ライフサイエンスコーパス: glycemic

1 ose) from CGM and continuous overlapping net glycemic action using a 4 hour interval (CONGA4).

2 Nineteen glycemic and 22 erythrocytic variants were associated wi

3 view the evidence for a reduction in fasting glycemic and insulinemic markers after chronic, isoenerg

4 was to review the evidence for postprandial glycemic and insulinemic responses after isoenergetic re

5 profibrotic markers that were independent of glycemic and lipid changes.

6 ies in large multiethnic cohorts with HbA1c, glycemic, and erythrocytic traits are required to better

7 e avoidance of smoking and the intake of low glycemic antioxidant-rich diets have largely followed fr

8 (also associated with erythrocyte traits) or glycemic (associated with other glucose-related traits).

9 onged, uninterrupted sedentary behavior with glycemic biomarkers in a cohort of US Hispanic/Latino ad

10 nt-centered care and shared decision making, glycemic biomarkers, hemoglobin A1c target ranges, indiv

11 were not associated with differences in any glycemic biomarkers.

12 cations received and improved study-selected glycemic, blood pressure, and lipid goal attainment (mod

13 High glycemic carbohydrate foods are linked to higher risk of

14 lucose tolerance and the insulin response to glycemic challenge were not perturbed in Gpr119(betacell

15 e are "first responder" islets to an in vivo glycemic challenge, which cannot be replicated by islets

16 R genotype, postpartum weight reduction, and glycemic changes between after delivery and pregnancy we

17 MC4R genotype was associated with postpartum glycemic changes; and the association with fasting gluco

18 en neighborhood supermarket gain or loss and glycemic control (assessed by glycated hemoglobin (HbA1c

19 s and Children Hospital, 28 of whom had poor glycemic control (average glycated hemoglobin [HbA1c] >/

20 s (P < 0.0001), insulin use (P = 0.002), and glycemic control (HbA1C < 7%) (P = 0.002) were used to d

21 Long-term glycemic control (HbA1c <7%) was seen in 63% of patients

22 27 age- and gender-matched subjects had good glycemic control (HbA1c <8%).

23 Intensive glycemic control (IGC) targeting HbA1c fails to show an

24 Participants who had diabetes had poor glycemic control (mean [+/-SD] glycated hemoglobin level

25 a-level attributes and according to baseline glycemic control (near normal, <6.5%; good, 6.5%-7.9%; m

26 sought to determine the relationship between glycemic control (random blood glucose [RBG], fasting bl

27 y and major adverse events despite favorable glycemic control after LVAD implantation.

28 he Behavioral Economic Incentives to Improve Glycemic Control Among Adolescents and Young Adults With

29 ded in a clinical setting improved long-term glycemic control among individuals with type 2 diabetes

30 vitamin D2 from 31 T1D patients with optimal glycemic control and 60 T1D patients with suboptimal gly

31 e analysis revealed association between poor glycemic control and arterial hypertension, presence of

32 control and 60 T1D patients with suboptimal glycemic control and assessed their tolerogenic properti

33 y during these years is associated with poor glycemic control and complications from diabetes in adul

34 This study demonstrates the importance of glycemic control and identifies potential therapeutic ta

35 nsplant recipients and examined the level of glycemic control and its associated factors, as well as

36 all margin between a dose that achieves good glycemic control and one that causes hypoglycemia.

37 Despite this, the current level of glycemic control and quality of screening strategies for

38 te the longitudinal association between poor glycemic control and subsequent changes in retinal micro

39 ected to have consequential bearings on IAPP glycemic control and T2D pathology.

40 d tremendous potential to improve the normal glycemic control and to reduce the incidence of hypergly

41 diabetes and chronic hyperglycaemia, liberal glycemic control appears to attenuate glycemic variabili

42 with more physiological profiles and better glycemic control are needed, especially analogues that p

43 New methods to improve glycemic control are needed.

44 chanism or mechanisms by which leptin exerts glycemic control are unclear.

45 imaging was obtained at the end of 1 year of glycemic control assessment.

