ライフサイエンスコーパス: SGLT

1 SGLT inhibition might also be considered in conjunction

2 SGLT-1 protein expression was unaltered; however, HS inc

3 SGLT-2 inhibitor initiators showed higher risk of genita

4 SGLT-2 inhibitors and GLP-1 receptor agonists are tradit

5 SGLT-2 inhibitors are associated with little or no effec

6 SGLT-2 inhibitors caused genital infection (high certain

7 SGLT-2 inhibitors had reduced hazards of hospital admiss

8 SGLT-2 inhibitors have demonstrated cardiovascular and k

9 SGLT-2 inhibitors were associated with an almost 3-fold

10 SGLT-2 inhibitors were more effective than DPP-4 inhibit

11 SGLT-2 inhibitors were more effective than sulfonylureas

12 SGLT-2 overexpression in diabetic patients contributes s

13 SGLT-2i combination therapies improved glucose homeostas

14 SGLT-mediated glucose transport can be estimated using a

15 SGLT-mediated glucose transport can be estimated using a

16 SGLTs are responsible for active glucose and galactose a

17 ut mice lacking sodium glucose tranporter-1 (SGLT-1) or the short chain fatty acid sensing receptor F

18 cells via the sodium glucose transporter 1 (SGLT-1) and glucose transporter 2 (GLUT2); various pepti

19 1 (PepT1), sodium/glucose co-transporter-1 (SGLT-1), potassium inwardly-rectifying channel, subfamil

20 nal SGLT-1 subtype as well as of dual SGLT-1/SGLT-2 inhibitors, representing a compelling strategy to

21 ition of the sodium glucose cotransporter 2 (SGLT-2) in the kidney and has been shown to lead to a ma

22 and chronic sodium-glucose cotransporter 2 (SGLT-2) inhibition increases endogenous glucose producti

23 Sodium-glucose cotransporter 2 (SGLT-2) inhibitors (gliflozins) represent the most recen

24 Sodium/glucose cotransporter 2 (SGLT-2) inhibitors are a novel class of antidiabetic age

25 Sodium-glucose cotransporter 2 (SGLT-2) inhibitors improve outcomes in patients with typ

26 nd safety of sodium-glucose cotransporter 2 (SGLT-2) inhibitors is mainly from placebo-controlled tri

27 nitiators of sodium-glucose cotransporter 2 (SGLT-2) inhibitors) between 2007 and 2019.

28 Sodium-glucose cotransporter 2 (SGLT-2) inhibitors, primarily used in diabetes and heart

29 expansion of sodium-glucose cotransporter-2 (SGLT-2) inhibitor use in patients with heart failure (HF

30 Sodium glucose cotransporter-2 (SGLT-2) inhibitors (odds ratio 0.88, 95% confidence inte

31 Sodium-glucose cotransporter-2 (SGLT-2) inhibitors could increase the risk for diabetic

32 (UTIs) with sodium-glucose cotransporter-2 (SGLT-2) inhibitors have reported conflicting findings.

33 Sodium-glucose cotransporter-2 (SGLT-2) inhibitors reduced heart failure hospitalization

34 benefits of sodium-glucose cotransporter-2 (SGLT-2) inhibitors, glucagon-like peptide-1 receptor ago

35 gonists with sodium-glucose cotransporter-2 (SGLT-2) inhibitors.

36 ibitors, and sodium-glucose cotransporter-2 (SGLT-2) inhibitors.

37 aPi-IIa) and sodium-glucose cotransporter-2 (SGLT-2).

38 Sodium-glucose co-transporters 2 (SGLT-2) inhibitors have emerged as a novel antidiabetic

39 abetic prescription on or after May 1, 2016: SGLT-2 inhibitors, DPP-4 inhibitors, GLP-1 agonists or o

40 iated by sodium-glucose cotransporters(2,3) (SGLTs).

