ライフサイエンスコーパス: blood glucose

1 sulin in proportion to postprandial rises in blood glucose.

2 es of >/=2 wk duration that measured fasting blood glucose.

3 le wasting and without a sustained impact on blood glucose.

4 azide diuretics is associated with a rise in blood glucose.

5 tion of blood volume/pressure/osmolality and blood glucose.

6 ergy expenditure, reduce adiposity and lower blood glucose.

7 etes model that induces a small elevation of blood glucose.

8 ttenuated renal pathology, and did not lower blood glucose.

9 lucose absorption and intestinal disposal of blood glucose.

10 hysiological importance in the regulation of blood glucose.

11 LUT4 in sensing and responding to changes in blood glucose.

12 g mice continued to have significantly lower blood glucose.

13 nificantly but only slightly lowered fasting blood glucose (-0.14 mmol/L; 95% CI: -0.24, -0.036 mmol/

14 mic (4x basal) hyperglycemic clamp (arterial blood glucose 146 +/- 2 mg/dL) with portal GLC infusion.

15 , -0.11 mmol/L; 95% CI, -0.17 to -0.04), and blood glucose (2 studies; mean differences, -0.18 mmol/L

16 se (-33.1% +/- 18.1%, P = 0.000005) and peak blood glucose (25.4% +/- 19.3%, P = 0.0004) were attenua

17 ental area under the curve for bread-derived blood glucose (-33.1% +/- 18.1%, P = 0.000005) and peak

18 n (HbA1c, -1.3 +/- 1.8%, P < 0.001), fasting blood glucose (-37.8 +/- 70.4 mg/dL, P < 0.001) and medi

19 eral: 10.3 [2.1] mmol/L; p = 0.02) and nadir blood glucose (4.4 [1.5] vs 5.5 [1.6] mmol/L; p < 0.01)

20 The median blood glucose 8 hours after admission in patients receiv

21 o (WHR), fasting blood glucose (FBG), 2-hour blood glucose after glucose overload (2h-OGTT), HbA1c, t

22 ain amino acids leucine and isoleucine lower blood glucose after oral glucose ingestion, and the intr

23 exogenous insulin is invariant regardless of blood glucose, aggravating the potential to cause hypogl

24 ice gained significantly more weight without blood glucose alteration.

25 Self-monitoring of blood glucose among people with type 2 diabetes not trea

26 o fat and muscle cells to lower postprandial blood glucose, an enforced change in cellular metabolism

27 central nervous system circuits controlling blood glucose and behaviour.

28 bition with a monoclonal antibody normalized blood glucose and beta-hydroxybutyrate levels.

29 P]) and systemic parameters (blood pressure, blood glucose and body mass index [BMI]) were assessed f

30 ulin resistance in fasted adult DKO pigs and blood glucose and C-peptide changes after intravenous gl

31 ed recommendations on screening for abnormal blood glucose and concluded that intensive lifestyle int

32 accounts for the inverse association between blood glucose and glioma.

33 Graft function was measured by nonfasting blood glucose and glucose tolerance testing.

34 The adjusted AUCs of random blood glucose and Homeostasis Model Assessment-Insulin R

35 t retains its ability to significantly lower blood glucose and improve glucose tolerance in diet-indu

36 ly, these agents have been reported to lower blood glucose and increase insulin sensitivity by alteri

37 The main outcomes analyzed were fasting blood glucose and insulin as well as fasting triglycerid

38 n food or beverages lowers peak postprandial blood glucose and insulin concentrations.

39 -3 fatty acid desaturase, mfat-1, normalized blood glucose and insulin levels for at least 182 days,

40 e insulin secretion through rapid sensing of blood glucose and integration of gut-derived signals.

41 Fasting blood glucose and lipid levels, the results of an oral g

42 animals demonstrated rapid normalization of blood glucose and perfectly normal glucose disposal duri

43 ity were measured over 4 hours using MRI and blood glucose and plasma concentrations of insulin, pept

44 with 100 mug (13)C-octanoic acid to measure blood glucose and plasma GLP-1 concentrations and gastri

45 mptying (3-dimensional ultrasonography), and blood glucose and plasma gut-hormone concentrations [ins

46 Fasting and postprandial blood glucose and plasma total GLP-1 as well as gastric

47 MTNR1B) is associated with increased fasting blood glucose and risk of T2D, but whether sleep or circ

48 015 recommendation on screening for abnormal blood glucose and type 2 diabetes; the 2016 recommendati

49 Blood glucose and weight were monitored until reversal o

50 otal cholesterol, triglycerides, and fasting blood glucose) and identified several cis-eGenes (ALDH2

51 display improved glucose tolerance, fasting blood glucose, and GSIS, whereas G6PC2 levels are decrea

52 d management during pregnancy, especially of blood glucose, and increased attention to post-partum we

53 nificant (P <0.05), for BW, WC, BMI, fasting blood glucose, and IPGTT-AUC.