46 ries for those with good, moderate, and poor glycemic control at baseline, while supermarket gain was

47 e neighborhood foreclosure rate could worsen glycemic control by activating stressors such as higher

48 These injectable analogs achieve robust glycemic control by increasing concentrations of "GLP-1

49 lifestyle intervention results in equivalent glycemic control compared with standard care and, second

50 mized clinical trials suggest that intensive glycemic control does not reduce major macrovascular eve

51 day-and-night closed-loop therapy maintained glycemic control during a high proportion of the time in

52 ia and diabetic ketoacidosis and with better glycemic control during the most recent year of therapy.

53 >/=9.0%) had the worst associated changes in glycemic control following either supermarket loss or ga

54 A) in the blood, are essential indicators of glycemic control for diabetes mellitus.

55 that encourage an individualized approach to glycemic control for U.S. adults with type 2 diabetes re

56 l trials consistently suggest that intensive glycemic control immediately increases the risk of sever

57 Although intensive glycemic control improves outcomes in type 1 diabetes me

58 , blood pressure was below 140/90 mm Hg, and glycemic control in 85% up to 15 years after onset.

59 borhood supermarket presence did not benefit glycemic control in a substantive way.

60 centives on glucose monitoring adherence and glycemic control in adolescents and young adults with ty

61 ing and modifying barriers impeding improved glycemic control in black persons with diabetes.

62 t it is unclear whether short period of poor glycemic control in children with T1D can cause evident

63 ent effect was fully attributed to the prior glycemic control in DCCT (explained treatment effect: 10

64 We assessed whether poor glycemic control in Hp 1-1 carriers is more strongly ass

65 ing cells offers the potential for restoring glycemic control in individuals with diabetes.

66 ation that correlated with an improvement of glycemic control in men with T2DM.

67 blockade similarly improved inflammation and glycemic control in obese WT mice.

68 important predictor of ischemic stroke than glycemic control in patients who have diabetes and AF.

69 ontinuous positive airway pressure (CPAP) on glycemic control in patients with diabetes.

70 to diagnose type 2 diabetes (T2D) and assess glycemic control in patients with diabetes.

71 ffect of positive airway pressure therapy on glycemic control in patients with relatively well-contro

72 abel subcutaneous semaglutide (secondary) on glycemic control in patients with type 2 diabetes.

73 fects of treating obstructive sleep apnea on glycemic control in patients with type 2 diabetes.

74 hether a lifestyle intervention can maintain glycemic control in patients with type 2 diabetes.

75 evelop new approaches to achieve near-normal glycemic control in real-world settings in people with t

76 e and health by examining annual measures of glycemic control in relation to local foreclosure activi

77 ery may achieve better and more long-lasting glycemic control in select patients with early-onset T2D

78 pharmacologic approaches for safer intensive glycemic control in T1DM.

79 subcutaneous adipocyte size predicted better glycemic control in T2D.

80 The incretin hormones improve glycemic control in T2DM by increasing insulin secretion

81 SIRT6 may be a viable strategy for improving glycemic control in T2DM.

82 ce that increased foreclosure rates worsened glycemic control in this continuously insured population

83 Poor glycemic control in Type 1 Diabetes (T1D) patients is st

84 Intensive glycemic control in type 2 diabetes (glycated hemoglobin

85 The challenges of achieving optimal glycemic control in type 2 diabetes highlight the need f

86 nt on GLP-1 secretion, gastric emptying, and glycemic control in type 2 diabetes.

87 g dietary intake variables with time-varying glycemic control indicators, controlling for age, height

88 Recent evidence suggests that glycemic control is associated with cognitive function i

89 most patients with type 1 diabetes, adequate glycemic control is not achieved with insulin therapy al

90 obesity and diabetes have become common and glycemic control may be poor.

91 gests that periodontal treatment may improve glycemic control of patients with DMt2 by eliminating pe

92 Glycemic control often deteriorates during adolescence a

93 ity after transplantation, but the effect of glycemic control on survival is unknown.We sought to det

94 lure cannot be explained by their actions on glycemic control or as osmotic diuretics.

95 rsons than in white persons are due to worse glycemic control or racial differences in the glycation

96 s to assess the overall long-term functional glycemic control or the possibility of unrecognized diab

97 Improvements in glycemic control over a 12-month period led to improveme

98 Achieving glycemic control remains a challenge for patients with t

99 of type 1 diabetes (T1D) treatment; however, glycemic control remains a challenge.

