ライフサイエンスコーパス: SGLT2

1 al sodium-dependent glucose cotransporter 2 (SGLT2).

2 otransporter sodium glucose cotransporter 2 (SGLT2).

3 bsorption is sodium-glucose cotransporter-2 (SGLT2).

4 re potent and highly selective inhibitors of SGLT2.

5 ng the sodium-dependent glucose transporter (SGLT2), a protein targeted pharmacologically to increase

6 Significant stimulation of SGLT2 activity also occurred in opossum kidney cells cot

7 e-associated protein (MAP17), that increased SGLT2 activity in RNA-injected Xenopus oocytes by two or

8 e inhibited the Na+-glucose cotransporter 2 (SGLT2) along the proximal convoluted tubule.

9 sodium/glucose cotransporter 2-encoding gene SGLT2 (also known as SLC5A2) in the family that segregat

10 d in opossum kidney cells cotransfected with SGLT2 and MAP17.

11 sodium by the sodium-glucose cotransporters SGLT2 and SGLT1 in the proximal tubule.

12 sorption of glucose in the kidney along with SGLT2 and SGLT1.

13 ing that this nephron segment also expresses SGLT2 and that the kidneys and intestine show significan

14 e injected i.v. into wild-type, Sglt1(-/-) , Sglt2(-/-) and Glut2(-/-) mice and their dynamic whole-b

15 alpha and of the glucose transporters SGLT1, SGLT2, and GLUT1.

16 Reabsorption is primarily handled by SGLT2, and SGLT2-specific inhibitors, including dapaglif

17 hrough the Na(+)-coupled glucose transporter SGLT2, and specific inhibitors of SGLT2 are now availabl

18 We propose that SSTR or SGLT2 antagonists should be considered as adjuncts to in

19 T2 expression at the protein level, the anti-SGLT2 antibody was first rigorously evaluated for specif

20 ransporter SGLT2, and specific inhibitors of SGLT2 are now available to patients with diabetes to inc

21 nhibitors of sodium-glucose cotransporter 2 (SGLT2) are a novel class of antidiabetes drugs, and memb

22 xperiments showed that NHE3 colocalizes with SGLT2 but not SGLT1 in the rat renal proximal tubule.

23 ent without any identifiable mutation in the SGLT2 coding gene (SLC5A2) displayed homozygosity for a

24 (i) immunohistochemical mapping of SGLT1 and SGLT2 distribution in tumors; (ii) measurement of glucos

25 nhibitors of sodium-glucose cotransporter 2 (SGLT2), exploratory results have suggested that such dru

26 esized that interindividual heterogeneity in SGLT2 expression and regulation may affect glucagon secr

27 To determine heterogeneity of SGLT2 expression at the protein level, the anti-SGLT2 an

28 gliflozin treatment had no effect on Agt and Sglt2 expression in HK-2 and in RPTCs of wild-type mice

29 ycosuria through modulation of renal Agt and Sglt2 expression in mice, respectively.

30 SPR gRNA up-regulated AGT and down-regulated SGLT2 expression.

31 ed, whereas sodium-glucose co-transporter 2 (Sglt2) expression was down-regulated in RPTs of both mal

32 Instead, in the kidneys, SGLT2 functionally interacts with the sodium-hydrogen ex

33 rter protein sodium-glucose cotransporter 2 (SGLT2) has emerged as a promising way to control blood g

34 In conclusion, SGLT2-I treatment improves impaired glucose effectivenes

35 l hyperglycemic-hyperinsulinemic clamp after SGLT2-I treatment, E-Rd increased by normalizing glucose

36 a sodium-glucose cotransporter 2 inhibitor (SGLT2-I) for 7 days.

37 The most potent inhibitors of SGLT2 (IC50 = 9-23 nM) were considerably weaker inhibito

38 a is freely filtered by the kidney, binds to SGLT2 in the apical membranes of the early proximal tubu

39 The sodium glucose cotransporter SGLT2 in the early proximal tubule is the major pathway

40 by inhibiting sodium glucose transporter 2 (SGLT2) in proximal tubular cells.

