ライフサイエンスコーパス: blood glucose

1 associated with liver enzymes or non-fasting blood glucose.

2 pendently and inversely correlated with mean blood glucose.

3 tion increases food intake, body weight, and blood glucose.

4 n response to body mass, feeding status, and blood glucose.

5 ior to significant changes in food intake or blood glucose.

6 d better approximate real-time deviations in blood glucose.

7 ERalpha(vlVMH) to DRN circuit both increase blood glucose.

8 hysiological importance in the regulation of blood glucose.

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

10 g mice continued to have significantly lower blood glucose.

11 evidence of mediation was found for average blood glucose.

12 nd improved mouse survival without affecting blood glucose.

13 igh-density lipoprotein, blood pressure, and blood glucose.

14 mmation, renal function, liver function, and blood glucose.

15 tivation of these VMNCCKBR neurons increased blood glucose.

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

17 Mean blood glucose 140-180 and greater than or equal to 180 m

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

19 72, -0.83, p = 0.002), and increased fasting blood glucose (16.14 mg/dL 95% CI: 6.25, 26.04, p = 0.00

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

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

22 , is the central obstacle to correcting high blood glucose, a primary cause of long-term microvascula

23 in caffeoylquinic acids and flavones reduced blood glucose, alanine aminotransferase (ALT), aspartate

24 Apo B, CRP, TNF-alpha, glucose, and fasting blood glucose among diabetic and cardiovascular disease

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

26 on of NDH and T2D and improved management of blood glucose and cardiovascular risk factors.

27 tus: its levels increased with body mass and blood glucose and decreased with fasting, RYGB, and in p

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

29 levels are inversely correlated with fasting blood glucose and hemoglobin A1c levels in men with T2DM

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

31 , hypertension, diabetes and smoking status, blood glucose and inflammatory markers, as well as distr

32 sc, twice a week) it resulted in lowering of blood glucose and inhibition of lens aldose reductase ac

33 is shown to modulate pathways that regulate blood glucose and is as effective as VNS in suppressing

34 outcomes (including blood pressure, fasting blood glucose and lipids) were assessed in a survey cond

35 ) and Taconic Biosciences were monitored for blood glucose and pilocarpine-induced salivation.

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

37 tivity up to 6 months; however, by 6 months, blood glucose and serum triglycerides in LIMP2 KO mice w

38 Blood glucose and weight were monitored until reversal o

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

40 of hepatic lipid droplets, body weight gain, blood glucose, and improved serum biochemical parameters

41 nitor (CGM) readings are delayed relative to blood glucose, and this delay is usually attributed to t

42 ermined by LM markers including breath H(2), blood glucose, and urinary galactose after a lactose tol

43 -1.06) and not practicing self-monitoring of blood glucose (AOR = 1.05, 95% CI 1.03-1.07), mediated t

44 t anti-asprosin monoclonal antibodies reduce blood glucose, appetite, and body weight, validating asp

45 gulate physiological processes like anxiety, blood glucose, appetite, inflammation and blood pressure

46 re, higher maternal BMI, and higher maternal blood glucose are associated with larger birth size thro

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

48 ir livers produce enough glucose to maintain blood glucose at viable levels even after a 23-hour fast

49 s is a chronic metabolic disease that causes blood glucose (BG) concentration to make dangerous excur

50 glycemic control, we examined the effect of blood glucose (BG) levels on GLP-1R-mediated exendin upt

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

52 vely, after adjustment for baseline HbA(1c), blood glucose, BMI, cholesterol, urine microalbumin-to-

53 Interrupting glucagon signaling lowers blood glucose but also results in hyperglucagonemia and

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

55 Nicotine increases levels of blood glucose by TCF7L2-dependent stimulation of the mHb

56 -specific deletion of WASH leads to impaired blood glucose clearance and reduced insulin release upon

57 face in response to postprandial insulin for blood glucose clearance.

58 on-free point-of-care (POC) device for whole blood glucose colorimetric detection.