41 -0.41; insulin RR = 0.28; 95% CI, 0.15-0.46; SGLT-2i RR = 0.42; 95% CI, 0.22-0.74).

42 peptidase-4 inhibitors (10.6% versus 7.5%), SGLT-2i (10.3% versus 8.1%), GLP-1 RA (3.4% versus 2.4%)

43 s are seen in real-world practice and across SGLT-2i class.

44 In addition, SGLT-2 inhibitors were not associated with increased ris

45 nd complications, we recommend administering SGLT-2 inhibitors (strong recommendation in favour).Reco

46 nd complications, we recommend administering SGLT-2 inhibitors (strong recommendation in favour)4.

47 and complications, we suggest administering SGLT-2 inhibitors (weak recommendation in favour)2.

48 and complications, we suggest administering SGLT-2 inhibitors (weak recommendation in favour)3.

49 In order to increase adoption, SGLT-2i and GLP-1RA must be reframed as primarily cardio

50 disease (CKD)): weak recommendation against SGLT-2 inhibitors or GLP-1 receptor agonists.* Moderate

51 fferences were found between the two agents: SGLT-2 inhibitors reduced admission to hospital for hear

52 GLT-2 inhibitors, the GLP-1 receptor agonist-SGLT-2 inhibitor combination was associated with a 29% l

53 his cohort study, the GLP-1 receptor agonist-SGLT-2 inhibitor combination was associated with a lower

54 rately, comparing the GLP-1 receptor agonist-SGLT-2 inhibitor combination with the background drug, e

55 is nationwide Medicare cohort, initiating an SGLT-2i was not associated with an increased risk of fra

56 Initiation of an SGLT-2 inhibitor or glucagon-like peptide-1 (GLP-1) rece

57 this study suggest that the initiation of an SGLT-2i was associated with a reduced risk of incident A

58 New users of an SGLT-2i, DPP-4i, or GLP-1RA without a previous fracture

59 ether with Western blot analysis revealed an SGLT-like protein.

60 benefits, harms, and burdens of starting an SGLT-2 inhibitor, incorporating the values and preferenc

61 ther a sulfonylurea, a thiazolidinedione, an SGLT-2 inhibitor, or a DPP-4 inhibitor to metformin to i

62 59.9 years; 63.6% female) and 18 537 used an SGLT-2 inhibitor (59.8 years; 63.7% female).

63 ong the 14 456 weighted patients who used an SGLT-2 inhibitor, compared with 853 events among the 587

64 g in the risk of DKA among patients using an SGLT-2 inhibitor as compared with placebo or an active c

65 ose uptake in fresh isolated tumors using an SGLT-specific radioactive glucose analog, alpha-methyl-4

66 pital admissions, or procedures, and when an SGLT-2 inhibitor was compared with a DPP-4 inhibitor (ra

67 espite at least 90 days of treatment with an SGLT-2 inhibitor, were randomly assigned (1:1) to receiv

68 by recommending GLP-1 receptor agonists and SGLT-2 inhibitors as initial glucose-lowering therapy.

69 Among users of GLP-1 receptor agonists and SGLT-2 inhibitors, the weighted risk per 1000 people was

70 P-4 inhibitors, GLP-1 receptor agonists, and SGLT-2 inhibitors and increased with sulfonylureas, thia

71 Alpha-blockers, antipsychotics, and SGLT-2 inhibitors were associated with up to 2-fold incr

72 ure of glucose utilization via both GLUT and SGLT transporters in health and disease stages.

73 ure of glucose utilization via both GLUT and SGLT transporters in health and disease states.

74 We determined levels of GLUT2 and SGLT-1 proteins and phosphorylation of AMPKalpha2 by imm

75 tion when compared with DPP-4 inhibitors and SGLT-2 inhibitors.

76 ve AMD compared with metformin, insulin, and SGLT-2i in logistic regression models.

