ライフサイエンスコーパス: metformin

1 on-DM, 76 DM of whom 35 [46%] were receiving metformin).

2 and are vulnerable to low glucose levels and metformin.

3 rgoing replicative senescence in presence of metformin.

4 hanced tumor growth, which were inhibited by metformin.

5 nd no serious adverse events associated with metformin.

6 ranslational and transcriptional response to metformin.

7 duced in DM, and glycolysis was increased by metformin.

8 l mechanism for the anti-diabetic actions of metformin.

9 biuret as a novel transformation product of metformin.

10 duced by starvation or the antidiabetic drug metformin.

11 PKalpha by using siRNA blunted the effect of metformin.

12 ed by 9 months of metformin, or 12 months of metformin.

13 itagliptin, or insulin glargine as add-on to metformin.

14 y and TB recurrence, when being treated with metformin.

15 PC maturation, which could not be rescued by metformin.

16 io was significantly reduced and reversed by metformin.

17 d G6P and also mimics the G6pc repression by metformin.

18 tophagic flux was enhanced by treatment with metformin.

19 Animals received saline (groups 1-2) or metformin (100 mg/kg; group 3) intravenously, followed b

20 of saline (normal and model control group), metformin (120 mg/kg.bw), and PLPE (600 mg/kg.bw) by ora

21 The effects of metformin + 2-DG on human T cells were accompanied by si

22 In this study, we report that metformin + 2-DG treatment more potently suppressed IFN-

23 into the effects of metabolic inhibition by metformin + 2-DG treatment on primary human T cells and

24 Accordingly, metformin + 2-DG treatment significantly suppressed MYC-

25 n sensitizes cells to ETC inhibitors such as metformin(5,6), suppressing growth of both cell line and

26 bo than exenatide (38.1% versus 28.8%), with metformin (6.1% versus 4.9%), sulfonylurea (8.7% versus

27 domly assigned to complete 12-week cycles of metformin (A) and placebo (B) in either an AB or BA sequ

28 ated the ultrahigh-throughput bioanalysis of metformin, a small polar substrate commonly used in high

29 the top tier includes rapamycin, senolytics, metformin, acarbose, spermidine, NAD(+) enhancers and li

30 er, up to 300 times higher concentrations of metformin accumulate in the intestine than in the circul

31 nthase (CBS) domain in the gamma1 subunit in metformin action and found that deletion of either CBS1

32 of each regulatory gamma subunit isoform to metformin action in this current study.

33 ntial role of this kinase and its targets in metformin action in vivo.

34 ut not gamma2 or gamma3, drastically reduced metformin activation of AMPK.

35 Metformin added to peripheral blood mononuclear cells fr

36 Metformin administered to healthy human volunteers led t

37 First, we assessed the effect of acute metformin administration on non-small cell lung cancer x

38 These data indicate that colchicine and metformin affect acute and chronic kidney injury differe

39 urrent glucose-lowering therapies, including metformin, affect intestinal-related IgA(+) B cell popul

40 sisted of a 2-week screening visit, a 3-week metformin-alone run-in period, and a 5-year treatment pe

41 s the antimetabolic drugs 2-deoxyglucose and metformin, also promoted the release of IL-6 and IL-8.

42 erlying mechanisms, we tested the effects of metformin, an oral antidiabetic drug, in mice fed an HFD

43 demonstrated that combination treatment with metformin and 2-DG was efficacious in dampening mouse T

44 y users; the weighted cohort included 24 679 metformin and 24 799 sulfonylurea users (median age, 70

45 There were 67 749 metformin and 28 976 sulfonylurea persistent monotherapy

46 inhibitor, 216 (71.5%) patients were taking metformin and 39 (12.9%) were taking sulphonylurea.

47 Using metformin and etomoxir as examples, we demonstrate that

48 Oral hypoglycaemic agents, principally metformin and glibenclamide (glyburide), are also used i

49 rstand the Genetics of the Acute Response to Metformin and Glipizide in Humans (SUGAR-MGH), we constr

50 The ability of metformin and increased intracellular free Ca(2+) concen

51 acological inhibition of CI function through metformin and macrophage infiltration through PLX-3397 i

52 While exercise, caloric restriction, metformin and many natural products increase AMPK activi

53 There were 174 882 persistent new users of metformin and sulfonylureas who reached a reduced kidney

54 We show that microbes integrate cues from metformin and the diet through the phosphotransferase si

55 The widely prescribed antidiabetic drug metformin and the glycolytic inhibitor 2-deoxyglucose (2

56 CM derived from HCT116 cells pretreated with metformin and then treated with LCA lost all stimulatory

57 ration and provides a potential link between metformin and wound healing impairment.