54 es were assessed for hemoglobin A1c, fasting blood glucose, and serum lipids.

55 s that systematically record blood pressure, blood glucose, and temperature data are required to furt

56 Blood pressure, blood glucose, and temperature data were collected for 5

57 , most notably heart rate, body temperature, blood glucose, and triglyceride concentration, all of wh

58 care test for identifying malaria parasites, blood glucose, and urea levels in whole blood samples fr

59 with the control, leucine-10g decreased the blood glucose area under the curve (AUC) (P < 0.05) and

60 Metformin controlled blood glucose as equally as insulin with no difference b

61 The USPSTF recommends screening for abnormal blood glucose as part of cardiovascular risk assessment

62 Ghrelin also regulates blood glucose, as emphasized by the hypoglycemia that is

63 expression of Ad36E4ORF1 lowered nonfasting blood glucose at a high dose of expression.

64 with the control, isoleucine-10g reduced the blood glucose AUC and peak blood glucose (P < 0.01), whe

65 gastric emptying was not correlated with the blood glucose AUC.

66 Blood glucose (BG) and hunger were measured 30 and 150 m

67 beta-cells to achieve meticulous control of blood glucose (BG) would revolutionize diabetes care.

68 ntrol received optimization of treatment for blood glucose, blood pressure, and cholesterol to recomm

69 ion of glucagon signaling effectively lowers blood glucose but results in compensatory glucagon hyper

70 ay for 2 weeks significantly reduced fasting blood glucose by 18%, with significant increase in fasti

71 Pancreatic islets respond to elevated blood glucose by secreting pulses of insulin that parall

72 tween patients with and without PEX included blood glucose, cholesterol, and homocysteine levels; blo

73 nce test clarified that the complex retained blood glucose clearance activity for 72 hours suggesting

74 bited significantly lower random and fasting blood glucose compared with mice transplanted with norma

75 nts were the percentage of time spent with a blood glucose concentration >10 mmol/L (%T >10) and peak

76 Infants with hypoglycemia (whole-blood glucose concentration <47 mg/dL) were treated to m

77 upplement) on the bread-derived postprandial blood glucose concentration in 2 randomized, crossover,

78 glycemic distance as the difference between blood glucose concentration in ICU and baseline blood gl

79 Tight control of blood glucose concentration in people with type 1 diabet

80 The mean daily blood glucose concentration in the sitagliptin-basal gro

81 c episode, defined as at least 1 consecutive blood glucose concentration less than 47 mg/dL, a severe

82 8-80 years with type 2 diabetes and a random blood glucose concentration of 7.8-22.2 mmol/L who were

83 On admission, 204 (62%) of 327 had blood glucose concentration of 70 mg/dL or less.

84 ntration <47 mg/dL) were treated to maintain blood glucose concentration of at least 47 mg/dL.

85 ohort of critically ill diabetic patients, a blood glucose concentration target of 10-14 mmol/L resul

86 Blood glucose concentration targets were 6-10 mmol/L dur

87 he first 48 ICU hours, we recorded absolute (blood glucose concentration, < 3.9 mmol/L) and relative

88 mponents-abdominal obesity, elevated fasting blood glucose concentration, low high-density lipoprotei

89 lar morphology, systemic blood pressure, and blood glucose concentration.

90 od glucose concentration in ICU and baseline blood glucose concentration.

91 insulin as indicated by transient dip in the blood glucose concentration.

92 ed hemoglobin to estimate premorbid baseline blood glucose concentration.

93 esults with plasmid-driven L. lactis Initial blood glucose concentrations (<350 mg/dL) and insulin au

94 d a negative glycemic distance in 248 of 488 blood glucose concentrations (50.8%) during the before p

95 ck stratification according to randomisation blood glucose concentrations (ie, higher or lower than 1

96 We investigated the association between blood glucose concentrations and glycemic variability an

97 an differences between groups in their daily blood glucose concentrations during the first 10 days of

98 eriod, 52 patients received insulin to treat blood glucose concentrations greater than 10 mmol/L wher

99 eriod, 31 patients received insulin to treat blood glucose concentrations greater than 14 mmol/L.

