metformin and sulfonylurea treatment was continued throu

71 When added to metformin and sulfonylurea, GLP-1 receptor agonists were

72 In primary hepatocytes from healthy animals, metformin and the IKKbeta (inhibitor of kappa B kinase)

73 ion of the mitochondrial complex I inhibitor metformin and the mitochondrial pyruvate carrier inhibit

74 In addition, we found that metformin and the structurally related compound aminogua

75 deaths occurred among patients allocated to metformin and two occurred among those allocated to plac

76 enetic and epigenetic biomarkers involved in metformin anticancer response.

77 atment burden and hypoglycemia risk (such as metformin) are required, a lower HbA1c target may be app

78 Most studies assessed the role of metformin as a monotherapy or dual therapy supplement an

79 To repurpose metformin as a precision anti-cancer therapy, we have de

80 , suggesting a potential role of nitrite and metformin as a preventative treatment for this disease.

81 of infectious virions, suggesting the use of metformin as a therapeutic agent for KSHV infection and

82 However, it is known to induce metformin-associated lactic acidosis (MALA), a severe me

83 in the subset of patients who were naive to metformin at the time of PDAC diagnosis (most representa

84 Finally, early treatments with nitrite and metformin at the time of SU5416 injection reduced pulmon

85 These findings show that metformin attenuated the development of atherosclerosis

86 ural proteome, we identified twenty putative metformin binding targets and their interaction models.

87 uch as acesulfame, perfluorobutanoic acid or metformin, but other novel pollutants were also identifi

88 However, whether metformin can effectively prevent thrombosis and its pot

89 ly present in the kidney, and a high dose of metformin caused a delayed renal uptake and clearance co

90 significantly reduced in patients receiving metformin compared with controls (interferon gamma, 30.3

91 wed reduced diabetes risk with lifestyle and metformin compared with placebo over 3.2 years.

92 Recently, we found that therapeutic metformin concentrations suppressed glucose production i

93 Metformin controlled blood glucose as equally as insulin

94 Here, we tested whether the AMPK activator metformin could affect the P23H rhodopsin synthesis and

95 thesis whether concomitant diet reversal and metformin could overcome HFD-induced metabolic memory an

96 Metformin cytotoxicity assay was performed using the MTS

97 Blocking metabolic pathways with metformin diminished cytokine production and increased m

98 Emerging genetic and pharmacologic (metformin) disruption of mitochondrial (mt) respiration

99 se AMPK activation requires liver kinase B1, metformin does not induce protein acetylation in liver k

100 In pigs, 80% of the injected metformin dose was rapidly present in the kidney, and a

101 9 trials (53,030 patients) of drugs added to metformin (dual therapy); and 29 trials (10,598 patients

102 In multivariate analysis, the metformin effect in men was not influenced by demographi

103 AC presence, 75% versus 84%, P=0.02), but no metformin effect was seen in women.

104 who had insufficient glycaemic control with metformin either alone or in combination with a sulfonyl

105 Metformin exemplifies a promising new class of antiplate

106 (-/-)/AMPK-alpha2(-/-) mice, indicating that metformin exerts an antiatherosclerotic action in vivo v

107 In a pilot study, LFS patients treated with metformin exhibited decreases in mitochondrial activity

108 We examined the impact of metformin exposure definitions, analytical methods, and

109 nt selection on the estimated effect size of metformin exposure on survival in a large cohort of pati

110 In this study, we find that metformin failed to suppress glucose production in prima

111 s study will shed new light into repurposing metformin for safe, effective, personalized therapies.

112 ning or treatment (behavior-based, orlistat, metformin) for overweight or obesity in children aged 2

113 Here the Metformin Genetics (MetGen) Consortium reports a three-s

114 5x10(-5)); alanine levels were higher in the metformin group (0.46 versus 0.44 mmol/L; P=2.4x10(-4)).