58 mitted transport of drugs (including DNA and metformin) and macromolecules (such as antibodies and pr

59 dazole-4-carboxamide ribonucleotide (AICAR), metformin, and a specific AMPKalpha activator (GSK621) a

60 e then treated with the hypoglycemic agents, metformin, and insulin to assess for appropriate reversi

61 ination treatment of R-alpha-lipoic acid and metformin, and niacin.

62 that include antisense HK2 oligonucleotides, metformin, and perhexiline prevent progression.

63 er cyst burden was observed compared to free metformin, and was well tolerated upon repeated dosages.

64 aOR] 2.84, 95% CI 1.10 to 7.37; p=0.031) and metformin (aOR 4.78, 95% CI 1.44 to 15.86; p=0.011) at h

65 e mechanisms of action of the biguanide drug metformin are still being discovered.

66 he mTORC1 pathway in the hepatic benefits of metformin are still ill defined.

67 Metformin as an add-on to insulin therapy resulted in gl

68 s subsets and were appropriately reverted by metformin as confirmed in vitro.

69 ide or DPP-4 inhibitors, who were also using metformin at baseline, matched 1:1 on age, sex, and prop

70 Metformin augmented expression of multiple autophagic pr

71 association that was significant was having metformin available, which was positively associated wit

72 ide-1 receptor agonists (GLP-1 RAs) added to metformin-based background therapy produced the greatest

73 s at increased cardiovascular risk receiving metformin-based background therapy, specific GLP-1 RAs a

74 s at increased cardiovascular risk receiving metformin-based background treatment (21 trials), oral s

75 atients at low cardiovascular risk receiving metformin-based background treatment (298 trials), there

76 cluded monotherapies (134 trials), add-on to metformin-based therapies (296 trials), and monotherapie

77 , we verified the effect of a single dose of metformin before radiotherapy on long-term treatment out

78 Interestingly, metformin, but not nec-1, improved brain insulin sensiti

79 Metformin can improve patients' hyperglycemia through si

80 Considering that metformin can reduce glucose consumption, we speculated

81 persisting with monotherapy, treatment with metformin, compared with a sulfonylurea, was associated

82 s admitted in an emergency context, a plasma metformin concentration greater than or equal to 9.9 mg/

83 characteristic curve analysis showed that a metformin concentration threshold of 9.9 mg/L was signif

84 ver, in-ICU death was less frequent when the metformin concentration was greater than or equal to 9.9

85 The antidiabetic drug metformin consistently had the highest concentration wit

86 a third antidiabetic agent after receiving a metformin-containing dual combination were identified.

87 inistration (FDA) changed labeling regarding metformin contraindications in patients with diabetes an

88 rmaceuticals (i.e., high = citalopram; low = metformin) contributed to complex mixture evolution alon

89 Interestingly, metformin decreased omental metastasis at least partiall

90 d leukocyte adhesion, whereas treatment with metformin decreased the SFA-induced leukocyte adhesion.

91 Administering the AMPK activator metformin decreases epithelial progenitor proliferation

92 and Drug Administration (FDA)-approved drug metformin, decreases RAN proteins, and improves behavior

93 Metformin-dependent activation of AMPK classically inhib

94 e an important function of CD8(+) T cells in metformin-derived host metabolic-fitness towards M. tube

95 The mechanisms by which metformin (dimethylbiguanide) inhibits hepatic gluconeog

96 in lactate/pyruvate ratio, whereas a higher metformin dose (>=5 nmol/mg) caused a more reduced mitoc

97 Study limitations include heterogeneity in metformin dosing, heterogeneity in diagnostic criteria f

98 zole-4-carboxamide ribonucleotide (AICAR) or metformin during sepsis improved the survival, while AMP

99 Metformin-educated CD8(+) T cells have increased (i) mit

100 A detailed experimental characterization of metformin effects downstream of Crp in combination with

101 uction of microbial agmatine, a regulator of metformin effects on host lipid metabolism and lifespan.