100 During surgery, glycemic control should be implemented using blood gluco

101 Glycemic control strongly correlates with survival after

102 active in rats, with an in vivo potency for glycemic control surpassing that of native GLP-1.

103 ith hyperglycemia did not benefit from tight glycemic control targeted to a blood glucose level of 80

104 In multicenter studies, tight glycemic control targeting a normal blood glucose level

105 LDL and duration of T1D, patients with poor glycemic control tended to have marginally wider retinal

106 iabetes, oral semaglutide resulted in better glycemic control than placebo over 26 weeks.

107 d with standard care resulted in a change in glycemic control that did not reach the criterion for eq

108 Interventions to improve glycemic control through early intensive treatment of di

109 ion of whether or not to recommend intensive glycemic control to patients to minimize microvascular a

110 d, 632 with type 2 diabetes and insufficient glycemic control using diet and exercise alone or a stab

111 rovided evidence that between 2007 and 2010, glycemic control was not associated with rates of comple

112 Dose-related worsening of glycemic control was noted in 14.5% of patients who rece

113 The improvement in glycemic control was observed without stimulation of the

114 high levels of obesity, diabetes was common, glycemic control was poor, and diabetes was associated w

115 or a DPP-4 inhibitor to metformin to improve glycemic control when a second oral therapy is considere

116 diabetes mellitus who do not achieve optimal glycemic control with insulin monotherapy, is the additi

117 lycemic medications are necessary to balance glycemic control with safety.

118 effects of the housing foreclosure crisis on glycemic control within a population of patients with di

119 o determine whether a " liberal" approach to glycemic control would reduce hypoglycemia and glycemic

120 e significantly higher in patients with poor glycemic control, although the plasma levels of both pro

121 Risk of insulin resistance, impaired glycemic control, and cardiovascular disease is excessiv

122 dy-composition metrics, appetite, markers of glycemic control, and gut microbiota were measured at 2

123 lood pressure, cholesterol and blood lipids, glycemic control, and the use of aspirin) management for

124 iologically with diabetic complications, and glycemic control, as reflected by HbA1c reduction, resul

125 ell accepted that physical activity improves glycemic control, but the knowledge on underlying mechan

126 n Americans with diabetes mellitus varies by glycemic control, health status, and calendar year (befo

127 ases in postprandial gut hormone secretions, glycemic control, pancreas morphology, and micronutrient

128 erapy to insulin in T1DM, heralding improved glycemic control, reduced body weight and total daily in

129 od pressure control, lipid control, diabetic glycemic control, smoking cessation, and target body mas

130 ere restricted to those with poorer baseline glycemic control, those with more severe sleep apnea, or

131 patic interaction of Ad36E4ORF1 in enhancing glycemic control, we expressed E4ORF1 of Ad36 or Ad5 or

132 igh-fat diet, Ocy-PPARgamma(-/-) mice retain glycemic control, with increased browning of the adipose

133 rition management is critical to maintaining glycemic control, yet it is difficult to achieve due to

134 - and gender- matched counterparts with good glycemic control.

135 ay be more vulnerable to the insults of poor glycemic control.

136 al for many homeostatic processes, including glycemic control.

137 nts, but little is known about the impact of glycemic control.

138 ears or longer at baseline, insulin use, and glycemic control.

139 36E4ORF1 but not Ad5E4ORF1 robustly improved glycemic control.

140 nts with type 2 diabetes, negatively affects glycemic control.

141 (vGMS) is associated with improved inpatient glycemic control.

142 tions among T1D pediatric patients with poor glycemic control.

143 n pharmacologic therapy is needed to improve glycemic control.

144 th HbA1c as a surrogate marker indicator for glycemic control.

145 abetes, is a major barrier to achieving good glycemic control.

146 stems, including in aldosterone function and glycemic control.

147 ects on food intake, energy homeostasis, and glycemic control.

148 ry intake than for biomarkers of longer-term glycemic control.

149 stinal glucose absorption in vivo to improve glycemic control.

150 does not appear to be effective in improving glycemic control.

151 nts with type 2 diabetes mellitus under poor glycemic control.

