ライフサイエンスコーパス: glucose-lowering

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

2 ng considered as potential new approaches to glucose lowering.

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

4 equivocal cardiovascular risk reduction with glucose lowering.

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

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

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

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

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

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

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

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

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

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

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

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

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

18 Its potent glucose-lowering activity results from enhanced insulin

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

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

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

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

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

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

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

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

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

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

29 The sustained glucose lowering and insulin sensitization attributed to

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 Some glucose-lowering drugs or strategies adversely affect ca

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

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

68 5, for large randomised controlled trials of glucose-lowering drugs or strategies that assessed cardi

69 Glucose-lowering drugs or strategies were associated wit

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 Its glucose-lowering effect results from decreased hepatic g

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

151 Reduction in glucose-lowering medications occurred in 47 participants

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

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

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

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

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

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

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

159 Glucose lowering occurred without signs of hypoglycemia

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 Glucose lowering remains important for the prevention of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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