100 Elevated maternal blood glucose concentrations may contribute to macrosomi

101 astric or intravenous glucose delivery (with blood glucose concentrations reaching >15 mmol/L), a sma

102 Blood glucose concentrations were tested with the use of

103 Four male Sprague-Dawley rats with different blood glucose concentrations were utilized to demonstrat

104 PAG LepRb neurons increased SNS activity and blood glucose concentrations, while ablating LepRb in PA

105 cant difference between groups in mean daily blood glucose concentrations.

106 wild-type littermate controls at comparable blood glucose concentrations.

107 e areas under the curves for serum 3-OMG and blood glucose concentrations.

108 cant difference between groups in mean daily blood glucose concentrations.

109 symptomatic hypoglycemic episodes (severe or blood glucose confirmed [<56 mg/dL]) during the maintena

110 symptomatic hypoglycemic episodes (severe or blood glucose confirmed, occurring between 12:01 am and

111 end point was the rate of overall severe or blood glucose-confirmed (<56 mg/dL) symptomatic hypoglyc

112 Severe or blood glucose-confirmed hypoglycaemia was reported by 16

113 e weight loss, reduce adiposity, and improve blood glucose control in diet-induced obese mice with pr

114 Blood glucose control is the primary strategy to prevent

115 augmented myogenic tone, despite reasonable blood glucose control.

116 rved to be associated with a higher level of blood glucose (Delta, 6.2 mg/dL; 95% CI, -2.0 to 14.3 mg

117 al-bolus group 9.4 mmol/L [2.7]) with a mean blood glucose difference of 0.1 mmol/L (95% CI -0.6 to 0

118 sts showed that Syn-1A-betaKO mice exhibited blood glucose elevation corresponding to reduced blood i

119 pancreatic beta-cells proliferate to prevent blood glucose elevations.

120 Body weight, organ mass, fasting blood glucose, energy expenditure, cardiac geometry and

121 The mice also had elevated fasting blood glucose, fatty liver, and insulin resistance.

122 mong nondiabetic individuals, higher fasting blood glucose (FBG) independently predicts diabetes risk

123 gatively with Waist hip ratio (WHR), fasting blood glucose (FBG), 2-hour blood glucose after glucose

124 control (random blood glucose [RBG], fasting blood glucose [FBG], and glycated hemoglobin [HbA1c]) an

125 cardiometabolic risk factor changes (fasting blood glucose [FBG], glycosylated hemoglobin [HbA1c], sy

126 protein level and prevented pyruvate-induced blood glucose from increasing.

127 Diagnostic accuracies of random blood glucose, glycated hemoglobin (HBA1c), fructosamine

128 e concentration >10 mmol/L (%T >10) and peak blood glucose (Gmax).

129 rate, blood pressure, pulse oxygenation, and blood glucose have applications in both fitness monitori

130 lucose absorption and intestinal disposal of blood glucose have not been directly compared between in

131 netic variants with LDL cholesterol, fasting blood glucose, HbA1c, fasting insulin, bodyweight, waist

132 ure and serum cholesterol, smoking, and high blood glucose), high body mass index, harmful alcohol us

133 y weight, liver and adipose tissue function, blood glucose homeostasis and survival in adult mice.

134 ptide 1), a critical incretin that regulates blood glucose homeostasis.

135 Targeted temperature management alters blood glucose homeostasis.

136 a higher risk of developing elevated fasting blood glucose (HR = 1.33, 95% CI: 1.14, 1.56).

137 Sustained dysregulation of blood glucose (hyper- or hypoglycemia) associated with t

138 tor, CDN1163, which markedly lowered fasting blood glucose, improved glucose tolerance, and ameliorat

139 nificantly decreased body weight and fasting blood glucose, improved lipid metabolism, and also reduc

140 that treatment with ApoA-IV lowered fasting blood glucose in both WT and diabetic KKAy mice by incre

141 ted a significant dose-dependent decrease in blood glucose in chronic studies in diabetic db/db mice

142 These results suggest that high blood glucose in diabetic patients contributes to develo

143 oring respiration, arterial blood gases, and blood glucose in mice exposed to 8% O2 for 2 or 6 h.

144 Particulate air pollution and fasting blood glucose in nondiabetic individuals: associations a

145 alate is a prodrug of salicylate that lowers blood glucose in patients with type 2 diabetes (T2D) and

146 ubjects, both leucine and isoleucine reduced blood glucose in response to a mixed-nutrient drink but

147 modest effects on their capacity to regulate blood glucose in streptozotocin-induced diabetic mice, i

148 approach to restore the physical response to blood glucose in type 1 diabetes.