152 ependent therapeutic effects on postprandial glycemic control.

153 to a weight-loss-independent improvement in glycemic control.

154 veness demonstrated therapeutically relevant glycemic control.

155 r for type 2 diabetes that adversely impacts glycemic control.

156 ive period but did not significantly improve glycemic control.

157 ar-daily basis for 24 weeks and had improved glycemic control.

158 tric patients with T1D after one-year's poor glycemic control.

159 Individualized versus uniform intensive glycemic control.

160 ht changes, on energy-metabolism metrics and glycemic control.The study was a randomized, controlled,

161 one cardiac surgery) to one of two ranges of glycemic control: 80 to 110 mg per deciliter (4.4 to 6.1

162 Here we report the first long-term glycemic correction of a diabetic, immunocompetent anima

163 ent progression of beta-cell dysfunction and glycemic deterioration in models of T1D.

164 a potential therapeutic approach to prevent glycemic deterioration in T1D.

165 f healthy individuals indicated that a lower glycemic diet may lead to important reductions in blood

166 ntrolling for age, sex, and education.A high-glycemic diet was associated with greater cerebral amylo

167 metabolic syndrome in a low-processed, lower-glycemic dietary context.

168 has uncovered dozens of loci that influence glycemic dysregulation.

169 Because Neu5Gc(-/-) mice exhibit glycemic dysregulations and pancreatic beta-cell dysfunc

170 renal function decline independently of its glycemic effects in a secondary analysis of a clinical t

171 renoprotective effects independently of its glycemic effects.

172 We classified variants as implicated in glycemic, erythrocytic, or unclassified biology and test

173 performed to determine the mean amplitude of glycemic excursion (MAGE) and postprandial incremental a

174 Glycemic excursions, independent of average glucose, hav

175 explained by diabetes duration or long-term glycemic exposure, suggesting the involvement of genetic

176 ohort (n = 900) with long-term postoperative glycemic follow-up, which, for the first time, categoriz

177 od profile, emphasizing low-processed, lower-glycemic foods.

178 hole-body glucose homeostasis is critical to glycemic function.

179 dicine approach can be used to individualize glycemic goals and prevent overtreatment, and can serve

180 Anticipating glycemic impact of different meals can be challenging no

181 fruit, which may reflect differences in the glycemic impact or phytochemical content.

182 ere performed to classify subjects with good glycemic improvements.

183 onstructed to classify weight maintainers or glycemic improvers.With RNAseq analyses, we identified 1

184 60% carbohydrate, 20% fat, 20% protein), low glycemic index (40% carbohydrate, 40% fat, 20% protein),

185 h fractions (3.87-10.96%) with low predicted glycemic index (62.97-53.13%), despite their higher tota

186 h for nutrition and with regard to estimated glycemic index (eGI) and glycemic load (eGL).

187 Expected glycemic index (eGI) was increased proportionally to the

188 (2.03-2.91%) correlated negatively with the glycemic index (GI) (r=-0.674; p</=0.05) and contributed

189 ts across eating patterns on meal or dietary glycemic index (GI) and glycemic load (GL) value determi

190 on on the postprandial glycemic response and glycemic index (GI) and glycemic load (GL) value determi

191 was to determine the associations of dietary glycemic index (GI) and glycemic load (GL) with systolic

192 t association in men was observed for higher-glycemic index (GI) fruit [HR: 1.51 (95% CI: 1.22, 1.86)

193 Australians have used the glycemic index (GI) since 1995; however, there are no da

194 were tested for their nutrient composition, glycemic index (GI), total phenolic content (TPC), total

195 An increase of expected glycemic index by 38% was determined for elicited sprout

196 Low-glycemic index diets have demonstrated health benefits a

197 could lower the glycemic response of a high-glycemic index food when consumed together and the mecha

198 luate the starch digestibility and predicted glycemic index in breads incorporated with pomelo fruit

199 The estimated glycemic index of porridge and injera of the varieties r

200 ents in the product formulations lowered the glycemic index probably by inhibiting carbohydrate hydro

201 cation by the carbohydrate:protein ratio and glycemic index was also investigated.A total of 29,152 p

202 commercial wholemeal pasta, and its in vitro glycemic index was even lower.

