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1 (depolarizing) sodium-glucose cotransporter (SGLT).
2  but requires sodium/glucose cotransporters (SGLT).
3 iated by sodium-glucose cotransporters(2,3) (SGLTs).
4 l tubules via sodium-glucose cotransporters (SGLTs).
5  active sodium-coupled glucose transporters (SGLTs).
6 es in sodium-dependent sugar cotransporters (SGLTs).
7  insights into the multifaceted functions of SGLTs.
8 ctivities of the Na(+)/glucose cotransporter SGLT-1 and GLUT2 were unaffected in LEPR-B-KO jejunum, w
9                The discovery that intestinal SGLT-1 inhibition can provide a novel opportunity to con
10                                              SGLT-1 protein expression was unaltered; however, HS inc
11 AMPKalpha2 and a rapid increase of the GLUT2/SGLT-1 protein ratio in the brush border membrane.
12            We determined levels of GLUT2 and SGLT-1 proteins and phosphorylation of AMPKalpha2 by imm
13 itors selectively directed to the intestinal SGLT-1 subtype as well as of dual SGLT-1/SGLT-2 inhibito
14  cells via the sodium glucose transporter 1 (SGLT-1) and glucose transporter 2 (GLUT2); various pepti
15 ut mice lacking sodium glucose tranporter-1 (SGLT-1) or the short chain fatty acid sensing receptor F
16  1 (PepT1), sodium/glucose co-transporter-1 (SGLT-1), potassium inwardly-rectifying channel, subfamil
17 intestinal SGLT-1 subtype as well as of dual SGLT-1/SGLT-2 inhibitors, representing a compelling stra
18 2 phosphorylation and modifying the ratio of SGLT-1:GLUT2.
19 se reuptake by sodium/glucose cotransporter (SGLT) 2 in the kidney, without affecting intestinal gluc
20 scribed GLP-1R agonists and those prescribed SGLT-2 (sodium-glucose cotransporter-2) inhibitors, DPP-
21                                   Therefore, SGLT-2 became a highly interesting therapeutic target, c
22 38 MAPK and caspase-1 activation and reduced SGLT-2 expression.
23 59.9 years; 63.6% female) and 18 537 used an SGLT-2 inhibitor (59.8 years; 63.7% female).
24 tly observed across individual agents in the SGLT-2 inhibitor (canagliflozin, dapagliflozin, empaglif
25  associations among individual agents in the SGLT-2 inhibitor and GLP-1 receptor agonist classes sugg
26 g in the risk of DKA among patients using an SGLT-2 inhibitor as compared with placebo or an active c
27  were identified in the GLP-1 cohort and the SGLT-2 inhibitor cohort after propensity score matching.
28  in the GLP-1 agonist cohort compared to the SGLT-2 inhibitor cohort.
29  in the GLP-1 agonist cohort compared to the SGLT-2 inhibitor cohort.
30 GLT-2 inhibitors, the GLP-1 receptor agonist-SGLT-2 inhibitor combination was associated with a 29% l
31 his cohort study, the GLP-1 receptor agonist-SGLT-2 inhibitor combination was associated with a lower
32 rately, comparing the GLP-1 receptor agonist-SGLT-2 inhibitor combination with the background drug, e
33                 The benefits associated with SGLT-2 inhibitor for patients with nephrolithiasis in th
34 of DME in the GLP-1 agonist group versus the SGLT-2 inhibitor group.