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

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

61 itoring facilitates the stringent control of blood glucose concentration in diabetic and intensive ca

62 Among them, the estimation of blood glucose concentration is one of the main diagnosti

63 8-80 years with type 2 diabetes and a random blood glucose concentration of 7.8-22.2 mmol/L who were

64 a computerized decision support tool (target blood glucose concentration of 80-130 mg/dL [4.4-7.2 mmo

65 that was administered subcutaneously (target blood glucose concentration of 80-179 mg/dL [4.4-9.9 mmo

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

67 of GABAergic NTS neurons increased systemic blood glucose concentration, whereas DREADD-mediated sil

68 (DMV) that is capable of modulating systemic blood glucose concentration.

69 bility to secrete/sense insulin and abnormal blood glucose concentration.

70 cell, a critical player in the regulation of blood glucose concentration.

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

72 imary outcomes were assessed through fasting blood glucose concentrations and 2-h oral glucose tolera

73 ffspring weight post-weaning, higher fasting blood glucose concentrations and greater gonadal adiposi

74 agents promote glycosuria, thereby reducing blood glucose concentrations and often resulting in mode

75 ty in mice, which reduces fetal and neonatal blood glucose concentrations by enhancing fetal beta-cel

76 tudied after either 6 or 16 h of fasting had blood glucose concentrations comparable with those of co

77 se glucagon secretion in response to falling blood glucose concentrations compromises the defense aga

78 nt HF feeding-induced reduction in offspring blood glucose concentrations during the perinatal period

79 Short-term CFTR inhibition increased blood glucose concentrations over the course of the stud

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

81 ession of locomotor activity correlated with blood glucose concentrations, was mitigated by exogenous

82 ncy significantly reduced fetal and neonatal blood glucose concentrations.

83 al-glucose-tolerance test (OGTT) would lower blood glucose concentrations.

84 Severe or blood glucose-confirmed hypoglycaemic events were report

85 is in a good accordance with the dynamics of blood glucose content without any time delay, thus offer

86 Recommendations address self-monitoring of blood glucose, continuous glucose monitors, and automate

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

88 Blood glucose control might be an adjuvant therapy for i

89 us insulin infusion) with self-monitoring of blood glucose (control group) or to the MiniMed 640G sys

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

91 The involved protective mechanisms include blood glucose-dependent and -independent mechanisms: SGL

92 emonstrated by the colorimetric detection of blood glucose directly from human whole bloodthout any s

93 phoresis produced profound hypoglycemia (63% blood glucose drop in 3 h) without damaging the intestin

94 nsitivity improved in NMES vs. sham (average blood glucose during ITT: 139.6 +/- 8.5 vs. 161.9 +/- 9.

95 by palmitoyl-carnitine that correlated with blood glucose dysregulation, while there was no differen

96 diabetes has focused on the understanding of blood glucose elevation and its detrimental metabolic se

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

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

99 lipids, blood pressure, augmentation index, blood glucose, endothelin, adhesion molecules, or clotti

100 ntral (aortic) pressure, augmentation index, blood glucose, endothelin, proprotein convertase subtili

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

102 rticipants with high vs. low average fasting blood glucose (FBG) and homeostasis model assessment ins

103 fat mass (BFM) with blood pressure, fasting blood glucose (FBG), and urinary kidney injury markers s

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

105 No differences in fasting blood glucose (FBS), random blood glucose (RBS), or glyc

106 (PGMs) have been used for the measurement of blood glucose for decades now such that they have become

107 identify neurons that specifically increase blood glucose from among the diversely functioning cell

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

109 c and diastolic blood pressure (BP), fasting blood glucose, glycated hemoglobin (HbA1c), triglyceride

110 qual to 8.0% treated in the second era, mean blood glucose greater than or equal to 180 mg/dL was ind

111 FKBPL was negatively correlated with fasting blood glucose, HbA1c and diastolic blood pressure (DBP),

112 Glucagon and insulin maintain blood glucose homeostasis and are used to treat hypoglyc

113 the role of islet delta cells in regulating blood glucose homeostasis in vivo.

114 need to be preserved, such as maintenance of blood glucose homeostasis, balancing the degradation of

115 ncreatic beta-cells is essential to maintain blood glucose homeostasis.

116 insulin, and diabetes-like dysregulation of blood glucose homeostasis.