115 n neonatal birth-weight z score (0.05 in the metformin group [interquartile range, -0.71 to 0.92] and

116 only 1 mild hypoglycemic episode (6%) in the metformin group, P < 0.05.

117 inued metformin in the originally randomized metformin group.

118 ges in cytosolic redox biology, suggest that metformin has a previously unrecognized effect on cardia

119 The widely prescribed diabetes medicine metformin has been reported to lower the risk of inciden

120 Biguanides such as metformin have previously been shown to antagonize hepat

121 cetylation and that AMPK activators, such as metformin, have the capacity to increase protein acetyla

122 [(11)C]-Metformin holds great potential as a tool to determine t

123 effects of treatments used for MetS, such as metformin hydrochloride and pioglitazone hydrochloride,

124 bit the upregulation of DDIT4 in response to metformin, hypoxia-like (CoCl2) or genotoxic stress.

125 ci or 5 DNA methylation loci associated with metformin IC50 through trans-regulation of expression of

126 , and 5 DNA methylation loci associated with metformin IC50 with P-values <10-4 or <10-5.

127 tudy, miR-21 was strikingly downregulated by metformin in a time- and dose-dependent manner.

128 account for the poor pro-apoptotic effect of metformin in cancer cells.

129 determine the pharmacokinetic properties of metformin in clinical studies.

130 Dose-dependent uptake of (11)C-metformin in LLC-PK1 cells was rapid.

131 and found significant benefit when including metformin in polycystic ovary syndrome treatment regimen

132 urn patients and further supports the use of metformin in severely burned patients for postburn contr

133 % of the mean PDC [82.3%], P = .003) and for metformin in the 2012 and 2013 cohorts (adjusted differe

134 To test whether the effects of metformin in the kidney are dependent on these transport

135 Even though exposure of metformin in the kidney was severely decreased in OCT1/2

136 T2 significantly reduced the distribution of metformin in the liver and small intestine.

137 E1 with pyrimethamine caused accumulation of metformin in the liver but did not affect distribution i

138 separate roles in uptake and elimination of metformin in the liver, but this is not due to changes i

139 e sessions to all participants and continued metformin in the originally randomized metformin group.

140 The inclusion of metformin in the treatment arms of cancer clinical trial

141 aphy with [(11)C]-labeled metformin ([(11)C]-metformin) in mice to investigate the role of OCT and MA

142 armacologic interventions such as the use of metformin, in obese populations may help to reduce their

143 Metformin increased the size of the hematopoietic stem c

144 Metformin increases alanine levels and reduces the phosp

145 the regulatory mechanism of miR-21 mediating metformin-induced anti-angiogenic effects, providing imp

146 miR-21 and its targets and their effects on metformin-induced antiangiogenic activity were assessed

147 te magnetic resonance spectroscopy to detect metformin-induced changes in cytosolic redox biology, su

148 e precise regulatory mechanisms by which the metformin-induced endothelial suppression and its effect

149 This metformin-induced H19 repression and alteration of gene

150 Despite the lack of recovery from metformin-induced impairment of mitochondrial energy met

151 1) glucose-responsiveness, 2) sensitivity to metformin-induced inhibition of the glucose effect at in

152 ted with a 0.17% (P = 6.6 x 10(-14)) greater metformin-induced reduction in hemoglobin A1c (HbA1c) in

153 We demonstrate that metformin induces endoplasmic reticulum (ER) stress, cal

154 Here we report that metformin induces genome-wide alterations in DNA methyla

155 criptional target, ACAD10, is activated when metformin induces nuclear exclusion of the GTPase RagC,

156 High-dose metformin inhibited GM-CSF and MMP9 release from WAT pro

157 lucose concentrations, and 3) alleviation of metformin inhibition by elevated glucose concentrations.