35                                              SGLT-2 inhibitor initiators showed higher risk of genita
36                             Initiation of an SGLT-2 inhibitor or glucagon-like peptide-1 (GLP-1) rece
37 red evidence regarding benefits and harms of SGLT-2 inhibitor therapy for adults with CKD over a five
38 F of 40% and less, optimal implementation of SGLT-2 inhibitor therapy for HF with LVEF more than 40%
39 cacy and safety of semaglutide when added to SGLT-2 inhibitor therapy in patients with inadequately c
40                        Adding semaglutide to SGLT-2 inhibitor therapy significantly improves glycaemi
41  nonsevere UTI events among those initiating SGLT-2 inhibitor therapy was similar to that among patie
42  Conservation in Heart Failure Patients With SGLT-2 Inhibitor Treatment [DAPA-Shuttle1]; NCT04080518)
43                                     Starting SGLT-2 inhibitor treatment was associated with a lower r
44  Conservation in Heart Failure Patients With SGLT-2 Inhibitor Treatment) was a single-center, double-
45 Existing antidiabetic medications, including SGLT-2 inhibitor treatment, were continued for the durat
46  diuretic therapy, the findings suggest that SGLT-2 inhibitor use was associated with a lower inciden
47                                 Furthermore, SGLT-2 inhibitor use was associated with a lower rate of
48                                Compared with SGLT-2 inhibitor use, GLP-1 receptor agonist use was not
49 pital admissions, or procedures, and when an SGLT-2 inhibitor was compared with a DPP-4 inhibitor (ra
50     In addition to randomised medication and SGLT-2 inhibitor, 216 (71.5%) patients were taking metfo
51 ong the 14 456 weighted patients who used an SGLT-2 inhibitor, compared with 853 events among the 587
52  benefits, harms, and burdens of starting an SGLT-2 inhibitor, incorporating the values and preferenc
53 ther a sulfonylurea, a thiazolidinedione, an SGLT-2 inhibitor, or a DPP-4 inhibitor to metformin to i
54 espite at least 90 days of treatment with an SGLT-2 inhibitor, were randomly assigned (1:1) to receiv
55   Compared with GLP-1 receptor agonists, the SGLT-2 inhibitor-GLP-1 receptor agonist combination was
56 ng GLP-1R agonists (reference) compared with SGLT-2 inhibitors (incidence rate ratio [IRR], 2.98; 95%
57                                Compared with SGLT-2 inhibitors (n = 366,067), GLP-1 RAs (n = 259,929)
58 .9%), DPP-4 inhibitors (n=34 464 ,45.5%), or SGLT-2 inhibitors (n=15 582, 20.6%).
59 s, moderate to high certainty evidence shows SGLT-2 inhibitors (relative to placebo or standard care
60 significant difference in MACE compared with SGLT-2 inhibitors (RR [95% CI]: 0.97 [0.85-1.09]).
61 nd complications, we recommend administering SGLT-2 inhibitors (strong recommendation in favour).Reco
62 nd complications, we recommend administering SGLT-2 inhibitors (strong recommendation in favour)4.
63  and complications, we suggest administering SGLT-2 inhibitors (weak recommendation in favour)2.
64  and complications, we suggest administering SGLT-2 inhibitors (weak recommendation in favour)3.
65  agonists reduced non-fatal stroke more than SGLT-2 inhibitors (which appeared to have no effect).
66 he second included 8942 patients who started SGLT-2 inhibitors and added on GLP-1 receptor agonists.
67                                              SGLT-2 inhibitors and GLP-1 receptor agonists are tradit
68                  These ancillary benefits of SGLT-2 inhibitors and GLP-1 receptor agonists further su
69 rticipants) of benefits and harms found that SGLT-2 inhibitors and GLP-1 receptor agonists generally
70          The study confirmed the benefits of SGLT-2 inhibitors and GLP-1 receptor agonists in reducin
71 ing the substantial benefits with the use of SGLT-2 inhibitors and GLP-1 receptor agonists in reducin
72        Low certainty evidence suggested that SGLT-2 inhibitors and GLP-1 receptor agonists might lowe
73                                 Benefits for SGLT-2 inhibitors and GLP-1 receptor agonists on the abs
74            In patients with type 2 diabetes, SGLT-2 inhibitors and GLP-1 receptor agonists reduced ca
75         All results refer to the addition of SGLT-2 inhibitors and GLP-1 receptor agonists to existin
76              In people with type 2 diabetes, SGLT-2 inhibitors and GLP-1 receptor agonists were assoc
77 CVD or CKD: Weak recommendation for starting SGLT-2 inhibitors and GLP-1 receptor agonists.* Establis
78 P-4 inhibitors, GLP-1 receptor agonists, and SGLT-2 inhibitors and increased with sulfonylureas, thia
79         GLP-1 receptor agonists and probably SGLT-2 inhibitors and tirzepatide improve quality of lif
80 CVD or CKD: Weak recommendation for starting SGLT-2 inhibitors and weak against starting GLP-1 recept
81  and CKD: Strong recommendation for starting SGLT-2 inhibitors and weak recommendation for starting G
82                                              SGLT-2 inhibitors are associated with little or no effec
83          The present study demonstrates that SGLT-2 inhibitors are effective as adjunct therapy to in
84  long-term studies focusing on GLP-1 RAs and SGLT-2 inhibitors are needed to validate these findings
85 1 receptor agonists reduce non-fatal stroke; SGLT-2 inhibitors are superior to other drugs in reducin
86     To assess the efficacy and safety of the SGLT-2 inhibitors as adjunct therapy to insulin in T1DM,
87  by recommending GLP-1 receptor agonists and SGLT-2 inhibitors as initial glucose-lowering therapy.