149 also lowered insulin levels while increasing blood glucose in vivo.

150 ain outcomes analyzed were peak postprandial blood glucose, insulin, and triglyceride concentrations.

151 fect on glycated hemoglobin (HbA1c), fasting blood glucose, insulin, and triglycerides.The objective

152 Blood glucose, insulin, C-peptide, the insulin-to-glucag

153 at tested effects of macronutrient intake on blood glucose, insulin, HbA1c, insulin sensitivity, and

154 ed from high-fat diet (HFD)-induced obesity, blood glucose intolerance, and insulin resistance.

155 Blood glucose is an important fuel for endurance exercis

156 Lastly, we found that blood glucose is elevated and serum adiponectin levels a

157 lonisation is significantly more likely when blood glucose is high.

158 sociation study gene associated with fasting blood glucose, is a negative regulator of glucose-stimul

159 mference, blood pressure, heart rate, HbA1c, blood glucose, LDL-to-HDL cholesterol ratio, C-reactive

160 failure, muscle weakness, and hyperglycemia (blood glucose level >150 mg/dL [to convert to millimoles

161 erval (CI): 1.06, 1.52), an elevated fasting blood glucose level (HR = 1.20, 95% CI: 1.03, 1.39), and

162 A lowered blood glucose level also was observed in overnight-faste

163 -)) display resistance to T1D as the rise in blood glucose level and islet inflammation were signific

164 y 98.3% degree of gelatinization and maximal blood glucose level at 30min).

165 ization ( approximately 53.8%) and a maximal blood glucose level at 60min (slower glycemic response)

166 population with diabetes, the change in the blood glucose level at the time of scan across longitudi

167 r rates of severe hypoglycemia, defined as a blood glucose level below 40 mg per deciliter (2.2 mmol

168 GLP-1 is capable of regulating the blood glucose level by insulin secretion after administr

169 Pancreatic islets manage elevations in blood glucose level by secreting insulin into the bloods

170 s, tight glycemic control targeting a normal blood glucose level has not been shown to improve outcom

171 2) has emerged as a promising way to control blood glucose level in diabetes patients.

172 ates whether perceived time has an effect on blood glucose level in people with type 2 diabetes.

173 Hyperglycemia was defined as a blood glucose level of 200 mg/dL or greater.

174 The rate of documented hypoglycemia with a blood glucose level of 55 mg per deciliter (3.1 mmol per

175 it from tight glycemic control targeted to a blood glucose level of 80 to 110 mg per deciliter, as co

176 8) We suggest that clinicians target a blood glucose level of less than 180 mg/dL in patients r

177 ibed on page 3115, effectively regulates the blood glucose level of type-1 diabetic mice, achieving a

178 ived time will have a greater influence over blood glucose level than actual time.

179 ation with glucose dehydrogenase to regulate blood glucose level, alcohol dissolution into carboxylic

180 ny actions that can raise or reduce falls in blood glucose level.

181 ociation being altered depending on maternal blood glucose level.

182 tures enabling potential seamless control of blood glucose level.

183 nsive insulin therapy (IIT) targeting normal blood glucose levels (81-108 mg/dl) increases the incide

184 al lipidome between participants with normal blood glucose levels (n = 26) and those with type 2 diab

185 red GcgR monoclonal antibody displayed lower blood glucose levels accompanied by elevated plasma ghre

186 mportantly, NT-ES-beta-cells maintain normal blood glucose levels after ablation of the mouse endogen

187 s and benefits, the significance of abnormal blood glucose levels and diabetes as cardiovascular risk

188 Blood glucose levels and disease severities were analyze

189 lockade in the NAc bidirectionally modulated blood glucose levels and glucose tolerance.

190 nally, we show that 13d significantly lowers blood glucose levels and increases concomitant beta-cell

191 n ventilation and CO2 sensitivity to restore blood glucose levels and prevent a fall in blood pH.

192 he vasculature that affect the regulation of blood glucose levels and the development of atherosclero

193 ccordingly, the Rosa-Lkb1 mice had increased blood glucose levels and were intolerant to glucose chal

194 e indicates that pre-diagnostic diabetes and blood glucose levels are inversely related to glioma ris

195 slet activity persist, and relatively normal blood glucose levels are maintained.