41 Inhibition of SGLT2 increases urinary glucose and calorie excretion, t

42 SGLT2 inhibition also is associated with an acute, dose-

43 SGLT2 inhibition also prevented inflammation via inhibit

44 Interestingly, SGLT2 inhibition also results in increased endogenous gl

45 We therefore studied whether SGLT2 inhibition altered cardiac oxidative substrate con

46 he metabolic adaptations that are induced by SGLT2 inhibition are similar to those observed in aestiv

47 Taken together, these data support SGLT2 inhibition as a viable insulin-independent treatme

48 We found that SGLT2 inhibition caused marked decreases in systolic blo

49 In conclusion, SGLT2 inhibition did not affect myocardial FFA uptake, b

50 The RECEDE-CHF trial (SGLT2 Inhibition in Combination With Diuretics in Heart

51 s are now investigating the potential use of SGLT2 inhibition in patients who have HF with and withou

52 wering, we also explore the potential use of SGLT2 inhibition in patients without T2D with HF or at r

53 otential mechanisms of beneficial effects of SGLT2 inhibition in the progression of diabetic renal di

54 SGLT2 inhibition is also associated with preservation of

55 However, glucosuria induction following SGLT2 inhibition is associated with a paradoxical increa

56 Although SGLT2 inhibition may have potential application beyond T

57 In summary, our study showed that SGLT2 inhibition modulates renal lipid metabolism and in

58 Effective SGLT2 inhibition needs adequate glomerular filtration an

59 -Reduced, we aimed to estimate the effect of SGLT2 inhibition on fatal and non-fatal heart failure ev

60 Furthermore, the effect of SGLT2 inhibition on renal lipid content and inflammation

61 provide a unique insight into the effects of SGLT2 inhibition on whole body metabolism.

62 SGLT2 inhibition prevented renal lipid accumulation via

63 SGLT2 inhibition promotes natriuresis and osmotic diures

64 Furthermore, the effects of SGLT2 inhibition to promote ketoacidosis are independent

65 SGLT2 inhibition was accompanied by a 26% relative reduc

66 SGLT2 inhibition with dapagliflozin leads to a sustained

67 abetes mellitus and coronary artery disease, SGLT2 inhibition with empagliflozin was associated with

68 n in patients with type 2 diabetes following SGLT2 inhibition, despite an overall decrease in fasting

69 may influence the glucose-lowering effect of SGLT2 inhibition, we subjected 12 patients with type 2 d

70 fuel switches that occur during therapeutic SGLT2 inhibition, we suggest that SGLT2 inhibitors induc

71 motic diuresis does not occur in humans with SGLT2 inhibition.

72 dition that is considered a natural model of SGLT2 inhibition.

73 slets of these donors to glucose sensing and SGLT2 inhibition.

74 partially to the cardioprotective effect of SGLT2 inhibition.

75 ortance for the glucose-lowering property of SGLT2 inhibition.

76 Sodium glucose cotransporter 2 (SGLT2) inhibition is a novel and promising treatment for

77 showed that sodium-glucose co-transporter-2 (SGLT2) inhibition reduced the combined risk of cardiovas

78 Sodium-glucose cotransporter 2 (SGLT2) inhibition reduces cardiovascular morbidity and m

79 rate was lower among patients prescribed an SGLT2 inhibitor (4.9 events per 1000 person-years) than

80 Matched SGLT2 inhibitor (n=22 830) and other glucose-lowering dr

81 Here we show that the SGLT2 inhibitor (SGLT2i) dapagliflozin promotes ketoacid

82 ation use of an ARNI, beta blocker, MRA, and SGLT2 inhibitor as a new therapeutic standard.

83 The Sglt2 inhibitor canagliflozin treatment had no effect on

84 e report analyses of renal outcomes with the SGLT2 inhibitor dapagliflozin in the DECLARE-TIMI 58 car

85 Here, we investigate the effect of the SGLT2 inhibitor dapagliflozin on haematocrit, red blood

86 n 58) studied the efficacy and safety of the SGLT2 inhibitor dapagliflozin versus placebo in 17 160 p

87 the GLP-1 receptor agonist exenatide and the SGLT2 inhibitor dapagliflozin with exenatide or dapaglif

88 blood pressure and glycaemic effects of the SGLT2 inhibitor dapagliflozin with placebo in patients w

