ライフサイエンスコーパス: glucose-lowering

1 ng considered as potential new approaches to glucose lowering.

2 n of HPA axis suppression to leptin-mediated glucose lowering.

3 equivocal cardiovascular risk reduction with glucose lowering.

4 F-1R(+/-) mice had enhanced insulin-mediated glucose lowering.

5 Concomitant with its effect on glucose lowering, 11g also caused a 50% reduction in ins

6 eased by SGLT2i, possibly compromising their glucose-lowering ability.

7 Unlike GLP-1, exendin-4 has a prolonged glucose-lowering action in vivo.

8 PP-4 inhibitors that may contribute to their glucose-lowering action.

9 nsulin analog designed to exhibit protracted glucose-lowering action.

10 vated receptors with insulin-sensitizing and glucose-lowering actions and favorable effects on lipid

11 that coapplication of metformin enhances the glucose-lowering actions of SGLT2I by restraining endoge

12 tidyl peptidase-4 (DPP-4) inhibition and its glucose-lowering actions were tested after an oral gluco

13 uconeogenesis, which might contribute to its glucose-lowering actions.

14 logues exhibited potent cellular and in vivo glucose-lowering activities, thus achieving proof-of-con

15 al for use as dietary ingredients with serum glucose lowering activity in humans.

16 The most potent compounds have glucose-lowering activity at doses as low as 0.01 mg/kg.

17 azolidinediones has shown potent and durable glucose-lowering activity in patients with type 2 diabet

18 We also show that the glucose-lowering activity of FGF1 can be dissociated fro

19 Its potent glucose-lowering activity results from enhanced insulin

20 activation, which likely contributes to the glucose-lowering activity.

21 that once daily administration of the novel glucose lowering agent, empagliflozin, an SGLT2 inhibito

22 f can trigger cardiac dysfunction and that a glucose-lowering agent can correct it.

23 ients aged 18 with a prescription of an oral glucose-lowering agent or GLP-1 receptor agonist were in

24 etes, there are little data to determine the glucose-lowering agent(s) of choice in KTR.

25 erapy to combination therapy with oral blood-glucose lowering agents, and 20 005 who had changed to r

26 sulin (2000-2007) after poor control on oral glucose-lowering agents (OGLD) were grouped by the numbe

27 The emergence of new glucose-lowering agents - sodium-glucose cotransporter 2

28 s, comorbidities, treatment (the use of oral glucose-lowering agents and insulin), control (hyperglyc

29 o treat diabetes and are the newest class of glucose-lowering agents approved in the United States.

30 meglimin is the first in a new class of oral glucose-lowering agents currently in phase 2b developmen

31 ally greater use of drop-in cardioprotective glucose-lowering agents demonstrated blunting of signal

32 Commonly used oral glucose-lowering agents include sulfonylureas, which are

33 ials comparing metformin treatment with oral glucose-lowering agents other than insulin.

34 d analyzing cardiovascular outcome trials of glucose-lowering agents under the premise of glycemic eq

35 d the District of Columbia, the use ratio of glucose-lowering agents with known cardiovascular benefi

36 ical study of Medicaid prescription rates of glucose-lowering agents with known cardiovascular benefi

37 cokinase is one of the promising targets for glucose-lowering agents, and the development of GK activ

38 Compared to diabetics treated with other glucose-lowering agents, MET-treated patients had better

39 Although initially considered to be only glucose-lowering agents, the effects of SGLT2i have expa

40 Only 1 class of glucose-lowering agents-sodium-glucose cotransporter 2 (

41 The sustained glucose lowering and insulin sensitization attributed to

42 in the newly introduced EOB mouse model for glucose lowering and lipid/cholesterol homeostasis.

43 magnitude of risk dependent on the method of glucose lowering and, potentially, weight gain.