88   For some secondary endpoints, evidence for SGLT-2 inhibitors being more effective was lacking-the h
89                                              SGLT-2 inhibitors caused genital infection (high certain
90             This study found that individual SGLT-2 inhibitors demonstrated comparable cardiovascular
91                        Existing guidance for SGLT-2 inhibitors does not account for the totality of c
92 iflozin, or empagliflozin without any use of SGLT-2 inhibitors during the prior 365 days.
93             Compared with the control group, SGLT-2 inhibitors group had significantly reduced fastin
94 iated with a reduced risk among those in the SGLT-2 inhibitors group.
95 etic ketoacidosis (DKA) (n = 16) was seen in SGLT-2 inhibitors group.
96         In cohort 1, persons newly receiving SGLT-2 inhibitors had 61 severe UTI events (incidence ra
97                 In cohort 2, those receiving SGLT-2 inhibitors had 73 events (IR, 2.15), compared wit
98 8 [10.7] years; 57.8% male), those receiving SGLT-2 inhibitors had a lower incidence of serious liver
99                                              SGLT-2 inhibitors had reduced hazards of hospital admiss
100 d background therapy, specific GLP-1 RAs and SGLT-2 inhibitors have a favorable effect on certain car
101                                              SGLT-2 inhibitors have demonstrated cardiovascular and k
102 pants) of benefits and harms associated with SGLT-2 inhibitors in adults with CKD with or without typ
103 indings further suggest a potential role for SGLT-2 inhibitors in cirrhosis management.
104                The strong recommendation for SGLT-2 inhibitors in patients with CVD and CKD reflects
105   A meta-analysis was conducted on trials of SGLT-2 inhibitors in patients with T1DM on insulin thera
106         Regarding medication-specific harms, SGLT-2 inhibitors increase genital infections (odds rati
107                     Our study suggested that SGLT-2 inhibitors is associated with lower mortality com
108 es yielded opposite effects, suggesting that SGLT-2 inhibitors might be as effective as, or potential
109  associated with similar HbA1C levels, while SGLT-2 inhibitors offered the lowest odds of hypoglycemi
110 tified recommendations concerning the use of SGLT-2 inhibitors or GLP-1 receptor agonists in adults w
111 e or no evidence was found for the effect of SGLT-2 inhibitors or GLP-1 receptor agonists on limb amp
112       Randomised controlled trials comparing SGLT-2 inhibitors or GLP-1 receptor agonists with placeb
113  disease (CKD)): weak recommendation against SGLT-2 inhibitors or GLP-1 receptor agonists.* Moderate
114 or CKD: Weak recommendation against starting SGLT-2 inhibitors or GLP-1 receptor agonists.* More than
115 lications): weak recommendation in favour of SGLT-2 inhibitors or GLP-1 receptor agonists; and a weak
116 failure): strong recommendation in favour of SGLT-2 inhibitors or GLP-1 receptor agonists; and a weak
117 d be prevented across the LVEF spectrum with SGLT-2 inhibitors over 3 years, of which 232 589 (95% CI
118                  Patients who were receiving SGLT-2 inhibitors plus furosemide and spironolactone wer
119 k, moderate to high certainty evidence shows SGLT-2 inhibitors probably reduce all-cause mortality an
120 D outcomes: Weak recommendation for starting SGLT-2 inhibitors rather than GLP-1 receptor agonists.
121 fferences were found between the two agents: SGLT-2 inhibitors reduced admission to hospital for hear
122 ative effectiveness and safety of individual SGLT-2 inhibitors remain unknown.
123 k, moderate to high certainty evidence shows SGLT-2 inhibitors result in similar benefits across outc
124 ce interval, CI]: 0.88 [0.81-0.96]), whereas SGLT-2 inhibitors showed a tendency (RR [95% CI]: 0.91 [
125 ematocrit was observed in EMPA-REG and other SGLT-2 inhibitors studies.
126 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
127 % 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
128 iabetes mellitus, and were initiating use of SGLT-2 inhibitors versus DPP-4 inhibitors (cohort 1) or
129 ylureas and -3.2 mmol/mol (-4.6 to -1.8) for SGLT-2 inhibitors versus DPP-4 inhibitors.