77 In addition to randomised medication and SGLT-2 inhibitor, 216 (71.5%) patients were taking metfo

78 s), GLP-1RA vs. DPP-4i (159545 patients) and SGLT-2i vs. GLP-1RA (93033 patients) were included.

79 long-term studies focusing on GLP-1 RAs and SGLT-2 inhibitors are needed to validate these findings

80 d background therapy, specific GLP-1 RAs and SGLT-2 inhibitors have a favorable effect on certain car

81 ice aiming to evaluate the role of GLUTs and SGLTs in controlling glucose distribution and utilizatio

82 and death in patients newly initiated on any SGLT-2i versus other glucose-lowering drugs in 6 countri

83 ose and alpha-MDG are abolished by arresting SGLT activity by sodium removal or the SGLT inhibitor ph

84 , 5319 individuals (2.3%) were identified as SGLT-2i users.

85 e matching, the absolute differences between SGLT-2i users and nonusers for incidence of mortality, M

86 were calculated to compare the risks between SGLT-2i users and nonusers, representing the mean treatm

87 limb amputations (LLAs) were similar between SGLT-2i and incretins [95% confidence interval (CI) rang

88 Both SGLT-2i and GLP-1RA were first studied as glucose-loweri

89 Randomised controlled trials comparing SGLT-2 inhibitors or GLP-1 receptor agonists with placeb

90 spite raising basal glucagon concentrations, SGLT inhibitor treatment did not restore the impaired gl

91 ctivities of the Na(+)/glucose cotransporter SGLT-1 and GLUT2 were unaffected in LEPR-B-KO jejunum, w

92 se reuptake by sodium/glucose cotransporter (SGLT) 2 in the kidney, without affecting intestinal gluc

93 selective for sodium-glucose cotransporter (SGLT) family members and the sweet taste receptor were t

94 Sodium-glucose cotransporter (SGLT) inhibitors increase glucagon concentrations.

95 The Na-glucose cotransporter (SGLT) was the first transporter ever to be cloned.

96 (depolarizing) sodium-glucose cotransporter (SGLT).

97 GLP-1 RAs) and sodium-glucose cotransporter (SGLT-2) inhibitors have been shown to prevent CVD in T2D

98 the sodium-dependent glucose cotransporters (SGLT) have appeared as viable therapeutics to control bl

99 but requires sodium/glucose cotransporters (SGLT).

100 gut and renal sodium-glucose cotransporters (SGLTs) has been proposed as a novel therapeutic approach

101 The two main sodium-glucose cotransporters (SGLTs), SGLT1 and SGLT2, provide new therapeutic targets

102 for sodium-dependent glucose cotransporters (SGLTs), which have recently been shown to be distributed

103 l tubules via sodium-glucose cotransporters (SGLTs).

104 es in sodium-dependent sugar cotransporters (SGLTs).

105 medications for adults with type 2 diabetes (SGLT-2 inhibitors, GLP-1 receptor agonists, finerenone a

106 In patients with type 2 diabetes, SGLT-2 inhibitors and GLP-1 receptor agonists reduced ca

107 In people with type 2 diabetes, SGLT-2 inhibitors and GLP-1 receptor agonists were assoc

108 intestinal SGLT-1 subtype as well as of dual SGLT-1/SGLT-2 inhibitors, representing a compelling stra

109 e 309 056 patients newly initiated on either SGLT-2i or other glucose-lowering drugs (154 528 patient

110 % confidence interval (CI) -3.7 to -1.3) for SGLT-2 inhibitors versus sulfonylureas and -3.2 mmol/mol

111 ylureas and -3.2 mmol/mol (-4.6 to -1.8) for SGLT-2 inhibitors versus DPP-4 inhibitors.

112 Benefits for SGLT-2 inhibitors and GLP-1 receptor agonists on the abs

113 age, 66 years) with HF would be eligible for SGLT-2 inhibitors.