102 lude that at a low pharmacological load, the metformin effects on the lactate/pyruvate ratio and gluc

103 These metformin effects result in the improvement of insulin s

104 In summary, metformin elevates circulating levels of GDF15, which is

105 odent cranial radiation model, we found that metformin enhanced the recovery of NPCs in the dentate g

106 In BCG-vaccinated mice and guinea pigs, metformin enhances immunogenicity and protective efficac

107 We hypothesized that nec-1 and metformin equally attenuated cognitive decline and brain

108 Nec-1 and metformin equally improved cognitive function, synaptic

109 dence suggest that the glucose-lowering drug metformin exerts a valuable anti-senescence role.

110 Despite lower average birth weight, metformin-exposed children appear to experience accelera

111 ty to increased adiposity versus insulin- or metformin-exposed groups.

112 In contrast to the neonatal phase, metformin-exposed infants were significantly heavier tha

113 Metformin-exposed neonates had decreased ponderal index

114 Metformin-exposed neonates had decreased ponderal index

115 Metformin-exposed neonates were born lighter (-191.73 g,

116 Metformin-exposed neonates were born lighter (-73.92 g,

117 Metformin-exposed neonates were lighter with reduced lea

118 Associations between metformin exposure and outcomes were estimated with inve

119 0.23 to 1.33, I2 = 7%, p = 0.005) following metformin exposure than following insulin exposure, alth

120 ups (n = 8/subgroup) with vehicle, nec-1, or metformin for 8 weeks.

121 ial was not intended to test the efficacy of metformin for cognitive recovery and brain growth, but t

122 Vildagliptin Efficacy in combination with metfoRmIn For earlY treatment of type 2 diabetes (VERIFY

123 a, or both, or basal insulin with or without metformin for the past 90 days were eligible.

124 vation of AMPK with the type 2 diabetes drug metformin (GlucoPhage) also increased mTORC2 signaling i

125 ted pregnancies randomised to treatment with metformin, glyburide, or insulin were included.

126 fter 1 year, 289 (28.5%) participants in the metformin group, 640 (62.6%) in the ILS group, and 137 (

127 9.5% (53-80.3 mmol/mol), on a stable dose of metformin (>=1500 mg or maximum tolerated) with or witho

128 Metformin had effects on both energy intake and energy e

129 year, those originally randomly assigned to metformin had the greatest loss during years 6 to 15.

130 Here, we show that metformin has a biphasic effect on the mitochondrial NAD

131 Metformin has been used to treat patients with type 2 di

132 I-T1D, n = 20), or treated with insulin plus metformin (IM-T1D, n = 20).

133 the renoprotective effects of colchicine or metformin in C57BL/6 mice challenged with renal ischemia

134 study, we describe the inhibitory effect of metformin in interleukin 8 (IL-8) upregulation by lithoc

135 ning to which drug add-ons to recommend when metformin in monotherapy does not achieve the therapeuti

136 s to lifestyle interventions with or without metformin in those at high atherosclerotic cardiovascula

137 overy and brain repair, focusing on the drug metformin, in parallel rodent and human studies of radia

138 In wild-type mice, oral metformin increased circulating GDF15, with GDF15 expres

139 Moreover, metformin increased hippocampal serotonergic neurotransm

140 on, providing a potential suggestion for why metformin increases acid secretion and reduces gastric c

141 t randomized controlled clinical trials-that metformin increases circulating levels of the peptide ho

142 In the subgroup receiving metformin, independently from immunosuppressive therapy

143 Challenge of hepatocytes with metformin-induced metabolic stress strengthened both AMP

144 irculating lactate:pyruvate ratio, blunted a metformin-induced rise in blood lactate:pyruvate ratio a

145 Interestingly, metformin-induced stimulation of AMP-activated protein k

146 In conclusion, metformin inhibited NADPH oxidase, which in turn suppres

147 Accordingly, metformin inhibited the phosphorylation of pSTAT1 (Y701)

148 nce suggest additional mechanisms at play in metformin inhibition of mTORC1.

