ライフサイエンスコーパス: plasma glucose

1 l parameters (fasting plasma glucose, 2-hour plasma glucose).

2 microbiota increased adiposity but decreased plasma glucose.

3 ssociated protein kinase results in elevated plasma glucose.

4 urrent levels of body mass index and fasting plasma glucose.

5 ons to prolonged sitting reduce postprandial plasma glucose.

6 energy intake, body weight, and circulating plasma glucose.

7 sis in the skeletal muscle of rats with high plasma glucose.

8 rols in skeletal muscle of animals with high plasma glucose.

9 and somatostatin, respectively, to regulate plasma glucose.

10 0.01; P = 0.04) and had no effect on fasting plasma glucose.

11 uncertain especially in the setting of high plasma glucose.

12 n of insulin secretion upon normalization of plasma glucose.

13 an a very moderate association with elevated plasma glucose.

14 uced glucosuria and markedly lowered fasting plasma glucose.

15 tion, despite an overall decrease in fasting plasma glucose.

16 obiota transplantation (FMT) on obesity, and plasma glucose.

17 ed signalling network, for varying levels of plasma glucose.

18 ted triglycerides, 18.95% for raised fasting plasma glucose.

19 weekly exenatide and albiglutide for fasting plasma glucose (-0.7 mmol/L [CI, -1.1 to -0.2 mmol/L]; -

20 0 years; HbA(1c) 8.5% [69 mmol/mol]; fasting plasma glucose 10 mmol/L).

21 Significant improvements in fasting plasma glucose (104.2 +/- 7.8 vs. 86.7 +/- 3.1 mg/dL) an

22 rinsulinemic-hypoglycemic clamp (stepwise to plasma glucose 2.7 mmol/L).

23 nition) or (2) additionally including 2-hour plasma glucose (2-hour PG) level of 200 mg/dL or greater

24 rmore, no significant differences in fasting plasma glucose (2.9%; 95% CI: -0.4, 6.3%; P = 0.09) or b

25 was superior to clinical parameters (fasting plasma glucose, 2-hour plasma glucose).

26 c), fasting plasma glucose (FPG), and 2-hour plasma glucose (2hPG).

27 It decreased fasting and postprandial plasma glucose (-5%, P < 0.01, and -8%, P < 0.03, respec

28 Changes in fasting plasma glucose (-9.7 +/- 10.1 vs. +1.8 +/- 8.1 mg/dL, P

29 ly less exogenous glucose was needed to keep plasma glucose above 2 mmol/L (155 +/- 36 [GIP] vs. 232

30 carbohydrates are important determinants of plasma glucose after meals.

31 blood pressure, dietary risks, high fasting plasma glucose, air pollution, and high LDL cholesterol)

32 ngerol supplementation significantly reduced plasma glucose, alanine aminotransferase, aspartate amin

33 ormal across categories of worsening fasting plasma glucose (all P <0.05).

34 ntation on blood pressure, plasma lipids, or plasma glucose, although there was a trend (P = 0.069) t

35 -h postprandial period to assess the rise in plasma glucose, amino acid, and gastrointestinal hormone

36 practices had 0.2 mmol/L lower mean fasting plasma glucose and 0.9% lower cardiovascular risk score

37 ts of rs2269023 were associated with fasting plasma glucose and 1-hour plasma glucose during OGTT.

38 jejunal feeding on postprandial circulating plasma glucose and amino acid concentrations and the ass

39 r, but more transient increases in levels of plasma glucose and amino acids were accompanied by highe

40 Oxytocin attenuated the peak excursion of plasma glucose and augmented the early increases in insu

41 n resistant during pregnancy, despite normal plasma glucose and body weight, and thus serve as a mode

42 cals could be effective in the regulation of plasma glucose and cholesterol levels.

43 We examined stress physiology (plasma glucose and corticosterone), mitochondrial perfor

44 dose exceeded conventional doses, depleting plasma glucose and electrolytes, such as potassium and p

45 ose-sensing neurons in this region increases plasma glucose and glucagon, lowers insulin levels and s

46 ndernutrition, were replaced by high fasting plasma glucose and high body-mass index by 2013.

