ライフサイエンスコーパス: plasma glucose

1 ons to prolonged sitting reduce postprandial plasma glucose.

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

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

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

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

6 and somatostatin, respectively, to regulate plasma glucose.

7 0.01; P = 0.04) and had no effect on fasting plasma glucose.

8 uncertain especially in the setting of high plasma glucose.

9 n of insulin secretion upon normalization of plasma glucose.

10 an a very moderate association with elevated plasma glucose.

11 uced glucosuria and markedly lowered fasting plasma glucose.

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

13 VMH attenuated the effect of systemic E2 on plasma glucose.

14 in the ventromedial nucleus (VMH), restored plasma glucose.

15 cortisol and curbed the meal-related rise in plasma glucose.

16 of type 2 diabetes risk variants on fasting plasma glucose.

17 ssociated protein kinase results in elevated plasma glucose.

18 urrent levels of body mass index and 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 Significant improvements in fasting plasma glucose (104.2 +/- 7.8 vs. 86.7 +/- 3.1 mg/dL) an

21 litazone also significantly improved fasting plasma glucose (-11+/-14 mg/dL; P=0.003), although the p

22 ficant decrease in concentrations of fasting plasma glucose (-17.1 +/- 14.8 compared with -0.9 +/- 16

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

24 Incremental venous plasma glucose (2-h area under the curve) was 2.4-fold g

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

26 y outcomes included fasting insulin, fasting plasma glucose, 2-hour plasma glucose, and lipid levels,

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

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

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

34 rimary outcome (difference in change in 2-hr plasma glucose among the three groups) did not reach sta

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

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

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

38 cident type 2 diabetes and 5-year changes in plasma glucose and beta-cell function.

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

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

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

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

43 ness (at 1 mm) and the levels of the fasting plasma glucose and glycosylated hemoglobin (HbA1c) were

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

45 el genome-wide significant associations: 2-h plasma glucose and HKDC1, and fasting C-peptide and BACE

46 21 days decreased body weight and nonfasting plasma glucose and increased circulating plasma insulin

47 When Ab1 was tested in vivo, it reduced plasma glucose and increased plasma GLP-1 concentration

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

49 mbination with glucose significantly lowered plasma glucose and increased plasma insulin in normal an

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

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

52 Fasting transgenic mice had decreased plasma glucose and insulin concentrations compared with

53 Plasma glucose and insulin concentrations were measured

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

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

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

57 Plasma glucose and insulin levels were higher in patient

58 howed normal plasma triglyceride levels, and plasma glucose and insulin levels were reduced by 40-60%

59 tive hyperglucagonemia and the rapid fall in plasma glucose and insulin levels.

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

61 Fasting plasma glucose and lipid levels were measured before and

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

63 comprised 64 individuals with normal fasting plasma glucose and normal glucose tolerance.

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

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

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

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

68 iation of TCF7L2 splicing with the levels of plasma glucose and serum free fatty acids (FFAs) in thre

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

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

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

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

73 atients with pre-DM showing impaired fasting plasma glucose and/or impaired oral glucose tolerance.

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

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

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

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

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

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

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

81 ting insulin, fasting plasma glucose, 2-hour plasma glucose, and lipid levels, insulin sensitivity, l

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

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

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

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

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

87 In both treatment groups, 2-hr plasma glucose at 3 months was significantly reduced com

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

89 nscriptional complexes to precisely modulate plasma glucose availability.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 here was a concentration-related increase in plasma glucose concentration and a decrease in blood lym

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

106 The sustained model raised the average plasma glucose concentration from 70 mg/dL to 180 mg/dL

107 ndiagnosed diabetes was defined as a fasting plasma glucose concentration of >/=126 mg/dL and was ass

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

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

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

111 Empagliflozin reduced the plasma glucose concentration threshold for glucose spill

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

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

114 ndex, systolic and diastolic blood pressure, plasma glucose concentration, height, years of attained

115 3 days of development caused daily spikes in plasma glucose concentration.

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

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

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

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

120 Pyruvate carboxylase ASO reduced plasma glucose concentrations and the rate of endogenous

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

122 ences in BMI, serum inflammatory markers, or plasma glucose concentrations between groups.

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

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

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

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

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

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

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

130 Prefilter plasma glucose concentrations were higher in patients wi

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

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

133 ed fasting, wild-type neonates recover their plasma glucose concentrations, but RagA(GTP/GTP) mice re

134 ned essentially identical effects on fasting plasma glucose concentrations.

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

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

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

138 At study initiation, plasma glucose, creatinine, triglyceride and cholesterol

139 ngested the same caloric dose, the change in plasma glucose depended upon individual differences in g

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

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

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

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

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

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

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

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

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

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

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

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

152 with HS progression were changes in fasting plasma glucose (FPG) between biopsies (per 10 mg/dL incr

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

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

155 commended for diabetes diagnosis but fasting plasma glucose (FPG) has been useful for identifying pat

156 The sensitivity of fasting plasma glucose (FPG) in screening for new-onset diabetes

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

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

159 Fasting plasma glucose (FPG) was measured from capillary blood u

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

161 (SBP), serum total cholesterol (TC), fasting plasma glucose (FPG), and body mass index (BMI) on the r

162 cut-point values of FINDRISC score, fasting plasma glucose (FPG), and HbA1c.