149 Metformin inhibits complex I and alpha-glycerophosphate

150 Metformin inhibits the expression of the plasma membrane

151 human systemic lupus erythematosus patients, metformin inhibits the transcription of IFN-stimulated g

152 Participants in both the lifestyle and metformin interventions had greater improvement in the m

153 ch as PKD, we loaded the candidate PKD drug, metformin, into chitosan nanoparticles, and upon oral ad

154 Metformin is an established AMPK agonist that can promot

155 Metformin is first-line therapy for type 2 diabetes mell

156 g mechanisms for the anti-diabetic effect of metformin is mediated by the stimulation of AMP-activate

157 ase in body weight gain in mice treated with metformin is not directly attributable to increased ener

158 survivors of pediatric brain tumors and that metformin is safe to use and tolerable in this populatio

159 Metformin is the first line of treatment for type 2 diab

160 Metformin is the first-line therapy for treating type 2

161 Metformin is the first-line treatment for type 2 diabete

162 Metformin is the regulatory-approved treatment of choice

163 summary, targeting PKR, including by use of metformin, is a promising therapeutic approach for C9orf

164 The metformin label change to an eGFR-based contraindication

165 f 30-44 ml/min per 1.73 m(2) were prescribed metformin less often than White counterparts (adjusted p

166 Cell metformin loads in the therapeutic range lowered cell G6

167 clude that therapeutically relevant doses of metformin lower G6P in hepatocytes challenged with high

168 At a functional level, metformin lowered ex vivo production of tumor necrosis f

169 The molecular mechanisms by which metformin lowers body weight are unknown.

170 determined the candidate mechanisms by which metformin lowers glucose 6-phosphate (G6P) in mouse and

171 Preconditioning with metformin lowers hepatobiliary injury and improves hepat

172 lung cancer xenograft model, we showed that metformin may act as a radiosensitizer by increasing tum

173 ells and provides a novel mechanism by which metformin may exert a therapeutic effect in autoimmune d

174 Metformin may improve tumor oxygenation and thus radioth

175 These actions depend on metformin-mediated activation of AMP kinase (AMPK).

176 fic and non-specific cytokine production via metformin-mediated increase in glycolytic activity.

177 lls from Cxcr3(-/-) mice do not exhibit this metformin-mediated metabolic programming.

178 Combining BPTES with metformin might achieve improved anti-cancer effects in

179 mg twice daily, or standard-of-care initial metformin monotherapy (stable daily dose of 1000 mg, 150

180 s which were 13 weeks apart, patients in the metformin monotherapy group received vildagliptin 50 mg

181 ombination treatment group or to the initial metformin monotherapy group, with the help of an interac

182 ith macrovascular disease; 59% had undergone metformin monotherapy) were treated and analyzed.

183 ference with both oxidative phosphorylation (metformin, oligomycin) and beta-oxidation of fatty acids

184 owever, the comparative effects of nec-1 and metformin on cognition and brain pathologies in prediabe

185 at a clinical trial examining the effects of metformin on cognition and brain structure is feasible i

186 62, 991, and C-13) had opposite effects from metformin on glycolysis, gluconeogenesis, and cell G6P.

187 The chronic effects of metformin on liver gluconeogenesis involve repression of

188 CREB seem to mediate the observed effects of metformin on NaCT.

189 e assay proved that the inhibitory effect of metformin on ROS production was derived from its strong

190 s the current understanding of the impact of metformin on systemic metabolism and its molecular mecha

191 alysis and in vitro validation revealed that metformin optimally reverts diabetogenic genes dysregula

192 rocesses, relative to treatments with either metformin or 2-DG alone.

193 ted primary human CD4(+) T cells than either metformin or 2-DG treatment alone.

194 HDL cholesterol in individuals randomized to metformin or placebo, but none of them achieved the mult

195 New users of metformin or sulfonylurea monotherapy who continued trea

196 and who had been receiving a stable dose of metformin or sulfonylurea, or both, or basal insulin wit

197 of insulin glargine followed by 9 months of metformin, or 12 months of metformin.

198 g with small molecules, including tretinoin, metformin, or TR4-shRNAs, all led to increase the suniti

199 ted with exposure to 1 defined daily dose of metformin over the previous 2-7 years were 0.98 (95% con

200 t with CB-839 (glutaminase 1 inhibitor) plus metformin/phenformin.

201 Metformin plus insulin resulted in a daily insulin dose

202 After orthotopic liver transplantation, metformin preconditioning significantly reduced transami

203 ssessed the association of race and sex with metformin prescription across eGFR level before and afte

204 rtently caused racial and sex disparities in metformin prescription among patients with low eGFR.