47 mbination with glucose significantly lowered plasma glucose and increased plasma insulin in mice.

48 Primary outcomes were postprandial plasma glucose and insulin (0-180 min).

49 EX reduced RaO, resulting in reduced plasma glucose and insulin concentration from 0 to 120 m

50 tivity, but directly correlated with 24-hour plasma glucose and insulin concentrations.

51 n with a decrease in hepatic DNL and 24-hour plasma glucose and insulin concentrations.CONCLUSIONSThe

52 er-specific BVRA KO mice exhibited increased plasma glucose and insulin levels and decreased glycogen

53 e 2 diabetes (T2D), along with decrements in plasma glucose and insulin levels and increments in gluc

54 Leptin reduced plasma glucose and insulin levels at 15 degrees C but no

55 reased the areas under the curve for 24-hour plasma glucose and insulin levels in both groups, with n

56 sensitivity, beta-cell function, and 24-hour plasma glucose and insulin profiles.

57 e liver, excessive postprandial excursion of plasma glucose and insulin, and a loss of metabolic flex

58 Fasting plasma glucose and lipid levels were measured before and

59 were no significant differences for fasting plasma glucose and lipid profiles within both groups aft

60 plements after a common meal on postprandial plasma glucose and plasma insulin in patients with type

61 Body weight, body composition, plasma glucose and plasma insulin were monitored.

62 th cardiovascular disease, including fasting plasma glucose and possibly HDL-C.

63 uggested an inverse association with fasting plasma glucose and serum C-reactive protein but not with

64 ose tolerance test (OGTT), with 7 samples of plasma glucose and serum insulin concentration measureme

65 glucose sensitivity and had lower levels of plasma glucose and serum potassium upon oral glucose sti

66 ective glucagon secretion, causing decreased plasma glucose and thus increased risk of hypoglycemia.

67 postprandial EF independent of reductions in plasma glucose and triglycerides.

68 Plasma glucose and urinary galactose/creatinine were unr

69 All three LM markers (breath H(2), plasma glucose and urinary galactose/creatinine) discrim

70 We measured plasma glucose and xylose appearance after oral loading,

71 ante-mortem case-control study, by contrast, plasma-glucose and plasma-copper levels did not differ b

72 s of nine AD patients and nine controls, and plasma-glucose and plasma-copper levels in an ante-morte

73 ucose tolerance test, basal insulin, fasting plasma glucose) and 1 postdonation RF, greater than 15%

74 on waist circumference, 4 trials on fasting plasma glucose, and 5 trials on C-reactive protein.

75 lf-reported physical activity level, fasting plasma glucose, and BMI were used.

76 showed a greater reduction of HbA1c, fasting plasma glucose, and body weight.

77 easures of fasting plasma glucose (FPG), 2 h plasma glucose, and HbA(1c).

78 timulating hormone (FSH), prolactin, fasting plasma glucose, and insulin levels were measured.

79 markers (HbA(1C) [hemoglobin A(1C)], fasting plasma glucose, and insulin resistance-homeostasis model

80 Body weights, plasma glucose, and insulin tolerance tests were perform

81 interaction for waist circumference, fasting plasma glucose, and lipid profiles within both groups ov

82 y mass index, fasting serum insulin, fasting plasma glucose, and type 2 diabetes.

83 5 and rs2284912 were associated with fasting plasma glucose, and variants of rs2269023 were associate

84 of measurement of lipid components, fasting plasma glucose, and visceral fat, and there might be pos

85 on in the duodenum, anandamide still reduced plasma glucose appearance in wild-type but not in CB1R(-

86 tively), and AM630 also reduced the delay of plasma glucose appearance induced by anandamide.

87 BCAA supplementation tended to decrease the plasma glucose area under the curve (AUC) measured by th

88 d a similar decrease in the 6-h postprandial plasma glucose area under the curve in both RYGB and LAG

89 for DM using glycated hemoglobin and fasting plasma glucose at TB treatment and after 3 months.

90 were screened for DM using HbA1c and fasting plasma glucose at TB treatment and after 3 months.