44 The hormone leptin has profound glucose-lowering and insulin-sensitizing action in type

45 ngs indicate that, in addition to its potent glucose-lowering and insulin-sensitizing effects, rFGF1

46 more, [dA(2)]GLP-1/GcG elicited a protracted glucose-lowering and insulinotropic effect in high fat-f

47 The SYNCHRONY study aimed to establish the glucose-lowering and lipid-modifying effects, and safety

48 of them were on diet treatment, 33% on oral glucose lowering, and 40% on insulin treatment.

49 psychotic-like, anxiolytic, weight-reducing, glucose-lowering, and wake-promoting activities.

50 The mechanisms underlying glucose lowering appear to differ; leucine stimulated in

51 Comparison of the magnitude of glucose lowering as a function of serum drug concentrati

52 rrent treatment strategies rely on intensive glucose lowering as well as strict blood pressure contro

53 betes Trial previously showed that intensive glucose lowering, as compared with standard therapy, did

54 mpaired oral glucose tolerance and a limited glucose-lowering benefit from exendin-4, suggesting that

55 mice at 25-50 mg/kg resulted in rapid (3 h) glucose lowering by 100-120 mg/dl (P < 0.001) without pr

56 these results suggest that the mechanism of glucose lowering by compound A was via inhibition of G-6

57 lucagon-like peptide 1 (GLP-1) secretion, on glucose lowering by dipeptidyl peptidase-4 (DPP-4) inhib

58 To determine whether glucose lowering by empagliflozin accelerates atheroscle

59 In summary, plasma glucose lowering by empagliflozin improves plaque regres

60 er, these results demonstrate that effective glucose lowering by G6PT1 inhibitors can be achieved wit

61 ss surgery, and mechanistic studies indicate glucose lowering by these procedures is driven by GLP-1.

62 We aimed to assess the extent to which glucose lowering by various drugs or strategies increase

63 The dose-dependent glucose-lowering capacity was profound regardless of whe

64 Finally, evidence that the blood glucose-lowering compound AZD7545 disrupts the interacti

65 Matched SGLT2 inhibitor (n=22 830) and other glucose-lowering drug (n=68 490) groups were well balanc

66 lic syndrome-related conditions, such as any glucose-lowering drug (PR = 0.28; 95% CI = 0.25-0.31) an

67 In recent clinical trials, new-generation glucose-lowering drug classes, the sodium-glucose co-tra

68 Increasing evidence suggest that the glucose-lowering drug metformin exerts a valuable anti-s

69 mmol/L; and diabetes >/=7.0 mmol/L or use of glucose-lowering drug).

70 the cardioprotective effect of exenatide, a glucose-lowering drug, is dependent on hyperglycemia rem

71 GRADE directly compared second line glucose lowering drugs for their ability to lower glycat

72 rkinson's disease of users of any other oral glucose lowering drugs.

73 s newly initiated on either SGLT-2i or other glucose-lowering drugs (154 528 patients in each treatme

74 ations between any of 9 available classes of glucose-lowering drugs (alone or in combination) and the

75 g of HbA1c concentrations by newly developed glucose-lowering drugs (alone or when added to other glu

76 led on stable daily doses of one or two oral glucose-lowering drugs (for 90 days or more before scree

77 2 consecutive HbA1c >=8.5% while on >=2 oral glucose-lowering drugs (OGLDs), with validation in anoth

78 o (n=2633), to be taken in addition to their glucose-lowering drugs and other medications.

79 Numerous glucose-lowering drugs are used to treat type 2 diabetes

80 GLP-1 RA were initially developed as glucose-lowering drugs because activation of the GLP-1 r

81 All patients who filled a prescription for glucose-lowering drugs between 2012 and 2015 were includ

82 r user was matched with three users of other glucose-lowering drugs by use of propensity scores.