196 Blood glucose levels are tightly controlled by the coord

197 h of gray and white matter in children whose blood glucose levels are well within the current treatme

198 Higher blood glucose levels at admission and during the first 3

199 patients then underwent treatment to control blood glucose levels before end blood samples were taken

200 CREBH deficiency leads to reduced blood glucose levels but increases hepatic glycogen leve

201 glucose homeostasis in vivo Nrf2 suppresses blood glucose levels by protecting pancreatic beta cells

202 an impact of a given meal on an individual's blood glucose levels can serve as the engine for a new g

203 report, we make the unexpected finding that blood glucose levels change significantly during the cou

204 Blood glucose levels changed in accordance with how much

205 Only 8% monitored their blood glucose levels daily, 15% monitored weekly, and 10

206 on to diabetes in patients who have abnormal blood glucose levels detected by screening.

207 successfully normalized and maintained host blood glucose levels for over 370 days in the absence of

208 Leptin treatment normalized blood glucose levels in both groups.

209 lly actuated to deliver Metformin and reduce blood glucose levels in diabetic mice.

210 e appeared as viable therapeutics to control blood glucose levels in diabetic patents.

211 sEPD of insulin was found to maintain blood glucose levels in normal range for at least 6h in

212 le subcutaneous injection failed to maintain blood glucose levels in normal range.

213 ghrelin receptor antagonist further reduced blood glucose levels into the markedly hypoglycemic rang

214 It is known that even normal blood glucose levels physiologically inhibit glycogen ph

215 ults suggest a mechanism whereby oscillatory blood glucose levels recruit non-oscillating islets to e

216 nt reactive oxygen species production, while blood glucose levels remained unchanged.

217 /-):Ins2(+/Akita) mice showed a reduction in blood glucose levels that correlated with the ameliorati

218 of Langerhans are the regulators of in vivo blood glucose levels through the secretion of endocrine

219 The authors demonstrate that high blood glucose levels trigger neutrophil release of S100

220 As expected, pre-diagnostic blood glucose levels were inversely related to glioma ri

221 Changes in blood glucose levels were measured in 46 participants wi

222 Body weights, blood glucose levels were monitored throughout the study

223 In Keap1MuKO mice, blood glucose levels were significantly downregulated an

224 ARA 290 treatment significantly improved the blood glucose levels when compared to those of control a

225 Normalization of blood glucose levels with GCGR-blocking antibody unexpec

226 HT decreased blood glucose levels, adipocyte size, and triglyceride a

227 tide that plays an important role regulating blood glucose levels, analogues of which are used for tr

228 UACR and 8-OHdG, low-density lipoprotein and blood glucose levels, and duration of diabetes in patien

229 Abnormal blood pressure, blood glucose levels, and fever in the setting of arteri

230 Abnormalities of blood pressure, blood glucose levels, and temperature are prevalent in c

231 e best medical management of blood pressure, blood glucose levels, and temperature in pediatric patie

232 ogether hormonal control of blood volume and blood glucose levels, and thus adding to our understandi

233 ot fibroblast cells significantly controlled blood glucose levels, delayed diabetes onset, ameliorate

234 Sulphonylurea therapy rapidly normalizes blood glucose levels, dissipates glycogen stores, increa

235 Lower fasting blood glucose levels, higher insulin, and lower islet am

236 bumin excretion, glomerular hyperfiltration, blood glucose levels, histological deterioration and sys

237 ot have hypertension, dyslipidemia, abnormal blood glucose levels, or diabetes to behavioral counseli

238 actors (hypertension, dyslipidemia, abnormal blood glucose levels, or diabetes).

239 rs, obtaining a close correlation with their blood glucose levels, simplifying and reducing the costs

240 r disease was associated with improvement in blood glucose levels, with evidence of altered expressio

241 homeostasis of hepatic glycogen storage and blood glucose levels.

242 rect, simple and less invasive monitoring of blood glucose levels.

243 involves the release of hormones to restore blood glucose levels.

244 erated the liver injury and normalization of blood glucose levels.

245 lipotoxicity and is associated with improved blood glucose levels.

246 ocin [HFD/STZ]) to induce a mild increase in blood glucose levels.

247 action was observed without any reduction in blood glucose levels.

248 r example, blood permittivity depends on the blood glucose levels.

249 versed diastolic dysfunction, and normalized blood glucose levels.

250 flozin, increase glucose excretion and lower blood glucose levels.