205 y have reduced racial and sex disparities in metformin prescription in moderate kidney dysfunction.

206 eGFR of 30-44 ml/min per 1.73 m(2) received metformin prescriptions less often than women counterpar

207 Metformin prevented weight gain in response to a high-fa

208 oenvironment induced by NCOA5 deficiency and metformin prevents HCC development via alleviating p21(W

209 These data suggest that metformin promotes natural host resistance to Mtb infect

210 fter long-term metformin treatment, and that metformin promotes the formation of the functional AMPK

211 Pre-emptive treatment with colchicine or metformin protected against AKI, with lower serum creati

212 e results suggest a novel mechanism by which metformin protects vascular endothelium from SFA-induced

213 in controls, the radiotherapy group, and the metformin + radiotherapy group, respectively (log-rank P

214 t renoprotective effects beyond therapy with metformin, ramipril, and empagliflozin (MRE).

215 HLA-A*24:02 CMV peptide was dampened, while metformin recovered multifunctionality.

216 Metformin reduced levels of circulating branched-chain a

217 Furthermore, metformin reduces blood lipopolysaccharides and its init

218 Because metformin reduces ectopic lipid accumulation, we evaluat

219 nistration of the type 2 diabetes medication metformin reduces mitochondrial respiration to control l

220 We investigated whether preconditioning with metformin reduces preservation injury and improves hepat

221 initiation of autophagy, we hypothesize that metformin reduces the accumulation of lipid droplets by

222 Aged OPCs treated with metformin regain responsiveness to pro-differentiation s

223 ration and nutrient sensing are modulated by metformin-regulated miRNAs and that some of the regulate

224 Our results show that metformin reshapes the senescence-associated miRNA/isomi

225 cate that the gamma1 subunit is required for metformin's control of glucose metabolism in hepatocytes

226 that deletion of either CBS1 or CBS4 negated metformin's effect on AMPKalpha phosphorylation at T172

227 Metformin significantly affects the relative abundance o

228 euptake inhibitors, allopurinol, mometasone, metformin, simvastatin, levothyroxine were inversely ass

229 either the early combination treatment with metformin (stable daily dose of 1000 mg, 1500 mg, or 200

230 re treated daily with the anti-diabetic drug metformin starting 4 weeks prior or concurrent with aero

231 rt that treatment of patients with estrogen, metformin, statins, vitamin D, and tumor necrosis factor

232 quate hemoglobin A1c (HbA1c) control despite metformin-sulfonylurea (Met-SU) dual therapy, a third-li

233 esponse with all noninsulin treatments after metformin (sulfonylureas, thiazolidinediones, dipeptidyl

234 The antidiabetic drug metformin suppressed insulin-induced hepatic cyclin D1 e

235 etion of the gamma1 subunit are resistant to metformin suppression of liver glucose production.

236 Inositol polyphosphate multikinase is a metformin target that regulates cell migration.

237 tified 2 commonly used drugs (colchicine and metformin) that alter inflammatory cell function and sig

238 ting in progressive MS: R-alpha-lipoic acid, metformin, the combination treatment of R-alpha-lipoic a

239 Metformin, the most widely administered diabetes drug, h

240 Metformin, the world's most prescribed anti-diabetic dru

241 A low cell dose of metformin (therapeutic equivalent: <2 nmol/mg) caused a

242 trials), and monotherapies versus add-on to metformin therapies (23 trials).

243 atients with type 2 diabetes uncontrolled on metformin therapy.

244 7.0-10.5% [53-91 mmol/mol]) on stable daily metformin therapy.

245 The ability of metformin to affect the biogenesis of selected microRNAs

246 his effect is attributable to the ability of metformin to lower body weight in a sustained manner(3).

247 bese mice on a high-fat diet, the effects of metformin to reduce body weight were reversed by a GFRAL

248 er, these findings suggest the capability of metformin to stimulate placental mitochondrial biogenesi

249 and CD8(+) T lymphocytes from Mtb infected, metformin treated animals maintained a more normal mitoc

250 he chronic stages of infection, Mtb infected metformin-treated animals had restored systemic insulin

251 t volumes) may be higher in children born to metformin-treated compared to insulin-treated mothers.