130 % confidence interval (CI) -3.7 to -1.3) for SGLT-2 inhibitors versus sulfonylureas and -3.2 mmol/mol
131               After adjustment, new users of SGLT-2 inhibitors were associated with 73% lower mortali
132                                              SGLT-2 inhibitors were associated with an almost 3-fold
133              Compared with DPP-4 inhibitors, SGLT-2 inhibitors were associated with an increased risk
134          Alpha-blockers, antipsychotics, and SGLT-2 inhibitors were associated with up to 2-fold incr
135                                   Effects of SGLT-2 inhibitors were interpreted in absolute terms app
136                         208 757 new users of SGLT-2 inhibitors were matched by using time-conditional
137                                              SGLT-2 inhibitors were more effective than DPP-4 inhibit
138                                              SGLT-2 inhibitors were more effective than sulfonylureas
139 emulation study of a target trial found that SGLT-2 inhibitors were more effective than sulfonylureas
140                                 In addition, SGLT-2 inhibitors were not associated with increased ris
141 Rs) with 95% CIs of DKA comparing receipt of SGLT-2 inhibitors with receipt of DPP-4 inhibitors, whic
142  using GLP-1 receptor agonists compared with SGLT-2 inhibitors within 30 days of the procedure; howev
143 relative to placebo or standard care without SGLT-2 inhibitors) decrease all-cause and cardiovascular
144 started GLP-1 receptor agonists and added on SGLT-2 inhibitors, and the second included 8942 patients
145 ound drug, either GLP-1 receptor agonists or SGLT-2 inhibitors, depending on the cohort.
146 abetic prescription on or after May 1, 2016: SGLT-2 inhibitors, DPP-4 inhibitors, GLP-1 agonists or o
147                         Absolute benefits of SGLT-2 inhibitors, GLP-1 receptor agonists, and finereno
148 medications for adults with type 2 diabetes (SGLT-2 inhibitors, GLP-1 receptor agonists, finerenone a
149 s with type 2 diabetes, including effects of SGLT-2 inhibitors, GLP-1RAs, finerenone and tirzepatide.
150 nal SGLT-1 subtype as well as of dual SGLT-1/SGLT-2 inhibitors, representing a compelling strategy to
151 c to drug class (eg, genital infections with SGLT-2 inhibitors, severe gastrointestinal adverse event
152                                Compared with SGLT-2 inhibitors, the GLP-1 receptor agonist-SGLT-2 inh
153   Among users of GLP-1 receptor agonists and SGLT-2 inhibitors, the weighted risk per 1000 people was
154 apy with GLP-1 agonists compared to those on SGLT-2 inhibitors.
155 age, 66 years) with HF would be eligible for SGLT-2 inhibitors.
156 tion when compared with DPP-4 inhibitors and SGLT-2 inhibitors.
157 t, excluding insulin, with GLP-1 agonists or SGLT-2 inhibitors.
158 ients on GLP-1 agonists compared to those on SGLT-2 inhibitors.
159 e warranted to conclude their superiority to SGLT-2 inhibitors.
160 nital mycotic infections were increased with SGLT-2 inhibitors.
161  the increased haematocrit levels noted with SGLT-2 inhibitors?
162                                              SGLT-2 overexpression in diabetic patients contributes s
163 ition of the sodium glucose cotransporter 2 (SGLT-2) in the kidney and has been shown to lead to a ma
164  and chronic sodium-glucose cotransporter 2 (SGLT-2) inhibition increases endogenous glucose producti
165 expansion of sodium-glucose cotransporter-2 (SGLT-2) inhibitor use in patients with heart failure (HF
166              Sodium-glucose cotransporter 2 (SGLT-2) inhibitors (gliflozins) represent the most recen
167              Sodium glucose cotransporter-2 (SGLT-2) inhibitors (odds ratio 0.88, 95% confidence inte
168              Sodium/glucose cotransporter 2 (SGLT-2) inhibitors are a novel class of antidiabetic age
169              Sodium-glucose cotransporter-2 (SGLT-2) inhibitors could increase the risk for diabetic
170 GLP-1 RAs) and sodium-glucose cotransporter (SGLT-2) inhibitors have been shown to prevent CVD in T2D
171            Sodium-glucose co-transporters 2 (SGLT-2) inhibitors have emerged as a novel antidiabetic
172  (UTIs) with sodium-glucose cotransporter-2 (SGLT-2) inhibitors have reported conflicting findings.