89 These data indicate that SGLT2 inhibitor elicits direct tubular effects in non-di

90 The mechanisms by which the SGLT2 inhibitor empagliflozin increases LDL cholesterol

91 In summary, the glucose-lowering SGLT2 inhibitor empagliflozin, used for type 2 diabetes,

92 94% of the total SGLT2 inhibitor exposure time was for use of dapaglifloz

93 iven by findings for empagliflozin (the only SGLT2 inhibitor for which data from a dedicated long-ter

94 Adults with type 2 diabetes prescribed an SGLT2 inhibitor had a lower rate of gout than those pres

95 We treated db/db mice with a selective SGLT2 inhibitor JNJ 39933673.

96 Our aim was to study the effects of SGLT2 inhibitor on circulating ZAG and ADI in nT2DM.

97 abetes mellitus who were newly prescribed an SGLT2 inhibitor or a GLP1 agonist.

98 Rather, patients on SGLT2 inhibitor therapy adjust to the reduction in energ

99 the crucial role for selecting patients for SGLT2 inhibitor therapy and highlight several crucial qu

100 Moreover, SGLT2 inhibitor therapy induces serious adverse events,

101 tes and a broad cardiovascular risk profile, SGLT2 inhibitor use was associated with reduced cardiova

102 Each SGLT2 inhibitor user was matched with three users of oth

103 ons with type 2 diabetes newly prescribed an SGLT2 inhibitor were 1:1 propensity score matched to pat

104 el glucose lowering agent, empagliflozin, an SGLT2 inhibitor which targets the kidney to block glucos

105 P-1 receptor agonist) with canagliflozin (an SGLT2 inhibitor) in patients with type 2 diabetes.

106 ogical therapy (ARNI, beta blocker, MRA, and SGLT2 inhibitor) versus conventional therapy (ACE inhibi

107 2 years after the FDA's first approval of an SGLT2 inhibitor, although the phenomenon had been known

108 ey disease to receive canagliflozin, an oral SGLT2 inhibitor, at a dose of 100 mg daily or placebo.

109 thod is demonstrated by the synthesis of the SGLT2 inhibitor, canagliflozin (1a), from commercially a

110 hod was demonstrated by the synthesis of the SGLT2 inhibitor, canagliflozin.

111 the efficacy and safety of canagliflozin, an SGLT2 inhibitor, with glimepiride in patients with type

112 e discovery of a highly selective and potent SGLT2 inhibitor.

113 ucose with a sodium-glucose cotransporter 2 (SGLT2) inhibitor could improve insulin-mediated tissue g

114 hypoglycemic sodium-glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin and the insulin sensitize

115 onse to the sodium-glucose co-transporter 2 (SGLT2) inhibitor dapagliflozin, which has been shown to

116 The sodium glucose cotransporter 2 (SGLT2) inhibitor empagliflozin promotes osmotic diuresis

117 nt with the sodium-glucose co-transporter-2 (SGLT2) inhibitor empagliflozin reduced albuminuria in pa

118 iflozin, the sodium-glucose cotransporter 2 (SGLT2) inhibitor, on renal hemodynamics and tubular func

119 gliflozin, a sodium glucose cotransporter 2 (SGLT2) inhibitor.

120 Time to onset after initiation of SGLT2-inhibitor therapy ranged from 5 days to 49 months.

121 tify other possible mechanisms of benefit of SGLT2-inhibitor therapy.

122 nital tract infections were more common with SGLT2 inhibitors (odds ratios, 1.42 [CI, 1.06 to 1.90] a

123 kely than White individuals to be prescribed SGLT2 inhibitors (OR 0.50, 95% CI 0.39-0.65; p < 0.001)

124 Unlike other agents, SGLT2 inhibitors act on the kidney to promote urinary gl

125 tes mellitus and chronic heart failure), but SGLT2 inhibitors activate SIRT1/PGC-1alpha/FGF21 signali

126 These data suggest net protection of SGLT2 inhibitors against cardiovascular outcomes and dea

127 ecause of their unique glycosuric mechanism, SGLT2 inhibitors also reduce weight.