83 nly a minor impact on microvascular disease; glucose-lowering drugs can delay conversion to diabetes,

84 een use of SGLT2 inhibitors and use of other glucose-lowering drugs for non-fatal myocardial infarcti

85 Comparative effectiveness of glucose-lowering drugs for type 2 diabetes: a systematic

86 Paradoxically, some glucose-lowering drugs have been shown to worsen heart f

87 that study the cardiovascular safety of new glucose-lowering drugs have improved our understanding o

88 newly initiated on any SGLT-2i versus other glucose-lowering drugs in 6 countries to determine if th

89 In particular, a patient's exposure to glucose-lowering drugs needs to be represented accuratel

90 sal absence in any large-scale trials of new glucose-lowering drugs of hospital admission for heart f

91 Some glucose-lowering drugs or strategies adversely affect ca

92 Few trials of glucose-lowering drugs or strategies in people with type

93 Overall, glucose-lowering drugs or strategies increased the risk

94 5, for large randomised controlled trials of glucose-lowering drugs or strategies that assessed cardi

95 Glucose-lowering drugs or strategies were associated wit

96 every 1.0 kg of weight gain associated with glucose-lowering drugs or strategies, there was a 7.1% (

97 ter 2 inhibitors (SGLT2i) are a new class of glucose-lowering drugs that act primarily in the kidney,

98 Incretin-based therapies are effective glucose-lowering drugs that have an increasing role in t

99 l study, treatment with SGLT-2i versus other glucose-lowering drugs was associated with a lower risk

100 rstanding of the current use and adoption of glucose-lowering drugs with cardiovascular benefit can i

101 9.5% (80 mmol/mol) on a maximum of two oral glucose-lowering drugs with or without basal insulin, an

102 istent with our findings, patients receiving glucose-lowering drugs with reno-protective properties h

103 lowering drugs (alone or when added to other glucose-lowering drugs) has been used, until recently, a

104 f SGLT2 inhibitors versus new users of other glucose-lowering drugs, in a population with a broad car

105 ticoagulants, blood pressure-lowering drugs, glucose-lowering drugs, or cholesterol-lowering drugs in

106 Compared with other glucose-lowering drugs, use of SGLT2 inhibitors was asso

107 Compared with other glucose-lowering drugs, use of SGLT2 inhibitors was asso

108 Use of SGLT-2i, versus other glucose-lowering drugs, was associated with lower rates

109 th SGLT-2i and GLP-1RA were first studied as glucose-lowering drugs, which may have impeded uptake by

110 ascular mortality compared with use of other glucose-lowering drugs-a finding consistent with the res

111 abetes limits the effectiveness of available glucose-lowering drugs.

112 in cardiovascular outcome trials of all new glucose-lowering drugs.

113 en largely excluded from clinical studies of glucose-lowering drugs.

114 orbidity or mortality compared with standard glucose-lowering drugs.

115 s of SGLT2 inhibitors and new users of other glucose-lowering drugs.

116 de-1 (GLP-1) receptor agonists are effective glucose-lowering drugs.

117 y high ligand efficiency that exhibit robust glucose lowering effect.

118 mice or ZDF rats, 46a,b showed a significant glucose-lowering effect and an increase in liver mass.

119 ve shown lower day-to-day variability in the glucose-lowering effect and lower rates of hypoglycemia

120 The glucose-lowering effect in mice is linked to activation

121 liver-specific protein prodrug to achieve a glucose-lowering effect in type 1 diabetic mice.

122 Lastly, the potent glucose-lowering effect of continuous intracerebroventri

123 Leptin mediated the glucose-lowering effect of early-life nutrition in women

124 logical dose of GLP-1 and fully reversed the glucose-lowering effect of GLP-1.

125 The surprising demonstration of a glucose-lowering effect of GMDeltaC in the background of

126 (HGU) contributes to the insulin-independent glucose-lowering effect of icv FGF1.

127 lin tolerance tests demonstrated an impaired glucose-lowering effect of insulin.

128 etic mouse model, compound 2 potentiated the glucose-lowering effect of insulin.