91 nts were the change from baseline in fasting plasma glucose at week 2 and week 28, and 2 h postprandi

92 nscriptional complexes to precisely modulate plasma glucose availability.

93 e marginally lower concentrations of fasting plasma glucose (beta = -0.18 mmol l(-1), P = 1.1 x 10(-6

94 roadways was associated with higher fasting plasma glucose (beta = 2.17 mg/dL; 95% CI: -0.24, 4.59),

95 riant have markedly higher concentrations of plasma glucose (beta = 3.8 mmol l(-1), P = 2.5 x 10(-35)

96 ood pressure, total cholesterol, and fasting plasma glucose, better health behaviors (diet, physical

97 men and in participants with normal baseline plasma glucose, body mass index, or blood pressure.

98 cose cotransport 2 inhibitors (SGLT2i) lower plasma glucose but stimulate endogenous glucose producti

99 tors group had significantly reduced fasting plasma glucose by 0.69 mmol/L [1.32; 0.07], glycosylated

100 dium-glucose cotransporter 2 (SGLT2) reduces plasma glucose by limiting glucose absorption in the kid

101 regulated by feeding time and could underpin plasma glucose changes.

102 ntestinal SCFA significantly decreased while plasma glucose, cholesterol and triglycerides, as well a

103 ls, SLMM elicited faster and sharper rise in plasma glucose compared with SG, with 88.2% and 42.9% of

104 nsulin concentration (1.62%, 0.53-2.72), and plasma glucose concentration (0.23%, 0.02-0.44).

105 icantly after RDN, whereas mean (SD) fasting plasma glucose concentration (5.9 +/- 0.7 mmol/L), media

106 terozygous carriers have a moderately higher plasma glucose concentration 2 hours after an oral gluco

107 n age 38 years, body weight 81.7 kg, fasting plasma glucose concentration 83 mg/dL, and fasting insul

108 roduces comparable glucosuria but lowers the plasma glucose concentration and improves beta-cell func

109 (n = 12); 2) repeat EGP measurement with the plasma glucose concentration clamped at the fasting leve

110 ated to achieve a self-measured prebreakfast plasma glucose concentration of 4-5 mmol/L.

111 stained physiologic increase of ~50 mg/dL in plasma glucose concentration on insulin secretion in nor

112 ession during OGTT, whereas the rise in mean plasma glucose concentration only became manifest when s

113 alipid, compared with saline, did not affect plasma glucose concentration or EGP throughout the study

114 Empagliflozin reduced the plasma glucose concentration threshold for glucose spill

115 n in Denmark, we found that impaired fasting plasma glucose concentration was associated with 44% (9-

116 lic risk factors (blood pressure and fasting plasma glucose concentration), along with binary variabl

117 inistration are secondary to the decrease in plasma glucose concentration, and 2) the dapagliflozin-i

118 g/dL, which is well below the normal fasting plasma glucose concentration.

119 to release insulin in response to changes in plasma glucose concentration.

120 ompared with GLU, FRU also resulted in lower plasma glucose concentrations and decreased exercise per

121 negatively correlated to changes in fasting plasma glucose concentrations and in the homeostatic mod

122 blocked corticosterone-induced increases in plasma glucose concentrations and rates of HGP and ketog

123 der normal physiological conditions, fasting plasma glucose concentrations are kept within a narrow r

124 tenuation of the sympathoadrenal response as plasma glucose concentrations fall.

125 res were similar in both genotypes; however, plasma glucose concentrations in Acsl1(M-/-) mice were a

126 utoimmunity, which correlated with HbA1c and plasma glucose concentrations in an oral glucose toleran

127 ol levels, plasma insulin concentrations and plasma glucose concentrations in men and women.

128 Mean +/- SEM pre- and postfilter venous plasma glucose concentrations in the aggregate group wer

129 tiveness" is a major contributor to elevated plasma glucose concentrations in type 2 diabetes (T2D).

130 phrine and glucagon secretion with declining plasma glucose concentrations is not in response to a de

131 g hyperinsulinemic glucose clamps at nominal plasma glucose concentrations of 90, 75, 60, and 45 mg/d

132 Prefilter plasma glucose concentrations were higher in patients wi

133 IN insulin dose-dependently decreased plasma glucose concentrations while reducing C-peptide a

134 eases in cytosolic redox state, decreases in plasma glucose concentrations, and inhibition of endogen

135 -with the exception of their effect to lower plasma glucose concentrations-is an area of active inves

136 in secretion persists in the presence of low plasma glucose concentrations.