203 odification by carbohydrate:protein ratio or glycemic index was found.Dietary intake and adipose tiss

204 om seven tef varieties and to estimate their glycemic index.

205 r disease (CVD) mainly because of their high glycemic index.

206 of rice flour, commonly known to have a high glycemic index.

207 starch digestibility and values of expected glycemic index; however, a decrease (up to 8%) of relati

208 diabetes incidence or prospective changes in glycemic indicators during the follow-up period.

209 ciated with diabetes incidence or changes in glycemic indicators during the follow-up period.

210 ncentrations with diabetes incidence and key glycemic indicators measured at baseline and annually ov

211 ciations between plasma PFAS concentrations, glycemic indicators, and diabetes incidence among high-r

212 tiple logistic regression models, the median glycemic level was an independent predictor of poor Cere

213 = 8.30, 95% CI = 3.56 to 19.35) and the high glycemic-level group (HbA1c levels >/= 5.6% and < 6.5%,

214 een periodontitis and LBW in both the normal glycemic-level group (HbA1c levels < 5.6%, unadjusted od

215 ciation continued to be strong in the normal glycemic-level group (OR adjusted = 7.59, 95% CI = 2.7 t

216 , is more sensitive to short term changes in glycemic levels, GA is expected to be used as an alterna

217 regard to estimated glycemic index (eGI) and glycemic load (eGL).

218 was the only one eliciting low GI of 50 and glycemic load (GL) of 13 while the rest exhibited GI ran

219 s on meal or dietary glycemic index (GI) and glycemic load (GL) value determinations has remained par

220 lycemic response and glycemic index (GI) and glycemic load (GL) value determinations remains unclear.

221 ociations of dietary glycemic index (GI) and glycemic load (GL) with systolic blood pressure (SBP) an

222 he aim was to compare average dietary GI and glycemic load (GL), and contributing carbohydrate foods,

223 rate, fat, saturated fat, dietary fiber, and glycemic load derived from self-report of dietary intake

224 P < 0.001) more on the high- than on the low-glycemic load diet, whereas normoglycemic individuals re

225 erweight patients consuming diets with a low glycemic load or with large amounts of fiber and whole g

226 ures (sugar intake, carbohydrate intake, and glycemic load) were also positively associated with glob

227 for 26 wk a diet with either a high or a low glycemic load.

228 ern, intakes of sugar and carbohydrates, and glycemic load] with cerebral amyloid burden (measured by

229 etary glycemic measures [adherence to a high-glycemic-load diet (HGLDiet) pattern, intakes of sugar a

230 and maintenance through diets with different glycemic loads or different fiber and whole-grain conten

231 t monitoring and pharmacologic approaches to glycemic management for type 1 diabetes.

232 Although intensive glycemic management has been shown to delay the onset an

233 poglycemia is the leading limiting factor in glycemic management of insulin-treated diabetes.

234 nce (WC), serum adipokines, cytokines, and a glycemic marker.

235 x SNPs were not associated with the clinical glycemic markers fasting glucose or the HbA1c, and vice

236 Individual dietary glycemic measures (sugar intake, carbohydrate intake, an

237 ed cross-sectional analyses relating dietary glycemic measures [adherence to a high-glycemic-load die

238 aging.We assessed the association of dietary glycemic measures with cerebral amyloid burden and cogni

239 d points comprising psychosocial and various glycemic measures, 6 met the hierarchical testing criter

240 ontinuation or dosage decrease of at least 1 glycemic medication without addition of, or uptitration

241 lucose normalization could contribute to the glycemic memory effect in DN.

242 d more frequent reviews for people with poor glycemic or blood pressure control.

243 pid signature of LCD success (for weight and glycemic outcome) in obese, nondiabetic patients.

244 g an LCD and the association with weight and glycemic outcomes both at LCD termination and 6 mo after

245 Pain and glycemic outcomes were recorded at follow-up visits ever

246 divided into 3 groups according to different glycemic outcomes.

247 ediates of blood lipids, blood pressure, and glycemic phenotypes.

248 The chemical composition and in vivo glycemic potential of popular Indian rice varieties name

249 anges in lipid profile but not with improved glycemic profile variables: the IPF relative reduction w

250 n obese mice, in addition to improving their glycemic profile.