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

118 Elevated blood glucose (hyperglycemia) is a hallmark metabolic ab

119 goal-setting features, reminders to measure blood glucose, hypoglycemia and hyperglycemia alerts, an

120 t also modulate the homeostatic setpoint for blood glucose in an insulin-independent manner, consiste

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

122 Insulin reduced blood glucose in diabetic rats, and rescued the pressure

123 e tolerance, insulin sensitivity and fasting blood glucose in diet-induced obesity (DIO) and db/db mo

124 d via in situ photopolymerization, regulated blood glucose in insulin-deficient diabetic mice and min

125 The fall in blood glucose in L-Ghr(-/-) mice was correlated with a p

126 and mice, venom insulins significantly lower blood glucose in the streptozotocin-induced model of dia

127 al and peripheral FGF1 significantly lowered blood glucose in vivo and increased ex vivo islet insuli

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

129 he putative secreted domain) reduces fasting blood glucose independently of body weight changes, sugg

130 RNAi-mediated LincIRS2 loss causes elevated blood glucose, insulin resistance and aberrant glucose o

131 utcomes: newborn weight, adiposity, and cord blood glucose, insulin, lipids, and leptin.

132 This elevated blood glucose is not due to altered pancreatic hormone r

133 reases with elevation of Ang-2, PDGF-BB, and blood glucose; is rapidly reversed on a timescale of day

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

135 tolerance test in mice, fraction 16C reduced blood glucose level (181 +/- 10 mg/dL) in comparison to

136 Elevated blood glucose level (BGL) and NLR were strongly associat

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

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

139 accurate, and non-invasive monitoring of the blood glucose level as an effective technique for diabet

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

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

142 mns in the range of Glc-1 to Glc-20 and high blood glucose level being retained in greater quantity.

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

144 cted normal chow-fed mice showed upregulated blood glucose level by increasing gluconeogenesis, and u

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

146 Proper control of the blood glucose level can delay, and to a greater extent,

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

148 zed formulation effectively lowered the high blood glucose level in a T2D db/db mice model to the nor

149 sample also showed significant drops of the blood glucose level in rats derived from hypoglycemic ac

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

151 rategies vary significantly, irrespective of blood glucose level or diabetic status.

152 The level of HbA1c reflects the mean blood glucose level over the prior 2-3 months and it is

153 , studies seldom focus precisely on maternal blood glucose level prior to pregnancy.

154 ormulation achieved a rapid reduction of the blood glucose level to the normal range within <12 h and

155 Moreover, GLP1(HepoK) decreased blood glucose level to the same level as GLP1(WT) in mic

156 During treatment, the mean blood glucose level was 118 mg/dL (6.6 mmol/L) in the in

157 The target blood glucose level was 90-120 mg/dL for patients admitt

158 control) in the percentage of time that the blood glucose level was lower than 70 mg per deciliter w

159 The blood glucose level was maintained to below the therapeu

160 outcome was the percentage of time that the blood glucose level was within the target range of 70 to

161 es of hypoglycemia with severity of level 2 (blood glucose level, <54 mg per deciliter) or level 3 (s

162 proliferation, hepatic inflammation, fasting blood glucose level, and glucose intolerance, compared w

163 refore, to stably and accurately control the blood glucose level, CGM should be stable and accurate f

164 d release of exendin-4, prolonged control of blood glucose level, reduced dosing frequency, and impro

165 e overt graft loss observed via uncontrolled blood glucose level.

166 mproved glucose tolerance and down-regulated blood glucose level.

167 islets play an essential role in regulating blood glucose level.

168 n capability and a remarkable sensitivity of blood glucose levels (BGLs).

169 s with type 2 diabetes and poorly controlled blood glucose levels (hemoglobin A1c (HbA1c) levels of >

170 and health state of the animals with normal blood glucose levels (Table 1).

171 Offspring exhibited similar weight, blood glucose levels and baseline water and chow intake

172 type 2 diabetes drug, dapagliflozin, reduces blood glucose levels and body weight by inhibiting sodiu

173 in diagnosis of NDH and T2D, and changes in blood glucose levels and cardiovascular risk score betwe

174 Blood glucose levels and disease severities were analyze

175 of high PM2.5 exposure during pregnancy with blood glucose levels and GDM risk in Chinese women.

176 gh PM2.5 exposure during pregnancy increases blood glucose levels and GDM risk in Chinese women.