114 For some secondary endpoints, evidence for SGLT-2 inhibitors being more effective was lacking-the h

115 Existing guidance for SGLT-2 inhibitors does not account for the totality of c

116 ere used to generate hazard ratios (HRs) for SGLT-2i compared with DPP-4i and GLP-1RA and Kaplan-Meie

117 isk was 2.4% (95% CI 2.1% to 2.7%) lower for SGLT-2 inhibitors than DPP-4 inhibitors (4.6% v 7.0%), 1

118 % v 7.5%), and 1.2% (0.9% to 1.5%) lower for SGLT-2 inhibitors than GLP-1 receptor agonists (4.7% v 6

119 The strong recommendation for SGLT-2 inhibitors in patients with CVD and CKD reflects

120 eally positioned to share responsibility for SGLT-2i and GLP-1RA treatment with primary care provider

121 indings further suggest a potential role for SGLT-2 inhibitors in cirrhosis management.

122 Propensity score for SGLT-2i initiation was used to match treatment groups.

123 is framework holds significance not only for SGLTs but also for other transporters and channels.

124 8]-fluoro-d-glucose (4-FDG), a substrate for SGLTs and GLUTs; and 2-deoxy-2-[F-18]-fluoro-d-glucose (

125 d-glucopyranoside (Me-4FDG), a substrate for SGLTs; 4-deoxy-4-[F-18]-fluoro-d-glucose (4-FDG), a subs

126 e potentially substantial role of functional SGLTs in glucose transport and use.

127 e potentially substantial role of functional SGLTs in glucose transport and utilization.

128 Furthermore, SGLT-2 inhibitor use was associated with a lower rate of

129 AMPKalpha2 and a rapid increase of the GLUT2/SGLT-1 protein ratio in the brush border membrane.

130 tested whether glucose transporters (GLUTs, SGLTs) destined for the plasma membrane are active durin

131 Compared with the control group, SGLT-2 inhibitors group had significantly reduced fastin

132 Regarding medication-specific harms, SGLT-2 inhibitors increase genital infections (odds rati

133 with those for alpha-glucosidases and human SGLT type 1 (hSGLT1), a well characterized sodium/glucos

134 was no difference in the risk of fracture in SGLT-2i users compared with DPP-4i users (HR, 0.90; 95%

135 analyses, the risk of LLA was not higher in SGLT-2i vs. GLP1-RA [hazard ratio (HR) (95% CI): 0.88 (0

136 ) (95% CI): 0.88 (0.73, 1.05)], and lower in SGLT-2i vs. DPP-4i/other ADD [HR (95% CI): 0.65 (0.56, 0

137 etic ketoacidosis (DKA) (n = 16) was seen in SGLT-2 inhibitors group.

138 Existing antidiabetic medications, including SGLT-2 inhibitor treatment, were continued for the durat

139 ative effectiveness and safety of individual SGLT-2 inhibitors remain unknown.

140 This study found that individual SGLT-2 inhibitors demonstrated comparable cardiovascular

141 h sodium/glucose cotransporter 2 inhibition (SGLT-2i).

142 he sodium-glucose cotransporter-2 inhibitor (SGLT-2i) empagliflozin in patients with type 2 diabetes

143 he sodium-glucose cotransporter 2 inhibitor (SGLT-2i) empagliflozin significantly reduces cardiovascu

144 odium-glucose transport protein 2 inhibitor (SGLT-2i) users, 286 066 metformin users, and 164 361 ins

145 e sodium glucose cotransporter-2 inhibitors (SGLT-2i) and glucagon-like peptide-1 receptor agonists (

146 f sodium-glucose cotransporter-2 inhibitors (SGLT-2i), glucagon-like peptide-1 receptor agonists (GLP

147 ium-glucose cotransporter type-2 inhibitors (SGLT-2i; no exposure to incretins); 149 826 received glu

148 um-glucose cotransport protein 2 inhibitors (SGLT-2is) have demonstrated associations with positive k

149 Sodium-glucose cotransporter-2 inhibitors (SGLT-2is) have demonstrated many cardiovascular and kidn

150 dium-glucose transport protein 2 inhibitors (SGLT-2is).