137 y in vivo, resulting in modest reductions in plasma glucose concentrations.

138 ned essentially identical effects on fasting plasma glucose concentrations.

139 gulated gluconeogenesis and resulted in high plasma glucose content by increasing PEPCK and G6P mRNA

140 Fasting plasma glucose did not differ between trials (P > 0.05)

141 t sustained inflammation results in elevated plasma glucose due to increased hepatic glucose producti

142 iated with fasting plasma glucose and 1-hour plasma glucose during OGTT.

143 sive gestational weight gain, raised fasting plasma glucose during pregnancy, short breastfeeding dur

144 nduced insulin resistance, increased fasting plasma glucose, enhanced ceramide accumulation and PP2A

145 clusion, endogenous GIP affects postprandial plasma glucose excursions and insulin secretion more tha

146 ensitivity to insulin and leptin and reduced plasma glucose excursions following the administration o

147 ly accounts for the lack of a dose effect on plasma glucose excursions.

148 /rs2269023 were also associated with fasting plasma glucose, fasting insulin and HOMA-IR.

149 y, nor did titrating treatment using fasting plasma glucose (for areas without HbA1c testing).

150 to 3 months after transplantation by fasting plasma glucose (fPG) >/= 7.0 mmol/L (>/= 126 mg/dL) and/

151 rum hemoglobin A1C (A1C) >/=6.5%, or fasting plasma glucose (FPG) >/=126 mg/dL, prediabetes as A1C 5.

152 tests such as hemoglobin A1c (HbA1c)/fasting plasma glucose (FPG) alone fail to diagnose or miscatego

153 rs964184 exhibited higher levels of fasting plasma glucose (FPG) and blood hemoglobin A1c (HbA1c) th

154 atients.We studied concentrations of fasting plasma glucose (FPG) and fasting insulin (FI) as prognos

155 inhibition with empagliflozin on the fasting plasma glucose (FPG) concentration and beta-cell functio

156 We investigated the association of fasting plasma glucose (FPG) concentrations during pregnancy wit

157 ciations between preconception blood fasting plasma glucose (FPG) level and subsequent pregnancy outc

158 in A1c level of 6.5% or greater or a fasting plasma glucose (FPG) level of 126 mg/dL or greater (hemo

159 of subgingival microbiota predicted fasting plasma glucose (FPG) longitudinally.

160 of 6.5% (48 mmol/mol) or greater or fasting plasma glucose (FPG) of 7.0 mmol/L or greater.

161 Gestational fasting plasma glucose (FPG) was positively associated with birt

162 -report, medication use, measures of fasting plasma glucose (FPG), 2 h plasma glucose, and HbA(1c).

163 surements of hemoglobin A1c (HbA1c), fasting plasma glucose (FPG), and 2-hour plasma glucose (2hPG).

164 ss index (BMI), blood pressure (BP), fasting plasma glucose (FPG), and type 2 diabetes (T2D).

165 moglobin (Hb) A1c (primary outcome), fasting plasma glucose (FPG), serum N(euro)-(carboxymethyl) lysi

166 od pressures, body mass index (BMI), fasting plasma glucose (FPG), triglycerides (TG) and cholesterol

167 We used fasting plasma glucose, glucose tolerance tests, and self-report

168 aist circumference, body mass index, fasting plasma glucose, glycohemoglobin, low-density lipoprotein

169 L (>/= 126 mg/dL) and/or 2 hr post-challenge plasma glucose >/= 11.1 mmol/L (>/= 200 mg/dL) during an

170 main outcome measures were diabetes (fasting plasma glucose >/= 126 mg/dL or taking medication), comm

171 Plasma glucose >/=11 mmol/L was associated with impaired

172 Participants who had a fasting plasma glucose >/=126 mg/dL and/or a 2-hour plasma gluco

173 and <6.5% and (2) diabetes mellitus: fasting plasma glucose >/=126 mg/dL, 2-hour postload glucose >/=