158 on of AMP-activated protein kinase (AMPK) by metformin, inhibition of mTORC by torin 1, or CRISPR/Cas

159 her studies show that treatment of mice with metformin inhibits obesity-associated tumour progression

160 We also demonstrated that metformin inhibits the opening of mPTP and induces mitoc

161 d sample size and statistical power for gene-metformin interactions (vs. placebo) using incidence rat

162 Thus, metformin is a potential FXS therapeutic.

163 search may be warranted to determine whether metformin is a preferred treatment for diabetes among br

164 Metformin is a widely used antidiabetic drug that exerts

165 ly, combined therapy of cisplatin (CDDP) and metformin is an effective treatment for non-small cell l

166 Metformin is an energy disruptor targeting complex I of

167 Metformin is currently considered as a promising antican

168 Metformin is one of the most widely used therapeutics fo

169 These results indicate that metformin is safe in burn patients and further supports

170 (11)C-metformin is suitable for imaging metformin uptake in ta

171 Metformin is the first-line antidiabetic drug with over

172 Metformin is the most commonly prescribed oral anti-diab

173 Metformin is the most commonly prescribed oral antidiabe

174 Metformin is the most widely prescribed oral antiglycemi

175 Our findings support the recent changes in metformin labeling.

176 Exposing cancer cells to metformin leads to hypermethylation of tumor-promoting p

177 Metformin may protect against coronary atherosclerosis i

178 g II-induced cardiac hypertrophy, and blunts metformin-mediated cardioprotective effects.

179 This Metformin-mediated effect was conserved in vivo; Metform

180 Overexpression of miR-21 abrogated the metformin-mediated inhibition of endothelial cells proli

181 n mice infused with Ang II and repressed the metformin-mediated reduction of cardiac hypertrophy and

182 ), purmorphamine (Pur), genistein (Gen), and metformin (Met).

183 of this study is to investigate efficacy of metformin (MF) 1% gel as an adjunct to scaling and root

184 Metformin might reduce insulin requirement and improve g

185 bA1c 8-12% [64-108 mmol/mol]) despite stable metformin monotherapy (>/=1500 mg/day) were randomly ass

186 h type 2 diabetes inadequately controlled by metformin monotherapy.

187 lusion of 26 985 patients being treated with metformin monotherapy: 23.3%, 20.4%, 20.3%, and 20% acro

188 Use of metformin (n = 2,558) was associated with 28% (95% CI, 0

189 chotic were assigned to take 1000 mg day(-1) metformin (n=103) or placebo (n=98) for 24 weeks, with e

190 omparing the effects of sulfonylureas versus metformin on body mass index, where the variables baseli

191 ndomized trials investigating the effects of metformin on cancer-related outcomes.

192 K-alpha2 deficiency abolished the effects of metformin on Drp1 expression, oxidative stress, and athe

193 or lifestyle versus placebo), but not in the metformin or placebo arms (P>0.05).

194 ted MI who were randomly assigned to receive metformin or placebo for 4 months.

195 53d/d mice with either the antidiabetic drug metformin or the antioxidant resveratrol activated AMPK

196 AMPK with the widely used antidiabetic drug metformin or with the AMP mimetic 5-aminoimidazole-4-car

197 ndomized high-risk individuals to lifestyle, metformin, or placebo interventions.

198 nly used for glycemic control as adjuncts to metformin, other oral antiglycemic agents, or insulin.

199 and many patients become less responsive to metformin over time.

200 h MALA induced through the administration of metformin per os and an intraperitoneal injection of lac

201 eclinical findings by a first-in-human (11)C-metformin PET dosimetry, biodistribution, and tissue kin

202 of U2OS cells to metabolic stress induced by metformin, PML loss did not inhibit the upregulation of

203 ically complexed with the cationic polymeric metformin (polymet).

204 Herein a polymeric construction of Metformin, PolyMetformin (PolyMet) is successfully synth

205 opose that neonatal administration of T4 and metformin post FAE affect memory via elevating Dnmt1 and

206 Here we show, metformin prevents both venous and arterial thrombosis w

207 mounts of extracellular mtDNA, we found that metformin prevents mtDNA release.