151 Compared with DPP-4 inhibitors, SGLT-2 inhibitors were associated with an increased risk

152 3-4 and type 2 diabetes who newly initiated SGLT-2i vs. DPP-4i (141671 patients), GLP-1RA vs. DPP-4i

153 nonsevere UTI events among those initiating SGLT-2 inhibitor therapy was similar to that among patie

154 The discovery that intestinal SGLT-1 inhibition can provide a novel opportunity to con

155 itors selectively directed to the intestinal SGLT-1 subtype as well as of dual SGLT-1/SGLT-2 inhibito

156 , with potential applicability to the larger SGLT family of important sodium:solute cotransporters.

157 e transport by vSGLT is similar to mammalian SGLTs and that further studies on vSGLT will provide nov

158 After 3-way matching, 45 889 (73%) new SGLT-2i users were matched to new users of DPP-4i and GL

159 ors of study drugs, 62 454 patients were new SGLT-2i users.

160 ike peptide 1 receptor agonists [GLP-1RA, no SGLT-2i or dipeptidyl peptidase-4 inhibitor (DPP-4i) exp

161 e insulin-independent mechanism of action of SGLT inhibitors seems to offer durable glucose-lowering

162 All results refer to the addition of SGLT-2 inhibitors and GLP-1 receptor agonists to existin

163 h type 2 diabetes and AKD, administration of SGLT-2is was associated with a significant reduction in

164 However, the association of SGLT-2is with outcomes among patients with type 2 diabet

165 These ancillary benefits of SGLT-2 inhibitors and GLP-1 receptor agonists further su

166 The study confirmed the benefits of SGLT-2 inhibitors and GLP-1 receptor agonists in reducin

167 Absolute benefits of SGLT-2 inhibitors, GLP-1 receptor agonists, and finereno

168 findings emphasize the potential benefits of SGLT-2is in managing AKD and mitigating the risks of maj

169 e or no evidence was found for the effect of SGLT-2 inhibitors or GLP-1 receptor agonists on limb amp

170 of this study was to determine the effect of SGLT-mediated glucose uptake on NHE3 activity in the ren

171 Effects of SGLT-2 inhibitors were interpreted in absolute terms app

172 s with type 2 diabetes, including effects of SGLT-2 inhibitors, GLP-1RAs, finerenone and tirzepatide.

173 shown the blood glucose-lowering efficacy of SGLT inhibitors in type 2 diabetes when administered as

174 lications): weak recommendation in favour of SGLT-2 inhibitors or GLP-1 receptor agonists; and a weak

175 failure): strong recommendation in favour of SGLT-2 inhibitors or GLP-1 receptor agonists; and a weak

176 red evidence regarding benefits and harms of SGLT-2 inhibitor therapy for adults with CKD over a five

177 F of 40% and less, optimal implementation of SGLT-2 inhibitor therapy for HF with LVEF more than 40%

178 with nonuse, underscoring the importance of SGLT-2is in care after acute kidney injury.

179 Notably, pharmacologic inhibition of SGLT activity by Phlorizin produced a marked inhibition

180 Initiation of SGLT-2i was associated with a lower risk of hyperkalemia

181 2 phosphorylation and modifying the ratio of SGLT-1:GLUT2.

182 Rs) with 95% CIs of DKA comparing receipt of SGLT-2 inhibitors with receipt of DPP-4 inhibitors, whic

183 However, the results of SGLT-2i use in primary prevention of atrial fibrillation

184 imaging in the investigation of the role of SGLT transporters in human physiology and diseases such

185 A meta-analysis was conducted on trials of SGLT-2 inhibitors in patients with T1DM on insulin thera

186 work provides further support for the use of SGLT imaging in the investigation of the role of SGLT tr

187 ing the substantial benefits with the use of SGLT-2 inhibitors and GLP-1 receptor agonists in reducin

188 iflozin, or empagliflozin without any use of SGLT-2 inhibitors during the prior 365 days.