129 In contrast, the chronic glucose-lowering effect of leptin in a STZ-induced mouse

130 The additive glucose-lowering effect of MTZ together with metformin h

131 The glucose-lowering effect of nitrite was abolished in SIRT

132 t whether and how glucagon may influence the glucose-lowering effect of SGLT2 inhibition, we subjecte

133 nd thereby unveil a previously unappreciated glucose-lowering effect of small intestinal mTOR.

134 tivation of small intestinal mTOR blunts the glucose-lowering effect of the oral anti-diabetic agent

135 Its glucose-lowering effect results from decreased hepatic g

136 ProINS-Tf also demonstrated a better glucose-lowering effect than native insulin, even with a

137 ame doses of exendin-4 resulted in a similar glucose-lowering effect that persisted for >4 h.

138 with a concomitant increase in glucagon, the glucose-lowering effect was lost.

139 A protracted glucose-lowering effect was observed 24 h following GIP(

140 Moreover, it displays a potent blood glucose-lowering effect when administrated orally in nor

141 ctor (higher C-peptide level equaled greater glucose-lowering effect).

142 acid metabolism could be independent of its glucose-lowering effect, and direct FGFR activation in a

143 In contrast, despite insulin exerting a glucose-lowering effect, it failed to improve myocardial

144 rstanding the mechanism of metformin's blood glucose lowering effects and provide a new therapeutic t

145 Accumulating evidence of the beyond-glucose lowering effects of a gut-released hormone, gluc

146 Research on the non-glucose lowering effects of troglitazone and, to a lesse

147 Furthermore, we demonstrated in vivo plasma glucose lowering effects with compound 12d in ob/ob mice

148 importantly good OBAV leading to robust oral glucose lowering effects.

149 the highest blood (23.5%) and serum (21.4%) glucose-lowering effects (P<0.05).

150 catechin gallate (EGCG), is reported to have glucose-lowering effects in animals.

151 Liraglutide treatment provided beneficial glucose-lowering effects in both chow- and high-fat-fed

152 ve shown clinically relevant weight loss and glucose-lowering effects in people with overweight, obes

153 intake and body weight reduction as well as glucose-lowering effects mediated by glucose-dependent i

154 ing, inhibition of duodenal Ampk reduced the glucose-lowering effects of a bolus metformin treatment

155 With the GLP-1r antagonist, the glucose-lowering effects of DPP-4 inhibition were reduce

156 We compared the potency and duration of glucose-lowering effects of exendin-4 and GLP-1 in hyper

157 cose tolerance in DIO mice, and enhanced the glucose-lowering effects of exogenous insulin administra

158 or mediating the acute, insulin-independent, glucose-lowering effects of FGF1 and FGF19 in rodents wi

159 w-dose insulin (to control for the transient glucose-lowering effects of IGF-I) failed to affect the

160 ffects that include the ability to mimic the glucose-lowering effects of insulin.

161 In support of this, MTZ enhanced the glucose-lowering effects of metformin in db/db mice.

162 In Oct1-deficient mice the glucose-lowering effects of metformin were completely ab

163 reduction in hyperglycemia, confirming that glucose-lowering effects of ranolazine are due to the bl

164 th insulin-insensitive and refractory to the glucose-lowering effects of TZD and AICAR.

165 class of antihyperglycemic agents that exert glucose-lowering effects via glycosuric actions.

166 positively correlates with adiposity and has glucose-lowering effects, thus it may mediate the associ

167 cts of liraglutide, but are not required for glucose-lowering effects.

168 actions that cannot solely be attributed to glucose-lowering effects.

169 betic sulfonylurea drugs to exert their full glucose-lowering effects.