252 The study population consisted of 194 metformin-treated diabetic patients (median age: 68.6; m

253 Despite persistent glucose intolerance, metformin-treated guinea pigs had a 2.8-fold reduction i

254 clear cells (PBMCs), which was normalized in metformin-treated guinea pigs.

255 Neonates born to metformin-treated mothers had lower birth weights (mean

256 In metformin-treated patients admitted in an emergency cont

257 and biomarkers of inflammation are lower in metformin-treated subjects with type 2 diabetes (T2D) an

258 with metabolic modeling of the microbiota in metformin-treated type 2 diabetic patients predicts the

259 In vivo, we show that maternal metformin treatment along with maternal high fat diet si

260 We used metformin treatment and anti-IL-6 (interleukin-6) antibo

261 esults do not support an association between metformin treatment and the incidence of major cancers (

262 Here, we use mass cytometry to show that metformin treatment expands a population of memory-like

263 An alternative hypothesis that metformin treatment improved clinical disease by having

264 Furthermore, in humans and animal models, metformin treatment leads to the loss of body weight, we

265 Metformin treatment of primary hepatocytes and intact mu

266 Metformin treatment on male diabetic placental explant a

267 Importantly, prophylactic metformin treatment reversed these characteristics inclu

268 However, metformin treatment still increases KLF4 levels and supp

269 Metformin treatment was associated with the differential

270 lytic alpha1 and alpha2 mice after long-term metformin treatment, and that metformin promotes the for

271 ducing IL-6, either by anti-IL-6 antibody or metformin treatment, reversed pulmonary vascular remodel

272 olism and inflammatory programs triggered by metformin treatment.

273 g evidence regarding the association between metformin use and cancer risk in diabetic patients.

274 1-7.3) fewer events per 1000 person-years of metformin use compared with sulfonylurea use.

275 M versus non-DM recipients, and, relevantly, metformin use was associated with fewer lipotoxic factor

276 Metformin use was associated with reduced lipid accumula

277 outcomes (23.0 per 1000 person-years) among metformin users and 1394 events (29.2 per 1000 person-ye

278 reatment regimen, beginning with neoadjuvant metformin+venetoclax to induce apoptosis and followed by

279 to induce apoptosis and followed by adjuvant metformin+venetoclax+anti-PD-1 treatment to overcome imm

280 e versus insulin, and 3 studies (n = 421) to metformin versus glyburide.

281 -two studies (n = 2,801) randomised women to metformin versus insulin, 8 studies (n = 1,722) to glybu

282 Lewis rats were administered metformin via oral gavage, after which a donor hepatecto

283 During follow-up (median, 1.0 year for metformin vs 1.2 years for sulfonylurea), there were 104

284 e-specific adjusted hazard ratio of MACE for metformin was 0.80 (95% CI, 0.75-0.86) compared with sul

285 participants with complete data in cycle 1, metformin was associated with better performance than pl

286 Metformin was demonstrated to block LCA-stimulated ROS p

287 sponse in mice on high-fat diet treated with metformin was largely ablated by AMPK deficiency under t

288 The G6P lowering by metformin was mimicked by a complex 1 inhibitor (rotenon

289 Effects of metformin were examined in human placental explants from

290 etic patients aged >= 60 years, those taking metformin were less likely to have age-related macular d

291 riment, rat donor livers preconditioned with metformin were stored on ice for 4 hours and transplante

292 Several oral drugs, including metformin, were predicted to have intestinal concentrati

293 The G6P lowering by metformin, which also occurs in hepatocytes from AMPK kn

294 tinamide (1-NMN), creatinine, carnitine, and metformin, which is a probe for OCT1 and OCT2 and MATE1

295 ering effect of the oral anti-diabetic agent metformin, while inhibiting small intestinal mTOR alone

296 hemoglobin level, 7.0 to 9.5%) while taking metformin with or without a dipeptidyl peptidase 4 inhib

297 Whether liraglutide added to metformin (with or without basal insulin treatment) is s

298 .5 and 11.0% if they were being treated with metformin (with or without insulin).

299 at a dose of up to 1.8 mg per day (added to metformin, with or without basal insulin), was efficacio

300 duce glucose consumption, we speculated that metformin would enhance the anti-neoplasia effect of BPT