189 tified recommendations concerning the use of SGLT-2 inhibitors or GLP-1 receptor agonists in adults w

190 iabetes mellitus, and were initiating use of SGLT-2 inhibitors versus DPP-4 inhibitors (cohort 1) or

191 Greater use of SGLT-2i and GLP-1RA will improve outcomes for patients w

192 Use of SGLT-2i, versus other glucose-lowering drugs, was associ

193 After adjustment, new users of SGLT-2 inhibitors were associated with 73% lower mortali

194 208 757 new users of SGLT-2 inhibitors were matched by using time-conditional

195 trol for potential confounding, new users of SGLT-2i were 1:1 propensity score (PS)-matched to new us

196 New users of SGLT-2is were 1:1 PS-matched to new users of a DPP-4i (n

197 ergometer workload (25 W) after 13 weeks of SGLT-2i treatment (25 mg once daily) compared with place

198 nctional studies, define the architecture of SGLTs, uncover the mechanism of substrate binding and se

199 insights into the multifaceted functions of SGLTs.

200 started GLP-1 receptor agonists and added on SGLT-2 inhibitors, and the second included 8942 patients

201 apy with GLP-1 agonists compared to those on SGLT-2 inhibitors.

202 ients on GLP-1 agonists compared to those on SGLT-2 inhibitors.

203 5 received DPP-4i (no exposure to GLP-1RA or SGLT-2i); and 1 954 353 received other ADDs.

204 d notably with or without use of GLP-1RAs or SGLT-2is and regardless of pretrial mealtime insulin reg

205 .9%), DPP-4 inhibitors (n=34 464 ,45.5%), or SGLT-2 inhibitors (n=15 582, 20.6%).

206 ound drug, either GLP-1 receptor agonists or SGLT-2 inhibitors, depending on the cohort.

207 t, excluding insulin, with GLP-1 agonists or SGLT-2 inhibitors.

208 ematocrit was observed in EMPA-REG and other SGLT-2 inhibitors studies.

209 tal structure of the Vibrio parahaemolyticus SGLT showed that residue Gln(428) interacts directly wit

210 Based on the treated population, SGLT-2i use was associated with a significantly lower ri

211 scribed GLP-1R agonists and those prescribed SGLT-2 (sodium-glucose cotransporter-2) inhibitors, DPP-

212 GLP-1 receptor agonists and probably SGLT-2 inhibitors and tirzepatide improve quality of lif

213 n by sodium glucose co-transporter proteins (SGLTs) in the kidneys is a relatively new strategy for t

214 he phytochemical phlorizin, the prototypical SGLT inhibitor, as well as in patients with familial ren

215 In cohort 1, persons newly receiving SGLT-2 inhibitors had 61 severe UTI events (incidence ra

216 In cohort 2, those receiving SGLT-2 inhibitors had 73 events (IR, 2.15), compared wit

217 8 [10.7] years; 57.8% male), those receiving SGLT-2 inhibitors had a lower incidence of serious liver

218 Patients who were receiving SGLT-2 inhibitors plus furosemide and spironolactone wer

219 published online in October 2018 recommends SGLT inhibitors as preferred add-on therapy for patients

220 38 MAPK and caspase-1 activation and reduced SGLT-2 expression.

221 Additionally, Phlorizin-sensitive SGLT transporters and NHE3 interact functionally in the

222 Seven SGLT isoforms (SGLT1 to 6 and sodium-myoinositol cotrans

223 s, moderate to high certainty evidence shows SGLT-2 inhibitors (relative to placebo or standard care

224 k, moderate to high certainty evidence shows SGLT-2 inhibitors probably reduce all-cause mortality an

225 k, moderate to high certainty evidence shows SGLT-2 inhibitors result in similar benefits across outc

226 he second included 8942 patients who started SGLT-2 inhibitors and added on GLP-1 receptor agonists.