170 nce-weekly treatment with insulin icodec had glucose-lowering efficacy and a safety profile similar t

171 domised clinical trials have shown the blood glucose-lowering efficacy of SGLT inhibitors in type 2 d

172 on of SGLT inhibitors seems to offer durable glucose-lowering efficacy with low risk of clinically si

173 uction in risk of microvascular disease with glucose lowering has resulted in guidelines worldwide re

174 The blood glucose-lowering hormone glucagon-like peptide-1 (GLP-1)

175 years of intensive as compared with standard glucose lowering in 1791 military veterans with type 2 d

176 insulin tolerance test showed similar plasma glucose lowering in Aqp7-/- and Aqp7+/+ mice, with no ev

177 effective on insulin receptor activation or glucose lowering in db/db mice.

178 Exendin-4 dose-dependently accelerated glucose lowering in diabetic rhesus monkeys by up to 37%

179 iver FBPase (IC(50) = 55 nM) and significant glucose lowering in normal fasted rats.

180 otency of this series with ED(50) values for glucose lowering in ob/ob mice of 3.0 mg/kg/day.

181 l line and ultimately demonstrating dramatic glucose lowering in ob/ob mice, a diabetic animal model.

182 glycemic agents as demonstrated by assessing glucose lowering in ob/ob mice.

183 enal function, resulting in less potency for glucose lowering in patients with kidney disease.

184 ment with compound 2 resulted in significant glucose lowering in several rodent models of diabetes.

185 line improved hyperglycemia and resulted in glucose lowering in streptozotocin-diabetic SCID mice.

186 ammatory stimuli as a relevant mechanism for glucose lowering in the critically ill.

187 effects of pharmacologic or strategy-driven glucose-lowering interventions for adults with type 2 di

188 myocardial infarction (AMI), enthusiasm for glucose lowering is tempered, in part, by concerns of in

189 The firing-dependent glucose lowering mechanism within POMC neurons is a pote

190 Thus, a significant DPP-4-sensitive glucose-lowering mechanism contributes to glycemic contr

191 notherapy who continued treatment with their glucose-lowering medication after reaching reduced kidne

192 response system and stratified by background glucose-lowering medication and country of origin, to on

193 web-response system, with stratification by glucose-lowering medication and renal function, to recei

194 eb-response system, stratified by background glucose-lowering medication at screening, to oral semagl

195 nsulin initiation, increase in the number of glucose-lowering medication classes, incidence of 5 or m

196 ally significant in the sulfonylurea and any glucose-lowering medication groups, while the ACM HR and

197 re and, secondarily, leads to a reduction in glucose-lowering medication in participants with type 2

198 or drug classes where >5% open-label drop-in glucose-lowering medication occurred, and for glucagon-l

199 ucose (FPG) >= 7.0 mmol/L, documented use of glucose-lowering medication or self-reported diabetes, a

200 Diabetes healthcare provision and glucose-lowering medication use between 1 January 2012 a

201 iation and then stabilized; treatment with a glucose-lowering medication was initiated in 74 of 162 p

202 ) of <=6.0% [42 mmol/mol] without the use of glucose-lowering medication) at 1 year after surgery.

203 type 2 diabetes mellitus and were taking >=1 glucose-lowering medication, 35 018 patients (8.3%) were

204 .6% [95%-CI: 14.5%, 23.4%] reported using no glucose-lowering medication, 57.3% [95%-CI: 53.1%, 61.4%

205 Adults with ASCVD and T2D taking at least 1 glucose-lowering medication, had end-stage kidney diseas

206 onylurea (Met-SU) dual therapy, a third-line glucose-lowering medication-including dipeptidyl peptida

207 ormed on the secondary outcome reductions in glucose-lowering medication.

208 physician-diagnosed diabetes, or the use of glucose-lowering medication.