128 SGLT2 inhibitors also reduced end-stage kidney disease (

129 way, sodium-related physiological effects of SGLT2 inhibitors and clinical correlates of natriuresis,

130 e on the cardiorenal protective effects with SGLT2 inhibitors and GLP-1 receptor agonists in patients

131 Patients were divided into new users of SGLT2 inhibitors and new users of other glucose-lowering

132 onsistent with data from clinical studies on SGLT2 inhibitors and provide a rationale for the mode of

133 iven to the balance of benefits and harms of SGLT2 inhibitors and risk mitigation strategies.

134 hanism underlying the cardiorenal effects of SGLT2 inhibitors and summarizes clinical trial evidence

135 summarize the key pharmacodynamic effects of SGLT2 inhibitors and the clinical evidence that support

136 ntify significant differences between use of SGLT2 inhibitors and use of other glucose-lowering drugs

137 SGLT2 inhibitors are antihyperglycemic drugs that protec

138 clinical trials, large clinical trials with SGLT2 inhibitors are now investigating the potential use

139 SGLT2 inhibitors are proximal tubule and osmotic diureti

140 he way towards the development of carbasugar SGLT2 inhibitors as potential antidiabetic/antitumor age

141 SGLT2 inhibitors attenuate the proximal reabsorption of

142 55 unique cases of FG in patients receiving SGLT2 inhibitors between 1 March 2013 and 31 January 201

143 e adenocarcinomas, and provide evidence that SGLT2 inhibitors block glucose uptake and reduce tumor g

144 synthetic route towards some small-molecule SGLT2 inhibitors by a chemo- and diastereospecific palla

145 We therefore investigated whether SGLT2 inhibitors could also reduce the risk of AF/AFL.

146 r government regulators nor manufacturers of SGLT2 inhibitors evinced an awareness of this extensive

147 However, maximal doses of SGLT2 inhibitors fail to inhibit >50% of the filtered gl

148 idence and safety data related to the use of SGLT2 inhibitors for cardiovascular and renal protection

149 1.73 m(2) To clarify and support the role of SGLT2 inhibitors for treatment of T2DM and CKD, the Nati

150 However, the clinical usage of carbasugar SGLT2 inhibitors has been underexplored, due to the leng

151 s may not be limited to diabetes management: SGLT2 inhibitors have also shown therapeutic promise in

152 The first SGLT2 inhibitors have been approved as a new class of an

153 t of SGLT2 to prevent renal glucose wasting, SGLT2 inhibitors have been developed to treat diabetes a

154 Preclinical studies and clinical trials of SGLT2 inhibitors have consistently demonstrated reductio

155 ar outcome trials in patients with diabetes, SGLT2 inhibitors improve cardiovascular and renal outcom

156 SGLT2 inhibitors improve glomerular hemodynamic function

157 However, SGLT2 inhibitors in clinical development inhibit only 30

158 rmacokinetic and pharmacodynamic profiles of SGLT2 inhibitors in clinical trials and examine possible

159 en done to assess the efficacy and safety of SGLT2 inhibitors in combination with insulin therapy in

160 The benefits of SGLT2 inhibitors in heart failure may be mediated by the

161 ce that support the rationale for the use of SGLT2 inhibitors in patients with HF who have T2D.

162 rong rationale to expect benefit from use of SGLT2 inhibitors in patients with type 2 diabetes at hig

163 ls designed to demonstrate the CVD safety of SGLT2 inhibitors in type 2 diabetes mellitus (T2DM), con

164 Important risks of SGLT2 inhibitors include euglycemic ketoacidosis, genita

165 herapeutic SGLT2 inhibition, we suggest that SGLT2 inhibitors induce aestivation-like metabolic patte

166 produced, it is important to understand why SGLT2 inhibitors inhibit <50% of the filtered glucose lo

167 Treatment with SGLT2 inhibitors is distinguished by 2 intriguing featur

168 SGLT2 inhibitors lower glomerular capillary hypertension

169 In particular, SGLT2 inhibitors lower risk of congestive heart failure,

170 ide decrease in environmental nutrients, but SGLT2 inhibitors may also upregulate SIRT1, PGC-1alpha,

171 ketogenic nutrient deprivation signaling by SGLT2 inhibitors may explain their cardioprotective effe