174 Diabetes was defined as nonfasting plasma glucose >/=200 mg/dl (11.1 mmol/l), glycated hemo

175 plasma glucose >/=126 mg/dL and/or a 2-hour plasma glucose >/=200 mg/dL during a 75-g oral glucose t

176 ma glucose >= 7.0 mmol/l (126 mg/dl), random plasma glucose >= 11.1 mmol/l (200 mg/dl), HbA1c >= 6.5%

177 Diabetes was defined as fasting plasma glucose >= 7.0 mmol/l (126 mg/dl), random plasma

178 ons of intermediate hyperglycaemia: IGT (2 h plasma glucose >=7.8 mmol/L [>=140 mg/dL]); IFG based on

179 al associations of glycemic markers (fasting plasma glucose, HbA(1C), and homeostasis model assessmen

180 include the lack of data on diet and midlife plasma glucose, high rate of attrition, as well as the l

181 ic factors (high SBP, high BMI, high fasting plasma glucose, high total cholesterol, and low glomerul

182 gnificant differences were found for fasting plasma glucose, high-density lipoprotein cholesterol, or

183 st p values and found some genes involved in plasma glucose homeostasis (GLP1R) and lipid metabolism

184 Supplementation with UT improved plasma glucose homeostasis and enhanced skeletal muscle

185 t of both wines on glycemic control (fasting plasma glucose, homeostatic model assessment of insulin

186 d with incident diabetes after adjusting for plasma glucose, implying a glucose independent associati

187 ion in WAT inversely correlated with fasting plasma glucose in both obese mice and humans.

188 s, high systolic blood pressure, and fasting plasma glucose in ranked attributable proportions within

189 Here, we investigated (13)C labeling in plasma glucose in rats given [U-(13)C3]glycerol under va

190 INI has been shown to lower plasma glucose in some studies, but whether it regulates

191 atory glycated hemoglobin (HbA1c) or fasting plasma glucose in TB patients.

192 tary group (-49%; p = 0.01) and postprandial plasma glucose in the Exercise group (-19%; p = 0.03).

193 Fasting plasma glucose increased from 94 +/- 2 to 142 +/- 4 mg/d

194 Among all fetuses, blood O2 saturation and plasma glucose, insulin and insulin-like growth factor-1

195 d to test for prediabetes, including fasting plasma glucose, insulin resistance (measured by the Home

196 Plasma glucose, insulin sensitivity and insulin secretio

197 the mixed meal induced a greater increase in plasma glucose, insulin, and GIP concentrations after su

198 ffect of dapagliflozin on EGP while clamping plasma glucose, insulin, and glucagon concentrations at

199 Silencing PEPCK-M lowers plasma glucose, insulin, and triglycerides, reduces whit

200 Furthermore, LT175 significantly reduced plasma glucose, insulin, non-esterified fatty acids, tri

201 Hypoglycaemia (low plasma glucose) is a serious and potentially fatal compl

202 Fetal plasma glucose, lactate or alpha-amino nitrogen concentr

203 glucose level, 100 to 125 mg per deciliter; plasma glucose level 2 hours after a 75-g oral glucose l

204 rved, while physiological effects, including plasma glucose level and blood leukocyte numbers were si

205 Data on 2-hour plasma glucose level and HbA1c concentration were not av

206 The fasting plasma glucose level had decreased at both time points i

207 compared with the wild-type Gly-297 allele) plasma glucose level in our study population (n = 410).

208 Control of plasma glucose level is essential to organismal survival

209 ined as a self-reported diagnosis or fasting plasma glucose level of 7.0 mmol/L (126 mg/dL) or more.

210 Among the adults, the mean plasma glucose level over the 5-day bionic-pancreas peri

211 Among the adolescents, the mean plasma glucose level was also lower during the bionic-pa

212 The performance in prediction of fasting plasma glucose level was measured using 100 bootstrap it

213 1.2% in each group, whereas the mean fasting plasma glucose level was significantly lower in the degl

214 nger duration of diabetes and higher fasting plasma glucose level were associated with lower normal (

215 e glycemic criteria for prediabetes (fasting plasma glucose level, 100 to 125 mg per deciliter; plasm

216 waist circumference, hypertension, elevated plasma glucose level, and dyslipidemia).