209 of type 2 diabetes and variable response to glucose lowering medications, current evidence on optima

210 e of DKD was stable despite increased use of glucose-lowering medications and renin-angiotensin-aldos

211 clinicians, receiving neither DM education, glucose-lowering medications at discharge, nor documenta

212 Baseline glucose-lowering medications for the 14 752 EXSCEL parti

213 Among persons with diabetes, use of glucose-lowering medications increased from 56.2% (95% C

214 Reduction in glucose-lowering medications occurred in 47 participants

215 Consequently, greater drop-in of open-label glucose-lowering medications occurred in the placebo gro

216 Other glucose-lowering medications or insulin could be added b

217 , there was limited evidence to suggest that glucose-lowering medications reduce the risk of cardiova

218 during hospitalization had been initiated on glucose-lowering medications versus 66% of those recogni

219 Association of glucose-lowering medications with cardiovascular outcome

220 with basal insulin, up to three non-insulin glucose-lowering medications without prandial insulin, a

221 baseline in terms of sex, use of concomitant glucose-lowering medications, and HbA(c) levels, and mor

222 ry end points, including body weight, use of glucose-lowering medications, and quality of life, also

223 ox model, adjusting for treatment with other glucose-lowering medications, as well as age, sex, ethni

224 idiabetic treatment or the initiation of new glucose-lowering medications, could be given to patients

225 azolidinediones, as compared with other oral glucose-lowering medications, in maintaining long-term g

226 The use of glucose-lowering medications, including insulin, was low

227 hemoglobin A(1c) of 6.5% or greater, use of glucose-lowering medications, or both (n = 1431 in NHANE

228 e comparative effectiveness of commonly used glucose-lowering medications, when added to metformin, w

229 s hemoglobin A1c greater than 6.5% or use of glucose-lowering medications.

230 d potentially to help guide the selection of glucose-lowering medications.

231 prandial insulin, with or without noninsulin glucose-lowering medications.

232 Glucose lowering occurred without signs of hypoglycemia

233 ing the effects of intensive versus standard glucose lowering on cardiovascular events, had baseline

234 ntional trials have shown no clear effect of glucose-lowering on CHD.

235 es Study, and of a meta-analysis of the four glucose-lowering outcome trials completed to date, sugge

236 his effect varied dependent on the method of glucose lowering (p for interaction=0.00021).

237 as how AKT might regulate lipid-lowering and glucose-lowering pathways that become insulin-resistant

238 enolics have been suggested to possess blood glucose lowering properties by inhibiting sugar transpor

239 unlike glucagon-like peptide (GLP)-1, lacks glucose-lowering properties in patients with type 2 diab

240 r CICR explains, at least in part, the blood glucose-lowering properties of an insulinotropic hormone

241 In vitro and in vivo studies on the glucose-lowering properties of antroquinonol indicate th

242 ptide 1 (GLP-1) also has insulin-independent glucose-lowering properties, and an elevated circulating

243 th factor 21 (FGF21) has insulin-independent glucose-lowering properties, we investigated whether FGF

244 cagonotropic effect is of importance for the glucose-lowering property of SGLT2 inhibition.

245 These data indicate that intensive glucose lowering reduces cardiovascular events in those

246 cipants to assess the effect of an intensive glucose-lowering regimen on death and cardiovascular out

247 lopment, provide summary recommendations for glucose-lowering regimens in specific patient types, und

248 be given in addition to their existing oral glucose-lowering regimens.

249 Glucose lowering remains important for the prevention of

250 On the basis of the potent glucose-lowering response elicited by activation of brai

251 Fgf3-elicited insulinotropic and glucose-lowering responses were recapitulated when overe

252 uced 14C-glycogen breakdown, confirming that glucose lowering resulted from inhibition of glycogenoly

253 In summary, the glucose-lowering SGLT2 inhibitor empagliflozin, used for

254 um can use cellulosic hydrolysate instead of glucose, lowering substrate costs for biolixiviant produ

255 s for longer durations, considering studying glucose-lowering therapies as first-line management of t

256 tered as monotherapy or in addition to other glucose-lowering therapies including insulin.

