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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
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
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-
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.
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
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
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)
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
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%
59 s, moderate to high certainty evidence shows SGLT-2 inhibitors (relative to placebo or standard care
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.
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.
69 rticipants) of benefits and harms found that SGLT-2 inhibitors and GLP-1 receptor agonists generally
71 ing the substantial benefits with the use of SGLT-2 inhibitors and GLP-1 receptor agonists in reducin
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
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
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
98 8 [10.7] years; 57.8% male), those receiving SGLT-2 inhibitors had a lower incidence of serious liver
100 d background therapy, specific GLP-1 RAs and SGLT-2 inhibitors have a favorable effect on certain car
102 pants) of benefits and harms associated with SGLT-2 inhibitors in adults with CKD with or without typ
105 A meta-analysis was conducted on trials of SGLT-2 inhibitors in patients with T1DM on insulin thera
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
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
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
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 [
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
130 % confidence interval (CI) -3.7 to -1.3) for SGLT-2 inhibitors versus sulfonylureas and -3.2 mmol/mol
139 emulation study of a target trial found that SGLT-2 inhibitors were more effective than sulfonylureas
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
146 abetic prescription on or after May 1, 2016: SGLT-2 inhibitors, DPP-4 inhibitors, GLP-1 agonists or o
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
153 Among users of GLP-1 receptor agonists and SGLT-2 inhibitors, the weighted risk per 1000 people was
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
170 GLP-1 RAs) and sodium-glucose cotransporter (SGLT-2) inhibitors have been shown to prevent CVD in T2D
172 (UTIs) with sodium-glucose cotransporter-2 (SGLT-2) inhibitors have reported conflicting findings.
174 nd safety of sodium-glucose cotransporter 2 (SGLT-2) inhibitors is mainly from placebo-controlled tri
176 benefits of sodium-glucose cotransporter-2 (SGLT-2) inhibitors, glucagon-like peptide-1 receptor ago
181 peptidase-4 inhibitors (10.6% versus 7.5%), SGLT-2i (10.3% versus 8.1%), GLP-1 RA (3.4% versus 2.4%)
185 eally positioned to share responsibility for SGLT-2i and GLP-1RA treatment with primary care provider
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
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
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
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
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
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
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
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
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
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
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
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
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.
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.
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.
262 selective for sodium-glucose cotransporter (SGLT) family members and the sweet taste receptor were t
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
270 n by sodium glucose co-transporter proteins (SGLTs) in the kidneys is a relatively new strategy for t
272 , the sodium-dependent glucose transporters (SGLTs), in pancreatic and prostate adenocarcinomas, and
274 ty, were either pair fed or treated with the Sglt inhibitor phloridzin, the insulin-sensitizer rosigl
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
284 on of the selectivity characteristics of the SGLT isoforms (SGLT1 transports both glucose and galacto
286 (GLUTs) and sodium-glucose co-transporters (SGLTs) may also function as glucose sensors independent
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
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
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