ライフサイエンスコーパス: glucose load

1 ng fasting and postprandial conditions (oral glucose load).

2 lucose-glucagon challenge as well as an oral glucose load.

3 ibitors fail to inhibit >50% of the filtered glucose load.

4 0% of the reabsorption of the renal filtered glucose load.

5 GLT2 inhibitors inhibit <50% of the filtered glucose load.

6 ls with a concomitant improved response to a glucose load.

7 y in the hypothalamus in response to an oral glucose load.

8 ominantly mediated by SGLT1, independent the glucose load.

9 elopment inhibit only 30-50% of the filtered glucose load.

10 lasma glucose >or=200 mg/dl after a 2-h oral glucose load.

11 h after glucose ingestion from the ingested glucose load.

12 pressure and the insulin response to an oral glucose load.

13 at 0 (fasting), 15, 45, and 75 minutes after glucose load.

14 ripheral glucose metabolism in response to a glucose load.

15 evels were measured before and after an oral glucose load.

16 before and 60 min after ingestion of a 75-g glucose load.

17 oglycemic when fasted and hyperglycemic when glucose-loaded.

18 n sensitivity by ~12% (P < 0.05) during oral glucose loading.

19 function both basally and during subsequent glucose loading.

20 ; control 3.8+/-0.5 ng/ml, P = 0.01) on oral glucose loading.

21 nd insulin excursions in response to an oral glucose load (2 g/kg) on day 11 were unaltered.

22 od after glucose ingestion from the ingested glucose load (75 g).

23 rance test ([14C]glucose given with the oral glucose load and [3H]glucose given by intravenous infusi

24 eached approximately 50% at 30 min after the glucose load and gradually decreased thereafter.

25 d glucose tolerance after an intraperitoneal glucose load and increased insulin-stimulated whole-body

26 Glucose and insulin response to oral glucose load and pancreas pathology were evaluated after

27 se and increased hepatic glycogen after oral glucose loading and also stimulated glycogen synthesis i

28 uirement for detailed accounting of vascular glucose loads and insulin availability.

29 ), peripheral glucose (to double the hepatic glucose load), and peripheral nicotinic acid (1.5 mg.kg(

30 from the islet microtissues in response to a glucose load applied in glucose tolerance tests on diffe

31 nclusion of small amounts of fructose with a glucose load augmented NHGU, increased hepatic glycogen

32 y glucose >11.1 mmol/l 120 min after an oral glucose load, but with normal fasting glucose levels.

33 1), P = 1.5 x 10(-20)) 2 hours after an oral glucose load compared with individuals with other genoty

34 ose values obtained 1 hour after a 50-g oral glucose load comprised the exposure.

35 paired the whole-body response to a systemic glucose load, demonstrating a role for glucose sensing b

36 agon, and glucose concentrations and hepatic glucose loads did not differ among groups.

37 Dissociation was studied by incubating glucose-loaded erythrocytes in PBS without glucose.

38 ted with glucose levels obtained 2 h after a glucose load given for OGTT (r = 0.69, P = 0.001).

39 Fasting and 2-h post-glucose load glucose and insulin levels, insulin-mediate

40 ogen activator inhibitor-1, fasting and post-glucose load glucose, and insulin concentrations were me

41 o ensure low levels of plasma FFA before the glucose load, GSIS was essentially ablated in fasted rat

42 vels of maternal glucose before and during a glucose load have been associated with reduced infant bi

43 atosis, glycemia, and insulin levels after a glucose load; however, db/db-PI3Kgamma(-/-) mice display

44 ce test with measurement of fasting and post-glucose load immunoreactive insulin (IRI), specific insu

45 insulin (IRI) release in response to an oral glucose load in 94 Japanese-American subjects with norma

46 a and the pancreatic beta-cell response to a glucose load in conscious 42-h-fasted dogs.