172 ure and diabetic glomerular hyperfiltration, SGLT2 inhibitors may induce protective effects on the ki

173 SGLT2 inhibitors may mimic systemic hypoxia and stimulat

174 ome evidence that the proportional effect of SGLT2 inhibitors might attenuate with declining kidney f

175 SGLT2 inhibitors might modulate glucose influx into rena

176 ociated ketosis and the ketogenic effects of SGLT2 inhibitors occur almost entirely independent of gl

177 We aimed to establish the effects of SGLT2 inhibitors on cardiovascular events, death, and sa

178 large-scale trials assessing the effects of SGLT2 inhibitors on cardiovascular outcomes in patients

179 y physiology predicts the salutary effect of SGLT2 inhibitors on hard renal outcomes, as shown in lar

180 Observations: The beneficial effect of SGLT2 inhibitors on heart failure cannot be explained by

181 w and meta-analysis to assess the effects of SGLT2 inhibitors on major kidney outcomes in patients wi

182 nately, these benefits are not without risk: SGLT2 inhibitors predispose to euglycemic ketoacidosis i

183 ucose-dependent and -independent mechanisms: SGLT2 inhibitors prevent both hyper- and hypoglycemia, w

184 ut not Sglt2-knockout mice, and injection of SGLT2 inhibitors prevented this binding.

185 If SGLT2 inhibitors protect the kidneys by reducing albumin

186 SGLT2 inhibitors protected against the risk of major adv

187 SGLT2 inhibitors provide multiple benefits, including de

188 Compared with other agents, SGLT2 inhibitors reduced body weight (mean difference, -

189 SGLT2 inhibitors reduced the risk of dialysis, transplan

190 ponsible for the cardioprotective effects of SGLT2 inhibitors remain incompletely understood.

191 SGLT2 inhibitors reverse this maladaptive signaling by t

192 SGLT2 inhibitors should be used when possible by people

193 SGLT2 inhibitors substantially reduced the risk of dialy

194 Additional mechanisms of SGLT2 inhibitors that might be beneficial include a redu

195 , cardiovascular or kidney outcome trials of SGLT2 inhibitors that reported effects on major kidney o

196 e substantive evidence supporting the use of SGLT2 inhibitors to prevent major kidney outcomes in peo

197 a signaling; this can explain the effects of SGLT2 inhibitors to promote ketonemia and erythrocytosis

198 fraction may be mitigated by the actions of SGLT2 inhibitors to reduce blood pressure, body weight,

199 ute importantly to the consistent benefit of SGLT2 inhibitors to slow the deterioration in glomerular

200 ecursors was synthesized and tested as SGLT1/SGLT2 inhibitors using a cell-based fluorescence assay o

201 ular mortality and morbidity in new users of SGLT2 inhibitors versus new users of other glucose-lower

202 ed with other glucose-lowering drugs, use of SGLT2 inhibitors was associated with a decreased risk of

203 ed with other glucose-lowering drugs, use of SGLT2 inhibitors was associated with decreased risk of c

204 However, the safety and efficacy of SGLT2 inhibitors when initiated soon after an episode of

205 estions about the risk-to-benefit profile of SGLT2 inhibitors when used as adjunctive therapy in pati

206 In patients with heart failure, SGLT2 inhibitors will likely be coprescribed with a loop

207 nical practice guidelines now recommend that SGLT2 inhibitors with proven cardiovascular benefit be p

208 ealed the unexpected SAR of these carbasugar SGLT2 inhibitors, and enabled the discovery of a highly

209 ge pancreatic and prostate cancers, and that SGLT2 inhibitors, currently in use for treating diabetes

210 ynthetic route towards some novel carbasugar SGLT2 inhibitors, featuring an underexploited, regiosele

211 summarizes proposed mechanisms of action for SGLT2 inhibitors, integrates these data with results of

212 discovery of two highly selective and potent SGLT2 inhibitors, thereby paving the way towards the dev

213 Recent developments include SGLT2 inhibitors, vericiguat, and transcatheter mitral v

214 ach of the beneficial and harmful effects of SGLT2 inhibitors-with the exception of their effect to l

215 ntified safety concern in patients receiving SGLT2 inhibitors.