251 n of dipeptidyl peptidase-4 (DPP-4) promotes glycemic reduction for the treatment of type 2 diabetes

252 riables enabled us to distinguish weight and glycemic responders from nonresponders.

253 t varied in macronutrient composition on the glycemic response and determination of GI and GL values

254 f prior meal composition on the postprandial glycemic response and glycemic index (GI) and glycemic l

255 composition of the prior meal influences the glycemic response and the determination of GI and GL val

256 ther pomegranate polyphenols could lower the glycemic response of a high-glycemic index food when con

257 in a supplement, can reduce the postprandial glycemic response of bread, whereas microbial metabolite

258 e intra- and inter-individual variability in glycemic response to a single food challenge and methodo

259 ve due to the high individual differences in glycemic response to nutrition.

260 maximal blood glucose level at 60min (slower glycemic response) than atmospheric counterparts ( appro

261 ed meat and low-fat dairy produced a similar glycemic response.

262 In the future, MPCCs under glycemic states can aid in novel drug discovery and mech

263 rogram Adult Treatment Panel III), including glycemic status (as defined by the Expert Committee on t

264 eolar bone loss and 2) determine whether the glycemic status affects the relationship between bone re

265 A dual relationship between glycemic status and bone remodeling was suggested recent

266 prove cardiometabolic risk factors including glycemic status in T2DM.

267 e prevalence of polyneuropathy stratified by glycemic status in well-characterized obese and lean par

268 tions of bone markers are either affected by glycemic status or detected at very low levels.

269 ial compared with enalapril, irrespective of glycemic status.

270 s; outcome assessors were masked to neonatal glycemic status.

271 pe 2 diabetes mellitus who have not achieved glycemic targets and who have prevalent atherosclerotic

272 with type 1 diabetes do not meet recommended glycemic targets.

273 Overall, 29,946 (59.3%) patients had a glycemic test within 3 y of follow-up, and 8,478 of them

274 e quarters with low HbA1C did not have their glycemic therapy deintensified, even after safety concer

275 Glycemic therapy was deintensified in 18.3% of patients

276 own associations between common variants and glycemic traits and identify new loci.

277 ation illuminate the genetic architecture of glycemic traits and suggest gene regulation as a target

278 Large genome-wide association studies of glycemic traits have identified genetics variants that a

279 wide association studies have been linked to glycemic traits in humans.

280 ound that tau haplotypes are associated with glycemic traits in humans.

281 3), IHD (0.96, 95% CI 0.80 to 1.14), lipids, glycemic traits, adiposity or adiponectin.

282 ed with higher left ventricular hypertrophy, glycemic traits, interleukin 6, and circulating lipids.

283 d variants were associated with diabetes and glycemic traits.

284 ariation influences type 2 diabetes risk and glycemic traits.

285 esis that hepatic PPP1R3B is associated with glycemic traits.

286 Ps) have pleiotropic and opposite effects on glycemic traits.

287 High-quality evidence about glycemic treatment in older adults is lacking.

288 Standards about pharmacologic approaches to glycemic treatment of type 2 diabetes.

289 Liberal therapy reduced glycemic variability (coefficient of variability, 33.2%

290 ycemic control would reduce hypoglycemia and glycemic variability and appear safe.

291 iberal glycemic control appears to attenuate glycemic variability and may reduce the prevalence of mo

292 nts (age, between 29 and 63 years) with high glycemic variability and problematic hypoglycemia receiv

293 ion between blood glucose concentrations and glycemic variability and the neurologic outcomes of pati

294 Dysglycemia and glycemic variability are associated with poor outcomes i

295 n, CSII decreased hypoglycemia frequency and glycemic variability compared with MDI whereas islet tra

296 t transplantation to reduce hypoglycemia and glycemic variability in type 1 diabetes subjects with se

297 n resolved hypoglycemia and further improved glycemic variability regardless of insulin independence.

298 on and during the first 36 hours, and higher glycemic variability, were associated with poor neurolog

299 ic scores of erythrocytic variants (GS-E) or glycemic variants (GS-G) were associated with higher T2D

300 tic risk-scores comprised of erythrocytic or glycemic variants on incident diabetes prediction and on