227 Starting SGLT-2 inhibitor treatment was associated with a lower r

228 or CKD: Weak recommendation against starting SGLT-2 inhibitors or GLP-1 receptor agonists.* More than

229 CVD or CKD: Weak recommendation for starting SGLT-2 inhibitors and GLP-1 receptor agonists.* Establis

230 CVD or CKD: Weak recommendation for starting SGLT-2 inhibitors and weak against starting GLP-1 recept

231 and CKD: Strong recommendation for starting SGLT-2 inhibitors and weak recommendation for starting G

232 D outcomes: Weak recommendation for starting SGLT-2 inhibitors rather than GLP-1 receptor agonists.

233 1 receptor agonists reduce non-fatal stroke; SGLT-2 inhibitors are superior to other drugs in reducin

234 sporters (GLUTs), sodium-glucose symporters (SGLTs), and SWEETs.

235 agonists reduced non-fatal stroke more than SGLT-2 inhibitors (which appeared to have no effect).

236 The present study demonstrates that SGLT-2 inhibitors are effective as adjunct therapy to in

237 rticipants) of benefits and harms found that SGLT-2 inhibitors and GLP-1 receptor agonists generally

238 emulation study of a target trial found that SGLT-2 inhibitors were more effective than sulfonylureas

239 diuretic therapy, the findings suggest that SGLT-2 inhibitor use was associated with a lower inciden

240 Low certainty evidence suggested that SGLT-2 inhibitors and GLP-1 receptor agonists might lowe

241 Our study suggested that SGLT-2 inhibitors is associated with lower mortality com

242 es yielded opposite effects, suggesting that SGLT-2 inhibitors might be as effective as, or potential

243 Compared with GLP-1 receptor agonists, the SGLT-2 inhibitor-GLP-1 receptor agonist combination was

244 were identified in the GLP-1 cohort and the SGLT-2 inhibitor cohort after propensity score matching.

245 tly observed across individual agents in the SGLT-2 inhibitor (canagliflozin, dapagliflozin, empaglif

246 associations among individual agents in the SGLT-2 inhibitor and GLP-1 receptor agonist classes sugg

247 iated with a reduced risk among those in the SGLT-2 inhibitors group.

248 2%, and 5% of the total exposure time in the SGLT-2i class, respectively.

249 The risk of incident AF was lower in the SGLT-2i group than the matched DPP-4i group or the match

250 cterized sodium/glucose cotransporter of the SGLT family.

251 sporter (vSGLT) is a bacterial member of the SGLT gene family.

252 on of the selectivity characteristics of the SGLT isoforms (SGLT1 transports both glucose and galacto

253 To assess the efficacy and safety of the SGLT-2 inhibitors as adjunct therapy to insulin in T1DM,

254 sting SGLT activity by sodium removal or the SGLT inhibitor phloridzin.

255 in the GLP-1 agonist cohort compared to the SGLT-2 inhibitor cohort.

256 in the GLP-1 agonist cohort compared to the SGLT-2 inhibitor cohort.

257 of DME in the GLP-1 agonist group versus the SGLT-2 inhibitor group.

258 Several members within the SGLT family transport key metabolites other than glucose

259 bgroups, and across single agents within the SGLT-2i and GLP-1RA classes.

260 Therefore, SGLT-2 became a highly interesting therapeutic target, c

261 Thus, SGLT-2i and GLP-1RA are associated with a lower risk of

262 cacy and safety of semaglutide when added to SGLT-2 inhibitor therapy in patients with inadequately c

263 Adding semaglutide to SGLT-2 inhibitor therapy significantly improves glycaemi

264 e warranted to conclude their superiority to SGLT-2 inhibitors.