208 How metformin protects against diabetes-related cardiovascul

209 Further we show that AMPK activation by metformin reduced collagen III levels and the ratio of C

210 Both AICAR and metformin reduced F-actin and significantly reduced the

211 Together with lifestyle modification, metformin remains the first-line therapy for adolescents

212 The metformin-rescued P23H rhodopsin was still intrinsically

213 It remains unknown how metformin resistance or insensitivity occurs.

214 etic screening in C. elegans, we uncover two metformin response elements: the nuclear pore complex (N

215 This ancient metformin response pathway is conserved from worms to hu

216 nd Igf2 in the adult male hippocampus, while metformin restored FAE-caused changes in Igf2 expression

217 Interestingly, the diabetes drug metformin reverses mutation-associated alterations on en

218 ersely, down-regulation of miR-21 aggravated metformin's action and revealed significant promotion ef

219 propose that aspirin/salicylate may augment metformin's hepatic action to suppress glucose productio

220 l systems pharmacology approach to elucidate metformin's molecular basis and genetic biomarkers of ac

221 xpression, further expanding the plethora of metformin's physiological effects.

222 regulation of 14 genes significantly altered metformin sensitivity in two breast cancer cell lines.

223 a1 KO mouse model, the protective effects of metformin still occurred in the 3dUUO model.

224 Compared with metformin, sulfonylurea (standardized mean difference [S

225 t failure (trial registration: NCT00473876), metformin suppressed plasma cytokines including the agin

226 lipid content of very large HDL was lower in metformin than in placebo-treated patients (28.89% versu

227 Here we show that metformin, the most widely used drug for type 2 diabetes

228 tissue, the liver, and a putative target of metformin, the small intestine.

229 To better individualize metformin therapy and explore novel molecular mechanisms

230 or MALA, which is a critical complication of metformin therapy.

231 Evaluated interventions included metformin, thiazolidinediones, sulfonylureas, dipeptidyl

232 There was no elimination of (11)C-metformin through the bile both during the intravenous a

233 RPRETATION: These data do not support use of metformin to improve glycaemic control in adults with lo

234 an SGLT-2 inhibitor, or a DPP-4 inhibitor to metformin to improve glycemic control when a second oral

235 Adding a sulfonylurea or metformin to insulin was associated with a decrease in h

236 We administered vehicle, thyroxine (T4) or metformin to neonatal rats post FAE and rats were tested

237 1: ACP recommends that clinicians prescribe metformin to patients with type 2 diabetes when pharmaco

238 metformin treatment in patients with varying metformin transport capacity.

239 the DPP for the rs8065082 SLC47A1 variant, a metformin transported encoding locus.

240 We aimed to investigate whether metformin treatment (added to titrated insulin therapy)

241 Compared with the placebo, metformin treatment also have a significant effect on re

242 In high glucose-exposed endothelial cells, metformin treatment and adenoviral overexpression of con

243 ulted in sensitization of MCF7-LTED cells to metformin treatment and impairment of 2-DG-induced motil

244 eractions between genetic risk scores (GRS), metformin treatment and intensive lifestyle intervention

245 idemia-associated loci modify the effects of metformin treatment and lifestyle intervention (versus p

246 Here, we used acute metformin treatment as a tool to induce metabolic decele

247 Metformin treatment attenuated inflammation, increased t

248 In cell models, metformin treatment improved P23H rhodopsin folding and

249 oss of SIRT2 blunted the response of AMPK to metformin treatment in mice infused with Ang II and repr

250 e dependent on these transporters, we tested metformin treatment in OCT1/2(-/-) mice.