217 1c level, and 171.3 (72.5) mg/dL for fasting plasma glucose level.

218 brain glucose content and have no effect on plasma glucose level.

219 ry end points included the change in fasting plasma glucose level.

220 RR = 1.64 [95% CI: 1.07-2.98]), high fasting plasma glucose levels (>/=126 mg/dL versus < 110 mg/dL,

221 cent of LQT2 patients developed hypoglycemic plasma glucose levels (<70 mg/dL) versus 36% control par

222 Fasting plasma glucose levels (Hedges g = 0.20; 95% CI, 0.02 to

223 us (IV) glucose administration under similar plasma glucose levels (incretin effect).

224 es g = 0.20; 95% CI, 0.02 to 0.38; P = .03), plasma glucose levels after an oral glucose tolerance te

225 reporting on fasting plasma glucose levels, plasma glucose levels after an oral glucose tolerance te

226 ifferences in fasting plasma glucose levels, plasma glucose levels after an oral glucose tolerance te

227 a GIP responses (P=0.03-0.001) and decreased plasma glucose levels after glucose ingestion (P=0.02) w

228 , which is far superior to measuring fasting plasma glucose levels alone.

229 cose and calorie excretion, thereby reducing plasma glucose levels and body weight.

230 In vivo, constitutively active YAP lowers plasma glucose levels and increases liver size.

231 n an inverted "U-shape" fashion dependent on plasma glucose levels and related to metabolic states.SI

232 iabetes in the ILS group, and higher fasting plasma glucose levels at baseline in the placebo group.

233 nhibiting small intestinal mTOR alone lowers plasma glucose levels by inhibiting glucose production i

234 rs glucagon secretion, which restores normal plasma glucose levels by stimulation of hepatic glucose

235 Despite a similar change in plasma glucose levels during the hyperglycemic clamp, in

236 tissue-specific GLUT4 expression and raised plasma glucose levels in LKO mice.

237 vivo, compound (R,R)-68 significantly lowers plasma glucose levels in mice during an oral glucose cha

238 onin treatment significantly reduced fasting plasma glucose levels in the rats with DM.

239 secretion and how the resulting decrease in plasma glucose levels leads to cessation of secretion.

240 Proportion of patients with fasting plasma glucose levels less than 126 mg/dL and HbA1c less

241 Plasma glucose levels were inversely correlated with HDL

242 Although plasma glucose levels were not affected by Tgfb1 genotyp

243 Mean 0-hour and 2-hour plasma glucose levels were significantly higher at follo

244 that high body mass index, elevated fasting plasma glucose levels, and nonalcoholic fatty liver dise

245 his haplotype had higher plasma CHGA levels, plasma glucose levels, diastolic blood pressure, and bod

246 of diabetes was evaluated by testing fasting plasma glucose levels, hemoglobin A1c levels, and durati

247 es were identified by fasting or non-fasting plasma glucose levels, oral glucose tolerance tests, hem

248 Overriding IR in an effort to lower plasma glucose levels, particularly with intensive insul

249 Case-control studies reporting on fasting plasma glucose levels, plasma glucose levels after an or

250 Standardized mean differences in fasting plasma glucose levels, plasma glucose levels after an or

251 an array of hormones that precisely regulate plasma glucose levels.

252 enal Ampk-dependent pathway to lower HGP and plasma glucose levels.

253 bolism, thereby linking insulin secretion to plasma glucose levels.

254 of anabolic bistable region with respect to plasma glucose levels.

255 chronic low-grade inflammation and elevated plasma glucose levels.

256 atments were equally efficacious in reducing plasma glucose levels.

257 In summary, plasma glucose lowering by empagliflozin improves plaque

258 zing drugs such as glitazones, which improve plasma glucose maintenance in patients with diabetes.

259 ratio 5.44 [2.63 to 11.27]), but not fasting plasma glucose (mean difference 0.03 mmol/L [-0.04 to 0.