173              Sodium-glucose cotransporter 2 (SGLT-2) inhibitors improve outcomes in patients with typ
174 nd safety of sodium-glucose cotransporter 2 (SGLT-2) inhibitors is mainly from placebo-controlled tri
175              Sodium-glucose cotransporter-2 (SGLT-2) inhibitors reduced heart failure hospitalization
176  benefits of sodium-glucose cotransporter-2 (SGLT-2) inhibitors, glucagon-like peptide-1 receptor ago
177              Sodium-glucose cotransporter 2 (SGLT-2) inhibitors, primarily used in diabetes and heart
178 gonists with sodium-glucose cotransporter-2 (SGLT-2) inhibitors.
179 ibitors, and sodium-glucose cotransporter-2 (SGLT-2) inhibitors.
180 aPi-IIa) and sodium-glucose cotransporter-2 (SGLT-2).
181  peptidase-4 inhibitors (10.6% versus 7.5%), SGLT-2i (10.3% versus 8.1%), GLP-1 RA (3.4% versus 2.4%)
182                                        Thus, SGLT-2i and GLP-1RA are associated with a lower risk of
183 bgroups, and across single agents within the SGLT-2i and GLP-1RA classes.
184               In order to increase adoption, SGLT-2i and GLP-1RA must be reframed as primarily cardio
185 eally positioned to share responsibility for SGLT-2i and GLP-1RA treatment with primary care provider
186                                         Both SGLT-2i and GLP-1RA were first studied as glucose-loweri
187                               Greater use of SGLT-2i and GLP-1RA will improve outcomes for patients w
188 limb amputations (LLAs) were similar between SGLT-2i and incretins [95% confidence interval (CI) rang
189  risk of amputation in patients treated with SGLT-2i and incretins was not higher compared with other
190 2%, and 5% of the total exposure time in the SGLT-2i class, respectively.
191 s are seen in real-world practice and across SGLT-2i class.
192                                              SGLT-2i combination therapies improved glucose homeostas
193 ere used to generate hazard ratios (HRs) for SGLT-2i compared with DPP-4i and GLP-1RA and Kaplan-Meie
194     The risk of incident AF was lower in the SGLT-2i group than the matched DPP-4i group or the match
195 ve AMD compared with metformin, insulin, and SGLT-2i in logistic regression models.
196                         Propensity score for SGLT-2i initiation was used to match treatment groups.
197 and insulin at all 3 years and compared with SGLT-2i only after 3 years of use (3 years: metformin re
198 ike peptide 1 receptor agonists [GLP-1RA, no SGLT-2i or dipeptidyl peptidase-4 inhibitor (DPP-4i) exp
199 e 309 056 patients newly initiated on either SGLT-2i or other glucose-lowering drugs (154 528 patient
200 -0.41; insulin RR = 0.28; 95% CI, 0.15-0.46; SGLT-2i RR = 0.42; 95% CI, 0.22-0.74).
201  ergometer workload (25 W) after 13 weeks of SGLT-2i treatment (25 mg once daily) compared with place
202 aluating the potential risks associated with SGLT-2i use for older adults outside of randomized clini
203                      However, the results of SGLT-2i use in primary prevention of atrial fibrillation
204             Based on the treated population, SGLT-2i use was associated with a significantly lower ri
205 e matching, the absolute differences between SGLT-2i users and nonusers for incidence of mortality, M
206 were calculated to compare the risks between SGLT-2i users and nonusers, representing the mean treatm
207 was no difference in the risk of fracture in SGLT-2i users compared with DPP-4i users (HR, 0.90; 95%
208  of 1233 patients with AKD patients who were SGLT-2i users confirmed the observed beneficial outcomes
209       After 3-way matching, 45 889 (73%) new SGLT-2i users were matched to new users of DPP-4i and GL
210 , 5319 individuals (2.3%) were identified as SGLT-2i users.
211 ors of study drugs, 62 454 patients were new SGLT-2i users.
212 and death in patients newly initiated on any SGLT-2i versus other glucose-lowering drugs in 6 countri
213 is large multinational study, treatment with SGLT-2i versus other glucose-lowering drugs was associat
214  3-4 and type 2 diabetes who newly initiated SGLT-2i vs. DPP-4i (141671 patients), GLP-1RA vs. DPP-4i
215 ) (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
216 s), GLP-1RA vs. DPP-4i (159545 patients) and SGLT-2i vs. GLP-1RA (93033 patients) were included.