177 KY sequence resulted in a reduction in basal blood glucose levels and increased circulating serum ins

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

179 Longitudinal changes in bodyweight, blood glucose levels and plasma insulin concentration we

180 units exhibited significantly higher fasting blood glucose levels and produced more glucose than flox

181 echnology now allows real time monitoring of blood glucose levels as a time series, and thus the expl

182 both precise dosing in response to real-time blood glucose levels as well as a feasible and low-burde

183 g insulin, glargine, resulted in fluctuating blood glucose levels between 91 and 443 mg/dL in type 1

184 of Cyp46a1(-/-) mice that had normal fasting blood glucose levels but up to a 1.8-fold increase in re

185 ring trimester 1 increased 1-hour and 2-hour blood glucose levels by 1.40% (95% CI: 0.42, 2.37) and 1

186 Insulin regulates blood glucose levels by binding its receptor and stimula

187 2 (SGLT2) inhibitors were developed to lower blood glucose levels by inhibiting glucose reabsorption

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

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

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

191 Of note, non-obese diabetic mice with high blood glucose levels displayed a healthy colonic mucus b

192 odulate insulin secretion to better regulate blood glucose levels during periods of changing metaboli

193 as it gives the stable and reliable value of blood glucose levels for a period of 90-120 days.

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

195 c blood glucose sensors at lower than normal blood glucose levels has blocked their practical applica

196 aced in the rat buccal pouch in vivo lowered blood glucose levels in a dose-dependent manner (up to 5

197 es require daily insulin therapy to maintain blood glucose levels in normoglycemic ranges to prevent

198 ion of exogenous insulin aimed at regulating blood glucose levels in the normoglycemic range.

199 ore and after beverage consumption show that blood glucose levels increase when participants believe

200 N subsets appear to be capable of regulating blood glucose levels independently from the central nerv

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

202 Tracking the fluctuations in blood glucose levels is important for healthy subjects a

203 Blood glucose levels measured four times before and afte

204 criteria are present - 'D', either elevated blood glucose levels or a family history of diabetes mel

205 onitored daily food intake, body weight, and blood glucose levels over a 3-week period.

206 rojecting melanocortinergic pathway elevates blood glucose levels that is associated with increased e

207 Empagliflozin reduces blood glucose levels via inhibition of the sodium glucos

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

209 in therapy was designed to rapidly normalize blood glucose levels with bolus doses of insulin and rap

210 bility of this insulin conjugate to regulate blood glucose levels within a normal range while mitigat

211 l insulin, causing a significant decrease in blood glucose levels within one hour.

212 roved several metabolic parameters including blood glucose levels, and insulin and glucose tolerance.

213 slet-seeded biomaterial coupled with reduced blood glucose levels, collectively resulting in increase

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

215 cardiovascular risk factors such as abnormal blood glucose levels, obesity, and smoking are not inclu

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

217 ediated by systolic blood pressure (SBP) and blood glucose levels, respectively.

218 re and promoted weight gain without altering blood glucose levels, silencing VMNCCKBR neurons decreas

219 tional satisfaction are linked to changes in blood glucose levels.

220 ut did not counter leptin's ability to lower blood glucose levels.

221 duce sufficient insulin to properly regulate blood glucose levels.

222 ulin secretion and maintaining physiological blood glucose levels.

223 with an irreversible and progressive drop of blood glucose levels.

224 s which undergo exocytosis upon elevation of blood glucose levels.

225 Collectively, these changes can normalise blood glucose levels.

226 cial effects on food intake, body weight and blood glucose levels.

227 olecules in the liver and kidney to maintain blood glucose levels.

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

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

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

231 otein-coupled receptor (GPCR) that regulates blood glucose levels.

232 tract in the DIO model and increased fasting blood glucose levels.

233 parasympathetic cholinergic fibers increases blood glucose levels.

234 neogenesis, glucose intolerance, and fasting blood glucose levels.

235 increased adiposity and decreased control of blood glucose levels.

236 in the fruit fly brain that directly senses 'blood' glucose levels and reciprocally regulates the sec

237 Interestingly, blood-glucose-levels drop severely in treated animals, p

238 outcomes (including blood pressure, fasting blood glucose, lipids) were assessed after 4 years' inte

239 polyphenolics have been suggested to possess blood glucose lowering properties by inhibiting sugar tr

240 or respiratory failure, severe hypoglycemia (blood glucose < 40 mg/dL) was uncommon, but any hypoglyc

241 25 (3.6%) who developed severe hypoglycemia (blood glucose < 40 mg/dL).