251 rove a valuable tool to assess the impact of metformin treatment in patients with varying metformin t

252 In obese syngeneic mice, metformin treatment mimicked the effects observed with G

253 nce spectroscopy to determine the effects of metformin treatment on heart and liver pyruvate metaboli

254 Here we report, for the first time, that metformin treatment overcomes metabolic memory and preve

255 In animal models of P23H RP, metformin treatment successfully enhanced P23H traffic t

256 We found that metformin treatment was effective in improving antipsych

257 ts either lack or have a delayed response to metformin treatment, and many patients become less respo

258 n combination with Mek-Erk1/2 inhibition and metformin treatment.

259 ormin-mediated effect was conserved in vivo; Metformin-treatment significantly reduced levels of KIC

260 Metformin treatments markedly reduced mitochondrial frag

261 Metformin triggers the disorganization of the cristae an

262 Hepatic metformin uptake depends on the expression of organic ca

263 (11)C-metformin is suitable for imaging metformin uptake in target tissues and may prove a valua

264 Rat small-animal PET images showed (11)C-metformin uptake in the kidney and liver, the kinetics o

265 Liver (11)C-metformin uptake was pronounced after oral administratio

266 Our findings did not suggest the benefit of metformin use after patients are diagnosed with PDAC.

267 Metformin use has been associated with a decrease in can

268 Metformin use in patients with moderate CKD, CHF, or CLD

269 To synthesize data addressing outcomes of metformin use in populations with type 2 diabetes and mo

270 ers must understand the clinical outcomes of metformin use in these populations.

271 yntheses involving 17 observational studies, metformin use is associated with reduced all-cause morta

272 Insulin use was higher and sulfonylurea/metformin use was lower among patients with lower renal

273 By the time-varying covariate analysis, metformin use was not statistically significantly associ

274 Randomization was stratified by metformin use.

275 ion of treatment in 59 (27%) participants on metformin versus 26 (12%) on placebo (p=0.0002) was main

276 ce were significantly lower among men in the metformin versus the placebo group (age-adjusted mean CA

277 Participants receiving metformin vs placebo experienced gastrointestinal advers

278 eas emerged: (1) lifestyle modification, (2) metformin vs placebo or estrogen-progestin oral contrace

279 n TEA and Arg was found, while the biguanide metformin was able to strongly inhibit uptake of both su

280 Renal clearance of (11)C-metformin was approximately 3 times the renal clearance

281 Cox model, an artificial survival benefit of metformin was detected (HR, 0.88; 95% CI, 0.77 to 1.01;

282 Additionally, metformin was effective in reducing the risk of HCC when

283 Notably, metformin was hierarchically the best when compared with

284 Only slow accumulation of (11)C-metformin was observed in muscle.

285 Whole-body PET revealed that (11)C-metformin was primarily taken up by the kidneys, urinary

286 itochondria, because the swelling induced by metformin was reversed by the inhibition of mitochondria

287 In summary, available evidence suggests that metformin was the most effective strategy to reduce HCC

288 ation dosimetry and biodistribution of (11)C-metformin were estimated in 4 subjects (2 women and 2 me

289 MRI, we found that the protective effects of metformin were OCT1/2 independent when tested in this mo

290 diet and exercise alone or a stable dose of metformin were randomized.

291 ss evidence, results for add-on therapies to metformin were similar to those for monotherapies.

292 2.Sle3 mice with either 2-deoxy-D-glucose or metformin were sufficient to prevent autoimmune activati

293 Furthermore, a common diabetes drug, metformin, which carries an AMPK-agonistic activity, dra

294 cose, which inhibits glucose metabolism, and metformin, which inhibits oxygen consumption, normalized

295 od and Drug Administration boxed warning for metformin will increase its use in persons with historic

296 eil a novel mechanism of action for the drug metformin with implications for the molecular basis of e

297 2) compared diabetes regimens that included metformin with those that did not; and 3) reported all-c

298 abetes who were inadequately controlled with metformin (with or without sulfonylureas).

299 yphosate) and two pharmaceuticals (caffeine, metformin) with detection frequencies ranging 66-84% of

300 Thus, we hypothesized that (11)C-labeled metformin would be a suitable PET tracer for quantificat