47 ic inhibition of STRs in response to an oral glucose load in healthy lean participants.Ten healthy le

48 ythm in GLP-1 secretory responses to an oral glucose load in rats, with increased release immediately

49 Mmp9(-/-) mice had an impaired response to a glucose load in vivo, with lower serum insulin levels.

50 educed glycogen accumulation with feeding or glucose load in vivo.

51 ed solely by hyperglycemia following an oral glucose load in whom islet function is normal at euglyce

52 nd hormone responses to oral and intravenous glucose loads in patients with glucokinase (GCK)-diabete

53 Insulinaemic responses to a standard glucose load increased 2-fold from baseline to follow-up

54 asures the body's capability to dispose of a glucose load, increased from 59.0 +/- 6.3 to 75.5 +/- 6.

55 sing in vivo and in vitro approaches, that a glucose load induces a massive secretion of 26RFa by the

56 gnetic resonance spectroscopy) and SGU (oral glucose load- insulin clamp technique) were quantitated

57 d muscle glucose uptake during an intestinal glucose load is counterbalanced by an increase in the ef

58 of small intestinal glucose exposure (i.e., glucose load) is a major determinant of the comparative

59 lled laboratory samples, such as water-based glucose-loaded liquid samples.

60 The large incretin secretion after the oral glucose load might contribute to the increased ISR.

61 of either G(o1) or any G(i) proteins, handle glucose loads more efficiently than wild-type (WT) mice,

62 lays a major role in the disposal of an oral glucose load (OGL).

63 asting and approximately 1 hour after a 75-g glucose load on the same morning in 89 older men and wom

64 as 2-h or area-under-the-curve glucose after glucose load or glycosylated hemoglobin (HbA1c), and mea

65 tions in the fasting state and after an oral glucose load, overweight, and a sedentary lifestyle--are

66 glucose concentrations 60 min. after an oral glucose load performed at week 28 of pregnancy, and offs

67 m insulin levels during fasting and 2-h post-glucose load periods.

68 Fa attenuates the hyperglycemia induced by a glucose load, potentiates insulin sensitivity, and incre

69 traction times the total (oral and arterial) glucose load presented to the liver.

70 The development of standardized glucose-loading protocols, including glucose-insulin-pot

71 ased approximately 10-fold shortly after the glucose load, reached a maximum at 60 min, and then drop

72 sion of catalytic amounts of fructose with a glucose load reduces postprandial hyperglycemia and the

73 Here, we show that glucose load results in mitochondrial fission and reduce

74 liver and blood data from paired fasting and glucose-loaded sessions in five adult human volunteers,

75 Glucose loading state is not a good predictor of myocard

76 glucose concentration 2 hours after an oral glucose load than non-carriers (beta = 0.43 mmol l(-1),

77 roximal tubule reabsorbs 90% of the filtered glucose load through the Na(+)-coupled glucose transport

78 o double the blood glucose level and hepatic glucose load throughout the study.

79 was delivered intraportally, and either the glucose load to the liver (CGMP/GLC; n = 5) or the gluco

80 Following the glucose load, transient improvement of clinical seizures

81 When yeast are given a large glucose load under aerobic conditions, the fluxes of the

82 women with GDM, plasma glucose after a 50-g glucose load was correlated with both increased liking f

83 Insulin response to a 75-g oral glucose load was evaluated in healthy nondiabetic Caucas

84 0 mU. m(-2). min(-1)) clamp, and a 75-g oral glucose load was ingested 3 h after starting the insulin

85 The hepatic glucose load was similar between periods and among group

86 Insulin levels in response to a glucose load were approximately twofold higher in IRKO c

87 glucose and insulin responses to a 75-g oral glucose load were measured in the volunteers.

88 nd peripheral glucose (to double the hepatic glucose load) were infused.

89 nd peripheral glucose (to double the hepatic glucose load) were infused.

90 spite maltose hydrolysis yielding double the glucose load yielded by sucrose hydrolysis, and despite