217  analyses, the risk of LLA was not higher in SGLT-2i vs. GLP1-RA [hazard ratio (HR) (95% CI): 0.88 (0
218                                Initiation of SGLT-2i was associated with a lower risk of hyperkalemia
219 this study suggest that the initiation of an SGLT-2i was associated with a reduced risk of incident A
220 is nationwide Medicare cohort, initiating an SGLT-2i was not associated with an increased risk of fra
221 trol for potential confounding, new users of SGLT-2i were 1:1 propensity score (PS)-matched to new us
222 e sodium glucose cotransporter-2 inhibitors (SGLT-2i) and glucagon-like peptide-1 receptor agonists (
223 he sodium-glucose cotransporter-2 inhibitor (SGLT-2i) empagliflozin in patients with type 2 diabetes
224 he sodium-glucose cotransporter 2 inhibitor (SGLT-2i) empagliflozin significantly reduces cardiovascu
225 odium-glucose transport protein 2 inhibitor (SGLT-2i) users, 286 066 metformin users, and 164 361 ins
226 f sodium-glucose cotransporter-2 inhibitors (SGLT-2i), glucagon-like peptide-1 receptor agonists (GLP
227 h sodium/glucose cotransporter 2 inhibition (SGLT-2i).
228 5 received DPP-4i (no exposure to GLP-1RA or SGLT-2i); and 1 954 353 received other ADDs.
229                              New users of an SGLT-2i, DPP-4i, or GLP-1RA without a previous fracture
230                                       Use of SGLT-2i, versus other glucose-lowering drugs, was associ
231 ium-glucose cotransporter type-2 inhibitors (SGLT-2i; no exposure to incretins); 149 826 received glu
232 d notably with or without use of GLP-1RAs or SGLT-2is and regardless of pretrial mealtime insulin reg
233  with nonuse, underscoring the importance of SGLT-2is in care after acute kidney injury.
234 findings emphasize the potential benefits of SGLT-2is in managing AKD and mitigating the risks of maj
235  Notably, the risk reduction associated with SGLT-2is remained significant even among patients withou
236 h type 2 diabetes and AKD, administration of SGLT-2is was associated with a significant reduction in
237                                 New users of SGLT-2is were 1:1 PS-matched to new users of a DPP-4i (n
238                  However, the association of SGLT-2is with outcomes among patients with type 2 diabet
239 um-glucose cotransport protein 2 inhibitors (SGLT-2is) have demonstrated associations with positive k
240   Sodium-glucose cotransporter-2 inhibitors (SGLT-2is) have demonstrated many cardiovascular and kidn
241 dium-glucose transport protein 2 inhibitors (SGLT-2is).
242 d-glucopyranoside (Me-4FDG), a substrate for SGLTs; 4-deoxy-4-[F-18]-fluoro-d-glucose (4-FDG), a subs
243 ibitor of the sodium-glucose co-transporter (SGLT), a component of a hypothesized alternate glucose-s
244         Notably, pharmacologic inhibition of SGLT activity by Phlorizin produced a marked inhibition
245 ose and alpha-MDG are abolished by arresting SGLT activity by sodium removal or the SGLT inhibitor ph
246 d by GLUTs; and (iii) measurement of in vivo SGLT activity in mouse models of pancreatic and prostate
247 rization and excitation by glucose-triggered SGLT activity may ensure that GE neurones continue to se
248 8]-fluoro-d-glucose (4-FDG), a substrate for SGLTs and GLUTs; and 2-deoxy-2-[F-18]-fluoro-d-glucose (
249 e transport by vSGLT is similar to mammalian SGLTs and that further studies on vSGLT will provide nov
250 ance of sodium-coupled glucose transporters (SGLTs) and facilitative glucose transporters (GLUTs) in
251 sporters (GLUTs), sodium-glucose symporters (SGLTs), and SWEETs.
252 ne (BBM) via a sodium-dependent transporter, SGLT, and exit across the basolateral membrane via facil
253 ose uptake into the brain and liver, whereas SGLTs are important in glucose recovery in the kidney.
254                                              SGLTs are responsible for active glucose and galactose a
255 diated by the sodium/glucose cotransporters (Sglts) because the Sglt inhibitor phlorizin could reduce
256 is framework holds significance not only for SGLTs but also for other transporters and channels.