257 d to ensure the cardiovascular safety of new glucose-lowering therapies to treat patients with type 2

258 Glucose-lowering therapies were granted regulatory appro

259 etes and cardiovascular risk, the actions of glucose-lowering therapies within the cardiovascular sys

260 Current glucose-lowering therapies, including metformin, affect

261 ocardial infarction, associated with certain glucose-lowering therapies, the US Food and Drug Adminis

262 shown unequivocally to be increased by some glucose-lowering therapies.

263 ar risk in diabetes remains elevated despite glucose-lowering therapies.

264 ons, which often exhibit limited response to glucose-lowering therapies.

265 nce and for cardiovascular outcome trials of glucose-lowering therapies.

266 er cardiovascular protection indications for glucose-lowering therapies.

267 ne the presence of remission: (1) absence of glucose-lowering therapy (GLT); (2) normoglycaemia; and

268 to support individualised choice of optimal glucose-lowering therapy are scarce for people with type

269 Although intensive glucose-lowering therapy did not significantly reduce ca

270 eliness of initiation and intensification of glucose-lowering therapy in individuals newly diagnosed

271 orbidity should be considered when tailoring glucose-lowering therapy in patients with type 2 diabete

272 Addition of rosiglitazone to glucose-lowering therapy in people with type 2 diabetes

273 lts regarding the effectiveness of intensive glucose-lowering therapy in reducing risk for cardiovasc

274 odic hypoglycemia that occurs as a result of glucose-lowering therapy is harmful in patients with AMI

275 ppropriate initiation and intensification of glucose-lowering therapy is key to reducing the risk of

276 itus failed to show a benefit from intensive glucose-lowering therapy on cardiovascular disease (CVD)

277 ment difference of intensive versus standard glucose-lowering therapy on risk of CVD events in the AC

278 the effectiveness of a strategy of selecting glucose-lowering therapy using clusters with one combini

279 Intensive glucose-lowering therapy was effective at preventing inc

280 efinitions were extracted and categorised by glucose-lowering therapy, glycaemic thresholds, and dura

281 rovided proof of concept of 3 as a potential glucose-lowering therapy.

282 diabetic fatty rats led to rapid and robust glucose lowering, thereby providing the first evidence t

283 angiotensin II receptor blocker therapy and glucose-lowering treatment for at least 12 weeks.

284 Dipeptidyl peptidase (DPP)-4 inhibition is a glucose-lowering treatment for type 2 diabetes.

285 e cognition or age; or intensive vs standard glucose-lowering treatment, blood pressure treatment, li

286 uding but extending beyond the initiation of glucose-lowering treatment, consideration should be give

287 sure, BMI, blood pressure-, cholesterol- and glucose-lowering treatment, prior cardiovascular events,

288 nsive medication, lipid-lowering drugs, or a glucose-lowering treatment.

289 that metformin is at least as safe as other glucose-lowering treatments in patients with diabetes me

290 inemia, suppression of glucagon release, and glucose lowering under endotoxic conditions, whereas inh

291 endotoxin, leading to insulin secretion and glucose lowering under inflammatory conditions in mice.

292 ycemic response was observed in fasted rats; glucose lowering was maximal 30 min after dosing with 10

293 This effect was comparatively short-lived; glucose lowering was maximal at 30 min after dosing with

294 proportional to baseline FBG; no significant glucose lowering was observed in euglycemic subjects, a

295 and AMG-3969 (but not GK activators), blood glucose lowering was restricted to diabetic and not norm

296 ffects presumably occur independent of blood glucose lowering, we also explore the potential use of S

297 in patients with type 2 diabetes, including glucose lowering, weight loss, blood pressure lowering,

298 type 2 diabetic subjects, with no additional glucose lowering when combined with sitagliptin.

299 In this model, blood glucose lowering with empagliflozin attenuated some mole

300 an ED50 of 65 micromol/kg, 28 mg/kg/day, for glucose lowering), yet by avoiding significant escape of