265 ibitor of the sodium-glucose co-transporter (SGLT), a component of a hypothesized alternate glucose-s

266 ne (BBM) via a sodium-dependent transporter, SGLT, and exit across the basolateral membrane via facil

267 Sodium-glucose co-transporters (SGLTs) in the kidneys play a pivotal role in glucose rea

268 (GLUTs) and sodium-glucose co-transporters (SGLTs) may also function as glucose sensors independent

269 or sodium-dependent glucose co-transporters (SGLTs), which have recently been shown to be distributed

270 ance of sodium-coupled glucose transporters (SGLTs) and facilitative glucose transporters (GLUTs) in

271 Sodium-dependent glucose transporters (SGLTs) couple a downhill Na(+) ion gradient to actively

272 , the sodium-dependent glucose transporters (SGLTs), in pancreatic and prostate adenocarcinomas, and

273 active sodium-coupled glucose transporters (SGLTs).

274 rization and excitation by glucose-triggered SGLT activity may ensure that GE neurones continue to se

275 d by GLUTs; and (iii) measurement of in vivo SGLT activity in mouse models of pancreatic and prostate

276 of 1233 patients with AKD patients who were SGLT-2i users confirmed the observed beneficial outcomes

277 ce interval, CI]: 0.88 [0.81-0.96]), whereas SGLT-2 inhibitors showed a tendency (RR [95% CI]: 0.91 [

278 ose uptake into the brain and liver, whereas SGLTs are important in glucose recovery in the kidney.

279 However, it remains to be determined whether SGLT-mediated glucose uptake regulates NHE3-mediated NaH

280 associated with similar HbA1C levels, while SGLT-2 inhibitors offered the lowest odds of hypoglycemi

281 The benefits associated with SGLT-2 inhibitor for patients with nephrolithiasis in th

282 pants) of benefits and harms associated with SGLT-2 inhibitors in adults with CKD with or without typ

283 aluating the potential risks associated with SGLT-2i use for older adults outside of randomized clini

284 Notably, the risk reduction associated with SGLT-2is remained significant even among patients withou

285 Compared with SGLT-2 inhibitor use, GLP-1 receptor agonist use was not

286 ng GLP-1R agonists (reference) compared with SGLT-2 inhibitors (incidence rate ratio [IRR], 2.98; 95%

287 Compared with SGLT-2 inhibitors (n = 366,067), GLP-1 RAs (n = 259,929)

288 significant difference in MACE compared with SGLT-2 inhibitors (RR [95% CI]: 0.97 [0.85-1.09]).

289 using GLP-1 receptor agonists compared with SGLT-2 inhibitors within 30 days of the procedure; howev

290 Compared with SGLT-2 inhibitors, the GLP-1 receptor agonist-SGLT-2 inh

291 and insulin at all 3 years and compared with SGLT-2i only after 3 years of use (3 years: metformin re

292 nital mycotic infections were increased with SGLT-2 inhibitors.

293 c to drug class (eg, genital infections with SGLT-2 inhibitors, severe gastrointestinal adverse event

294 the increased haematocrit levels noted with SGLT-2 inhibitors?

295 Conservation in Heart Failure Patients With SGLT-2 Inhibitor Treatment [DAPA-Shuttle1]; NCT04080518)

296 Conservation in Heart Failure Patients With SGLT-2 Inhibitor Treatment) was a single-center, double-

297 d be prevented across the LVEF spectrum with SGLT-2 inhibitors over 3 years, of which 232 589 (95% CI

298 risk of amputation in patients treated with SGLT-2i and incretins was not higher compared with other

299 is large multinational study, treatment with SGLT-2i versus other glucose-lowering drugs was associat

300 relative to placebo or standard care without SGLT-2 inhibitors) decrease all-cause and cardiovascular