216 of the potential cardiovascular benefits of SGLT2 inhibitors.

217 f ongoing cardiovascular outcome trials with SGLT2 inhibitors.

218 accounts for the high kidney specificity of SGLT2 inhibitors.

219 of canagliflozin therapy compared with other SGLT2 inhibitors.

220 ts), which provided data for seven different SGLT2 inhibitors.

221 o interindividual differences in response to SGLT2 inhibitors.

222 ecretion by human alpha-cells in response to SGLT2 inhibitors.

223 met our inclusion criteria, assessing three SGLT2 inhibitors: empagliflozin (EMPA-REG OUTCOME), cana

224 ; p < 0.01), sodium-glucose cotransporter-2 (SGLT2) inhibitors (OR 0.68, 95% CI 0.58-0.79; p < 0.001)

225 Sodium-glucose transport protein 2 (SGLT2) inhibitors are a class of anti-diabetic agents; h

226 Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a new class of antidiabetic drugs.

227 Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a newer class of antihyperglycemic

228 g effects of sodium-glucose cotransporter 2 (SGLT2) inhibitors are already established, guidance is n

229 Sodium-glucose cotransporter 2 (SGLT2) inhibitors are effective antidiabetic therapies i

230 Carbasugar sodium-glucose cotransporter 2 (SGLT2) inhibitors are highly promising drug candidates f

231 agonists and sodium-glucose cotransporter-2 (SGLT2) inhibitors are increasingly used as second-line a

232 2 diabetes, sodium-glucose cotransporter-2 (SGLT2) inhibitors are known to reduce glucose concentrat

233 Sodium-glucose cotransporter 2 (SGLT2) inhibitors are the most recently approved class o

234 istration of sodium-glucose cotransporter-2 (SGLT2) inhibitors could lead to ketoacidosis in patients

235 rofile, the sodium-glucose co-transporter-2 (SGLT2) inhibitors empagliflozin and canagliflozin have b

236 Use of sodium-glucose cotransporter-2 (SGLT2) inhibitors has been associated with Fournier gang

237 re recently, sodium-glucose cotransporter 2 (SGLT2) inhibitors have further improved disease outcomes

238 treated with sodium glucose cotransporter 2 (SGLT2) inhibitors have improved cardiovascular (CV) outc

239 Sodium-glucose co-transporter-2 (SGLT2) inhibitors have several beneficial effects in pat

240 Sodium-glucose co-transporter-2 (SGLT2) inhibitors have shown beneficial effects on renal

241 Sodium-glucose cotransporter 2 (SGLT2) inhibitors improve glycaemia in patients with typ

242 implicating sodium-glucose cotransporter 2 (SGLT2) inhibitors in glucagon secretion by pancreatic al

243 gon release, sodium-glucose cotransporter 2 (SGLT2) inhibitors induce stimulation of endogenous gluco

244 Sodium-glucose cotransporter 2 (SGLT2) inhibitors lower glycemia by enhancing urinary gl

245 e effects of sodium-glucose cotransporter-2 (SGLT2) inhibitors may be related primarily to enhanced S

246 effects of sodium-glucose co-transporter-2 (SGLT2) inhibitors on kidney failure, particularly the ne

247 Sodium-glucose cotransporter-2 (SGLT2) inhibitors prevent glucose reabsorption and lower

248 gonists and sodium-glucose co-transporter-2 (SGLT2) inhibitors reduce glycaemia and weight, and impro

249 Sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce the risk of hospitalization for

250 Sodium/glucose cotransporter 2 (SGLT2) inhibitors were developed to lower blood glucose

251 own that the sodium-glucose cotransporter-2 (SGLT2) inhibitors, a newer generation of antihyperglycem

252 a) agonists, sodium glucose cotransporter 2 (SGLT2) inhibitors, and farnesoid X receptor (FXR) agonis

253 Sodium-glucose cotransporter-2 (SGLT2) inhibitors, including empagliflozin, dapagliflozi

254 ering agents-sodium-glucose cotransporter 2 (SGLT2) inhibitors-has been reported to decrease the risk

255 eported with sodium-glucose cotransporter 2 (SGLT2) inhibitors.