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

164 for glycated hemoglobin A1c (HbA1c), fasting plasma glucose (FPG), total cholesterol (TC), triglyceri

165 , systolic blood pressure (SBP), and fasting plasma glucose (FPG), triglyceride, and high-density lip

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 tion rate constant increased with decreasing plasma glucose (Gp), in particular at a Gp of less than

170 s) and >/= 88 cm (female adults); 2) fasting plasma glucose >/= 100 mg/dl; 3) blood pressure of >/= 1

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

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

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

174 pBG] >/=11.1 mmol/L, FPG >/=7.0 mmol/L, 2-hr plasma glucose >/=11.1 mmol/L, or glycated hemoglobin [H

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

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

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

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

179 Fasting plasma glucose had weaker associations with these countr

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

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

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

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

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

185 Plasma glucose iAUC also differed between interventions

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

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

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

189 ks on a high fat diet, the decreased fasting plasma glucose in transgenic mice compared with controls

190 aloric low-GI meal, a high-GI meal decreased plasma glucose, increased hunger, and selectively stimul

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

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

193 d DeltaISR/DeltaG x MI) were calculated from plasma glucose, insulin, and C-peptide concentrations du

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

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

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

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

198 The OGCT and fasting plasma glucose level (at a threshold of 4.7 mmol/L [85 m

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

200 ip was found between CMT, HbA1c, and fasting plasma glucose level in either group (p=0.05).

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

202 Control of plasma glucose level is essential to organismal survival

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

204 had poorer test characteristics than fasting plasma glucose level or the OGCT.

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

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

207 1.2% in each group, whereas the mean fasting plasma glucose level was significantly lower in the degl

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

209 1c level, and 171.3 (72.5) mg/dL for fasting plasma glucose level.

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

211 exhibited a 37% (P<0.05) decrease in fasting plasma glucose level.

212 e of one of four parameters: (i) two fasting plasma glucose levels >/= 126 mg/dL (>/= 7.0 mmol/L) >/=

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

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

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

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

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

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

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

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

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

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

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

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

225 ssion of hepatic CES1 lowered hepatic TG and plasma glucose levels in both wild-type and diabetic mic

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

227 ies, administration of 2-AAA lowered fasting plasma glucose levels in mice fed both standard chow and

228 Fasting plasma glucose levels in nondiabetic individuals were al

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

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

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

232 was strongly associated with the changes in plasma glucose levels produced by ingestion of the bever

233 betic phenotype, evidenced by higher fasting plasma glucose levels than wild-type mice.

234 st, exogenous insulin-induced suppression of plasma glucose levels was significantly greater in RYGB

235 Increasing fasting and 2-h plasma glucose levels were associated with elevated leve

236 In the diabetic state, plasma glucose levels were increased in CTGF+/+ and CTGF

237 Plasma glucose levels were inversely correlated with HDL

238 Although plasma glucose levels were not affected by Tgfb1 genotyp

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

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

241 ucagon infusion was accompanied by a rise in plasma glucose levels, but addition of GLP-1 to glucagon

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

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

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

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

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

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

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

249 atments were equally efficacious in reducing plasma glucose levels.

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

251 the body's only hormone capable of lowering plasma glucose levels.

252 nses that can occur in response to declining plasma glucose levels.

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

254 Blood samples were taken to assess fasting plasma glucose, low-density lipoprotein, high-density li

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

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

257 Plasma glucose measured during an emergency hospital adm

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

259 ce of moderate-dose prednisolone, where peak plasma glucose occurs 7 to 8 hr after administration.

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

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

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

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

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

265 ass index, high blood pressure, high fasting plasma glucose, physical inactivity, and alcohol use.

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

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

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

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

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

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

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

273 sociations of body mass index (BMI), fasting plasma glucose, systolic blood pressure, and serum total

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

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

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

277 17:0 were inversely associated with fasting plasma glucose, the area under the curve for glucose dur

278 For a fasting plasma glucose threshold of 4.7 mmol/L (85 mg/dL), they

279 Plasma glucose, total cholesterol, LDL cholesterol, and

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

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

282 Plasma glucose, urea, and electrolytes were analyzed and

283 ive increase in fasting, 30-min, and 120-min plasma glucose values and a relative decrease in measure

284 oglobin A1c levels less than 6.5% or fasting plasma glucose values less than 126 mg/dL without pharma

285 Plasma glucose values obtained 1 hour after a 50-g oral

286 Fasting plasma glucose was also inversely correlated with ischem

287 This association between TCF7L2 splicing and plasma glucose was independent of the TCF7L2 genotype.

288 Plasma glucose was lower (mean +/- SE: 4.7 +/- 0.14 comp

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

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

291 Plasma glucose was maintained by infusion of glucose in

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

293 etic risk score on 5-year changes in fasting plasma glucose was stronger in individuals who increased

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

298 OVX caused a 17% decrease in plasma glucose, which was completely restored by systemi

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