251 MN patches, leading to a gradual decrease in blood glucose levels.

252 In this model, blood glucose lowering with empagliflozin attenuated som

253 able effects presumably occur independent of blood glucose lowering, we also explore the potential us

254 PHH was defined as blood glucose < 50 mg/dL AND plasma insulin > 3 mU/L at

255 weeks, were the differences from baseline in blood glucose measured 2 h after a 75 g oral glucose tol

256 verweight or obese population who received a blood glucose measurement (median 22% [IQR 11-37]); and

257 o reported that they (2) had ever received a blood glucose measurement (median 36% [IQR 27-63]); (3)

258 fasting and 2-h oral-glucose-tolerance test blood glucose measurement at re-examination rounds 4, 11

259 prehensively assessing the validity of whole blood glucose measurement in critically ill patient care

260 The efficacy was determined by nonfasting blood glucose measurements and glucose tolerance tests.

261 n the effects of exendin-4 on the control of blood glucose metabolism and beta-cell mass.

262 s special article will review the history of blood glucose meter hospital use and current issues surr

263 , including death, attributable to erroneous blood glucose meter measurements and leading to question

264 the accuracy and interference limitations of blood glucose meters and aware of the current regulatory

265 rvices are moving toward eliminating current blood glucose meters for use with critically ill patient

266 manufacturers to evaluate the performance of blood glucose meters in critically ill patient settings.

267 ance and hence insulin action in response to blood glucose, mitigating risk for hypoglycemia.

268 me's potential for the use as the enzyme for blood glucose monitor enzyme sensor strips was evaluated

269 presented can serve as a good candidate for blood glucose monitoring and for other glucose based bio

270 All participants were given daily blood glucose monitoring goals of 4 or more checks per d

271 more than 30% during lipid-lowering therapy, blood glucose monitoring is suggested to detect incident

272 tools to assess the performance of the study blood glucose monitoring system compared with laboratory

273 ools, to evaluate the clinical accuracy of a blood glucose monitoring system in critically ill patien

274 Monte Carlo simulation modeling of the study blood glucose monitoring system showed low probability o

275 y assessment algorithm demonstrated that the blood glucose monitoring system was acceptable for use i

276 ge, diabetes duration, regimen, frequency of blood glucose monitoring, physical activity, and treatme

277 ; neither HFD nor STZ alone had an effect on blood glucose or resistance artery myogenic tone.

278 contribute to platelet hyperreactivity-high blood glucose, oxidative stress, and elevated vascular s

279 e-10g reduced the blood glucose AUC and peak blood glucose (P < 0.01), whereas effects of isoleucine-

280 e (AUC) (P < 0.05) and tended to reduce peak blood glucose (P = 0.07), whereas effects of leucine-5g

281 d in significantly lowered peak postprandial blood glucose, particularly in people with prediabetes a

282 ric emptying ((13)C-acetate breath test) and blood glucose, plasma insulin, C-peptide, glucagon, gluc

283 stimulates feeding, while inhibition reduces blood glucose, raises insulin levels and suppresses feed

284 idence interval [CI], 1.04-1.16), low CSF to blood glucose ratio (HR, 1.16 per 0.10 decrease; 95% CI,

285 elationship between glycemic control (random blood glucose [RBG], fasting blood glucose [FBG], and gl

286 ings for metabolic syndrome and high fasting blood glucose remained significant for PM2.5 levels belo

287 Regulation of blood glucose requires precise coordination between diff

288 d isoleucine on the gastric emptying of, and blood glucose responses to, a physiologic mixed-macronut

289 equent ECG abnormalities but not with higher blood glucose, serum cholesterol, or serum homocysteine

290 ted a small molecule, SR-18292, that reduces blood glucose, strongly increases hepatic insulin sensit

291 ses in blood gases and a slower reduction in blood glucose suggest stress, which was accompanied by w

292 The optimal blood glucose target in critically ill patients with pre

293 glycemic control should be implemented using blood glucose target levels less than 200 mg/dL, and nor

294 for a maximum of 15 years after their first blood glucose test until glioma diagnosis, death, emigra

295 SREBP1c(-/-) and CRY1(-/-) mice show higher blood glucose than wild-type (WT) mice in pyruvate toler

296 ng with diet reversal restored the levels of blood glucose, triglycerides, cholesterol, blood urea ni

297 Diabetes increased blood glucose, urine albumin-to-creatinine ratio (ACR),

298 Lowering blood glucose using a sodium-glucose cotransporter 2 inh

299 During the year before diagnosis, blood glucose was inversely associated with glioma in th

300 , NR greatly reduced non-fasting and fasting blood glucose, weight gain and hepatic steatosis while p