260 incremental area under the curve (iAUC) for plasma glucose [mg/dL . min; mean (95% CI)] did not diff

261 ceeded the possible contribution from either plasma glucose or muscle oxaloacetate.

262 ctor to discern the concentration of average plasma glucose over a long-drawn-out period.

263 gy expenditure, whole-body glucose disposal, plasma glucose oxidation, and insulin sensitivity in the

264 ly), average 24-h BP values (all p < 0.001), plasma glucose (p = 0.008), TG (p = 0.003), TG: HDL-C ra

265 G (p = 0.001), HbA1c (p = 0.019) and fasting plasma glucose (p = 0.019) and significant increase in H

266 wer rate of diabetes onset p = 0.027), lower plasma glucose (p = 0.043), and lower HbA1c (p = 0.008)

267 artum weight reduction on changes in fasting plasma glucose (P-interaction = 0.03).

268 rent postprandial hypoglycemia documented by plasma glucose (PG) <=3.4 mmol/L were examined on 2 d wi

269 rter 2 inhibitors (SGLT2i) effectively lower plasma glucose (PG) concentration in patients with type

270 Higher maternal plasma glucose (PG) concentrations, even below gestation

271 ificantly lower glycated hemoglobin, fasting plasma glucose, plaque index, gingival index, probing de

272 O2 saturation (r(2) = 0.80, P < 0.0001) and plasma glucose (r(2) = 0.68, P < 0.0001), insulin (r(2)

273 lues ranging from 5.7% to 6.4% or 2) fasting plasma glucose ranging from 100 to 125 mg/dL.

274 .004), but the percentage of time with a low plasma glucose reading was similar during the two period

275 Following late meals, however, plasma glucose rhythms were delayed by 5.69 +/- 1.29 hr

276 between cholesterol intake and risk of T2D, plasma glucose, serum insulin, and C-reactive protein we

277 o -0.07], P<0.001, respectively; for fasting plasma glucose, standardized B=-0.09 [-0.15 to -0.04], P

278 ated weekly to a pre-breakfast self-measured plasma glucose target of 4.0-5.5 mmol/L [72-99 mg/dL]) f

279 ce-weekly GLP-1RAs reduced HbA1c and fasting plasma glucose; taspoglutide, 20 mg, once-weekly exenati

280 ce lacking hepatic Ppp1r3b had lower fasting plasma glucose than controls.

281 17:0 were inversely associated with fasting plasma glucose, the area under the curve for glucose dur

282 specificity of breath H(2) was greater than plasma glucose to detect LNP following lactose challenge

283 dex [BMI] as behavioral CVH metrics; fasting plasma glucose, total cholesterol, and blood pressure as

284 Plasma glucose, total cholesterol, LDL cholesterol, and

285 ificantly reduced body weight, heart weight, plasma glucose, triglyceride, and insulin levels in db/d

286 tory blood pressure monitoring (BP), fasting plasma glucose, triglycerides (TG), cholesterol levels (

287 Plasma glucose, urea, and electrolytes were analyzed and

288 Fasting plasma glucose was also inversely correlated with ischem

289 Each 10-mg/dL increase in fasting plasma glucose was associated with higher odds of LV hyp

290 The first hour, plasma glucose was lowered by insulin infusion, and the

291 mp experiments conducted in healthy dogs, as plasma glucose was lowered stepwise from 280 mg/dL to 80

292 Plasma glucose was maintained by infusion of glucose in

293 Plasma glucose was significantly higher for both O-GDM a

294 tion, higher glycohemoglobin A1c and fasting plasma glucose were associated with lower retinal arteri

295 e) against periodontal bacteria and elevated plasma glucose were in qualitatively opposite directions

296 e, blood pressure, serum lipids, and fasting plasma glucose) were collected.

297 76.4) for FPG, and 77.1% (75.4-78.8) for 2 h plasma glucose, whereas the AUC for a score composed of

298 2.70% dietary arginine level results in high plasma glucose, which could lead to negative feedback of

299 Here, we examined whether reduction of plasma glucose with a sodium-glucose cotransporter 2 (SG

300 ogether, our data indicate that reduction of plasma glucose with an agent that works specifically on