242 0 mg/dL) was uncommon, but any hypoglycemia (blood glucose < 60 mg/dL) remained common and was associ

243 Cases were children with any hypoglycemia (blood glucose < 60 mg/dL), whereas controls were childre

244 correlated with efficient glycemic control (blood glucose <120 mg/dL), prevention of diabetic ketoac

245 which delays their onset of action and makes blood glucose management difficult for people with diabe

246 future interventional studies to explore new blood glucose management strategies and to substantiate

247 casion to diagnose hypertension and a single blood glucose measurement to diagnose diabetes.

248 uterized algorithm that guided the timing of blood glucose measurements and titration of insulin infu

249 ant function was assessed through nonfasting blood glucose measurements, intraperitoneal glucose tole

250 These studies relied on intermittent blood glucose measurements, which may have introduced de

251 GM (CGM group; n = 74) or usual care using a blood glucose meter for glucose monitoring (blood glucos

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

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

254 In addition to blood glucose meters, devices used by people with type 1

255 nitored firing rate changes in breathing and blood glucose modulated conditions.

256 lored the molecular mechanism underlying the blood glucose modulating effect of CO-EtOAc using L6 myo

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

258 blood glucose meter for glucose monitoring (blood glucose monitoring [BGM] group; n = 79).

259 Thus, blood glucose monitoring is a requisite tool in the mana

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

261 us glucose monitoring compared with standard blood glucose monitoring resulted in a small but statist

262 us glucose monitoring compared with standard blood glucose monitoring resulted in a small but statist

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

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

265 State-of-the-art ultra-sensitive blood glucose-monitoring biosensors, based on glucose ox

266 Blood glucose of the treated mice was monitored post inj

267 l fibrosis and glycosuria without changes in blood glucose or glomerular filtration rate compared wit

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

269 aximum current versus 2 +/- 1 min to maximum blood glucose (P = 0.0017).

270 used occasional transient elevation in their blood glucose, peri-insulitis, and Th1 responses to EGFP

271 ice did not significantly alter body weight, blood glucose, plasma insulin or glucagon levels, glucos

272 increased fructose intake, inflammation, and blood glucose (r > 0.6).

273 ICCs) of five major CVD risk factors (raised blood glucose, raised blood pressure, smoking, overweigh

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

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

276 ences in fasting blood glucose (FBS), random blood glucose (RBS), or glycated haemoglobin (HbA1c) wer

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

278 Regulation of blood glucose requires precise coordination between diff

279 Ms were implanted in mice, and sensor versus blood glucose responses were measured after an intraveno

280 commonly used approaches for the control of blood glucose responses.

281 factory sensitivity at high pH, nonenzymatic blood glucose sensing has finally been achieved, elimina

282 The saturation of nonenzymatic blood glucose sensors at lower than normal blood glucose

283 and advanced enzymes for self-monitoring of blood glucose sensors; however, the achievement of direc

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

285 s, constructing temporal profiles of fasting blood glucose, serum lipids including triglycerides, cho

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

287 ugh avoidance of bolus dosing, a liberalized blood glucose target, and gradual insulin titration.

288 atins might need greater prioritisation than blood glucose therapies, which contrasts with observed t

289 in, induced by fasting/hypoglycemia to raise blood glucose through action mediated in the liver.

290 l psychopathology subscore, higher levels of blood glucose, total cholesterol and high-density lipopr

291 and some glucagon secretagogues, and elevate blood glucose upon transplantation in mice.

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

293 Blood glucose was monitored for islet function, and miR-

294 glycemic effects on brain function; because blood glucose was not clamped prior to or during scannin

295 Blood glucose was reduced from 5 (90 mg/dl) to hypoglyce

296 ully increase subjective hunger and decrease blood glucose, we do not find significant effects of hun

297 s, systolic blood pressure (SBP) and fasting blood glucose were also contributors, and WMH volume was

298 ntitis, the dynamics of renal parameters and blood glucose were minimal whereas statistically signifi

299 production, insulin-independently decreasing blood glucose without altering energy balance.

300 ificant effect of nut consumption on fasting blood glucose (WMD: -0.52 mg/dL; 95% CI: -1.43, 0.38 mg/