256 [ARNIs], and sodium/glucose cotransporter 2 [SGLT2] inhibitors) reduce mortality in patients with hea

257 gonists, and sodium-glucose cotransporter 2 [SGLT2] inhibitors) using routinely available clinical fe

258 nfirm the physiologic relevance of the MAP17-SGLT2 interaction, we studied a cohort of 60 individuals

259 We found that SGLT2 is functionally expressed in pancreatic and prosta

260 their cardioprotective effects, even though SGLT2 is not expressed in the heart.

261 It is widely accepted that SGLT2 is responsible for >80% of the reabsorption of the

262 SGLT2 is responsible for reabsorption of most of the glu

263 SGLT2 knockout mice were protected from HFD-induced hype

264 Here, we used a SGLT2 knockout mouse to investigate the effect of increa

265 nd wild-type and Sglt1-knockout mice but not Sglt2-knockout mice, and injection of SGLT2 inhibitors p

266 tion of the sodium-glucose co-transporter 2 (SGLT2) leads to substantial loss of energy (in the form

267 stantial amounts of carbohydrate into urine, SGLT2-mediated glycosuria results in a progressive shift

268 It generally is accepted that SGLT2 mediates 90% of renal glucose reabsorption.

269 inary excretion of Me-4FDG in Sglt1(-/-) and Sglt2(-/-) mice.

270 into the heart of wild-type, Sglt1(-/-) and Sglt2(-/-) mice.

271 SGLT1 and SGLT2 mRNA and protein expression decreased under the th

272 We have found that the expression of SGLT2 mRNA and protein is increased in renal biopsies fr

273 The first aim of this study was to determine SGLT2 mRNA and protein levels in human and animal models

274 dient-dependent glucose transporter protein (SGLT2) mRNA and protein expression data reported in the

275 he index family, with simultaneous MCT12 and SGLT2 mutation.

276 inhibitor of sodium-glucose co-tranporter-2; SGLT2) or when the action of secreted somatostatin is pr

277 Selective inhibition of SGLT2 over SGLT1 is critical for minimizing adverse side

278 ata suggest that heterogeneous expression of SGLT2 protein and variability in glucagon secretory resp

279 on with MAP17 did not change the quantity of SGLT2 protein at the cell surface in either cell type.

280 sis of 665 human islets showed a significant SGLT2 protein colocalization with glucagon but not with

281 ts revealed a high interdonor variability of SGLT2 protein expression.

282 t to db-db mice that had no changes in renal SGLT2 protein expression.

283 proach to map the distribution of functional SGLT2 proteins in rodents using positron emission tomogr

284 um-glucose cotransporters (SGLTs), SGLT1 and SGLT2, provide new therapeutic targets to reduce hypergl

285 ition of the sodium-glucose cotransporter 2 (SGLT2) reduces plasma glucose by limiting glucose absorp

286 asses of antihyperglycemic agents, including SGLT2 (sodium glucose cotransporter 2) inhibitors and GL

287 SGLT2 (sodium-glucose cotransporter 2) inhibitors have b

288 SGLT2 (sodium-glucose cotransporter 2) inhibitors lower

289 The cardioprotective effects of SGLT2 (sodium-glucose cotransporter 2) inhibitors may be

290 SGLT2 (sodium-glucose cotransporter-2) inhibitors improv

291 bsorption is primarily handled by SGLT2, and SGLT2-specific inhibitors, including dapagliflozin, cana

292 itor of sodium-glucose cotransporter type 2 (SGLT2) that is marketed in United States, Europe, and ma

293 ted cellular glucose uptake independently of SGLT2, this did not account for AMPK activation.

294 inhibitor of the kidney glucose transporter SGLT2 to lower their blood level of 1,5-anhydroglucitol

295 Based on the impact of SGLT2 to prevent renal glucose wasting, SGLT2 inhibitors

296 en overexpressed in HEK293 cells, the mutant SGLT2 transporter did not efficiently translocate to the

297 The high density of functional SGLT2 transporters detected in the apical membrane of th

298 d controlled trials assessing the effects of SGLT2 treatment compared with controls.

299 ession of the glucose transporters SGLT1 and SGLT2 under hypoxic conditions which implies a possible

300 asis for a more thorough characterization of SGLT2 which would include the possible effects of its in