257       Sodium-dependent glucose transporters (SGLTs) couple a downhill Na(+) ion gradient to actively
258  tested whether glucose transporters (GLUTs, SGLTs) destined for the plasma membrane are active durin
259 , with potential applicability to the larger SGLT family of important sodium:solute cotransporters.
260                   Several members within the SGLT family transport key metabolites other than glucose
261 cterized sodium/glucose cotransporter of the SGLT family.
262  selective for sodium-glucose cotransporter (SGLT) family members and the sweet taste receptor were t
263 sporter (vSGLT) is a bacterial member of the SGLT gene family.
264 gut and renal sodium-glucose cotransporters (SGLTs) has been proposed as a novel therapeutic approach
265 the sodium-dependent glucose cotransporters (SGLT) have appeared as viable therapeutics to control bl
266 work provides further support for the use of SGLT imaging in the investigation of the role of SGLT tr
267 ice aiming to evaluate the role of GLUTs and SGLTs in controlling glucose distribution and utilizatio
268 e potentially substantial role of functional SGLTs in glucose transport and use.
269 e potentially substantial role of functional SGLTs in glucose transport and utilization.
270 n by sodium glucose co-transporter proteins (SGLTs) in the kidneys is a relatively new strategy for t
271              Sodium-glucose co-transporters (SGLTs) in the kidneys play a pivotal role in glucose rea
272 , the sodium-dependent glucose transporters (SGLTs), in pancreatic and prostate adenocarcinomas, and
273                                              SGLT inhibition might also be considered in conjunction
274 ty, were either pair fed or treated with the Sglt inhibitor phloridzin, the insulin-sensitizer rosigl
275 sting SGLT activity by sodium removal or the SGLT inhibitor phloridzin.
276 m/glucose cotransporters (Sglts) because the Sglt inhibitor phlorizin could reduce STZ uptake in the
277 spite raising basal glucagon concentrations, SGLT inhibitor treatment did not restore the impaired gl
278 he phytochemical phlorizin, the prototypical SGLT inhibitor, as well as in patients with familial ren
279  published online in October 2018 recommends SGLT inhibitors as preferred add-on therapy for patients
280 shown the blood glucose-lowering efficacy of SGLT inhibitors in type 2 diabetes when administered as
281 e insulin-independent mechanism of action of SGLT inhibitors seems to offer durable glucose-lowering
282                Sodium-glucose cotransporter (SGLT) inhibitors increase glucagon concentrations.
283                                        Seven SGLT isoforms (SGLT1 to 6 and sodium-myoinositol cotrans
284 on of the selectivity characteristics of the SGLT isoforms (SGLT1 transports both glucose and galacto
285 ether with Western blot analysis revealed an SGLT-like protein.
286  (GLUTs) and sodium-glucose co-transporters (SGLTs) may also function as glucose sensors independent
287                                              SGLT-mediated glucose transport can be estimated using a
288                                              SGLT-mediated glucose transport can be estimated using a
289 of this study was to determine the effect of SGLT-mediated glucose uptake on NHE3 activity in the ren
290 However, it remains to be determined whether SGLT-mediated glucose uptake regulates NHE3-mediated NaH
291  The two main sodium-glucose cotransporters (SGLTs), SGLT1 and SGLT2, provide new therapeutic targets
292 tal structure of the Vibrio parahaemolyticus SGLT showed that residue Gln(428) interacts directly wit
293 ose uptake in fresh isolated tumors using an SGLT-specific radioactive glucose analog, alpha-methyl-4
294            Additionally, Phlorizin-sensitive SGLT transporters and NHE3 interact functionally in the
295 ure of glucose utilization via both GLUT and SGLT transporters in health and disease stages.
296 ure of glucose utilization via both GLUT and SGLT transporters in health and disease states.
297  imaging in the investigation of the role of SGLT transporters in human physiology and diseases such
298  with those for alpha-glucosidases and human SGLT type 1 (hSGLT1), a well characterized sodium/glucos
299 nctional studies, define the architecture of SGLTs, uncover the mechanism of substrate binding and se
300                The Na-glucose cotransporter (SGLT) was the first transporter ever to be cloned.
301 or sodium-dependent glucose co-transporters (SGLTs), which have recently been shown to be distributed
302 for sodium-dependent glucose cotransporters (SGLTs), which have recently been shown to be distributed

 
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