ライフサイエンスコーパス: after meal

1 d anaphylactic reactions induced by exercise after meals.

2 s rated their hunger and fullness before and after meals.

3 es for plasma Cys occurred approximately 3 h after meals.

4 d by using visual analogue scales before and after meals.

5 ysis from adipose tissue by insulin released after meals.

6 whereas they were less likely to brush teeth after meals.

7 Gastroesophageal reflux typically occurs after meals.

8 are important determinants of plasma glucose after meals.

9 were fasting and at 30, 60, 90, and 120 min after meals.

10 +/- 3.3% at fasting, peaked at 18.2 +/- 7.1% after meal 1 (P = 0.003 compared with fasting), rose fur

11 Peak insulin concentrations after meal 1 correlated with peak DNL (R = 0.838, P = 0.

12 with fasting), rose further to 23.1 +/- 8.9% after meal 2 (P = 0.01 for difference between meals), an

13 ere abdominal pain (90%), pain predominantly after meals (76%), nausea (85%), and early fullness afte

14 eals (76%), nausea (85%), and early fullness after meals (79%).

15 c oxide were measured at baseline and 30 min after meal administration.

16 rent subjects were collected both before and after meals and analyzed in a double-blind fashion in tw

17 ured by weighing the feeding bowl before and after meals, and breast milk intake was measured by test

18 CAP values declined after meals at early fibrosis stages and across all stag

19 tly more acidic than the body of the stomach after meals but not during fasting.

20 PA) to aspirate gastric contents 20 minutes after meal consumption.

21 of satiety at defined time points up to 6 h after meal consumption.

22 before and 30, 60, 90, 120, 150, and 180 min after meal consumption.

23 Portal blood flow increased similarly after meals containing dark or white chocolate (median i

24 texercise energy balance, appetite responses after meals differing in GI are of particular interest.

25 se data confirm the acute stimulation of DNL after meals in healthy subjects and validate the contrib

26 increased during head-up tilt-table testing after meal ingestion (12% during preprandial testing and

27 umes, maximal gastric volume occurred 20 min after meal ingestion (189% +/- 25% of baseline).

28 g/3 hours and 9.2 [IQR, 5.2] g/3 hours) and after meal ingestion (median, 29.0 [IQR, 12.5] g/5 hours

29 sed by CA plus diet treatment vs. diet alone after meal ingestion (P = 0.004).

30 After meal ingestion and head-up tilt-table testing, 22%

31 ed (P < 0.05) to a peak of 353 +/- 55 nmol/l after meal ingestion but did not change after saline inf

32 meal; serum was collected before and 1 hour after meal ingestion for quantitative determination of 1

33 Glucose tolerance after meal ingestion in vivo is the result of multiple p

34 arent alterations in DNA methylation 160 min after meal ingestion mainly reflect changes in the estim

35 tal-body cortisol and D3 cortisol production after meal ingestion originated in extrasplanchnic tissu

36 ension tended to occur more often and sooner after meal ingestion than before meal ingestion (P = 0.0

37 The increase in cortisol after meal ingestion was associated with an increase in

38 The relative increase in insulin secretion after meal ingestion was comparable in diabetic and nond

39 Furthermore, the decrease in insulin action after meal ingestion was compensated in all groups by an

40 st, glucose disappearance (R(d)) immediately after meal ingestion was lower (P < 0.001) in subjects w

41 Resting energy expenditure rates and those after meal ingestion were unchanged.

42 After meal ingestion, glucose and insulin AUC decreased,

43 Glucose and insulin concentrations increased after meal ingestion, peaking at 11.0 +/- 1.0 mmol/l and

44 After meal ingestion, plasma insulin was lower for oat t

45 - 12% of baseline; P < 0.05) occurred 40 min after meal ingestion, when only 69% +/- 3% of the radiol

46 for a rapid increase during the first 30 min after meal ingestion.

47 s and lean subjects in the fasting state and after meal ingestion.

48 were collected at different times during 7h after meal ingestion.

49 mulating glucose-dependent insulin secretion after meal ingestion.

50 sma samples were collected over a 7 h-period after meal ingestion.

51 response) and minutes 30-180 (late response) after meal ingestion.

52 9% +/- 13% of baseline) occurred immediately after meal ingestion; total CSA remained significantly i

53 A significant increase in LS values after meal intake was observed within 15 to 120 min, wit

54 619-induced fibrinogen binding was unchanged after meal intake with placebo but was markedly enhanced

55 Similarly, after meal intake, arterial baroreflex-MSNA gain for bur

56 id was administered 1 hour before or 2 hours after meals on days 1 through 5, with escalated doses of

57 tients were administered oral GTE with water after meals one or three times daily for 4 weeks, to a m

58 Postprandial blood samples were collected after meal or physiological serum (control) administrati

59 tryptamine (5-HT) and releases large amounts after meals or exposure to toxins.

60 ferences in hunger or fullness before meals, after meals, or over the 2 d across conditions.

61 s were taken at fasting (0 and 24 hours) and after meals over the day to mimic typical food consumpti

62 0.001), glucagon during the first 30 minutes after meal (P < 0.05), and leptin levels (P < 0.05).

63 Fibrinolytic activity is not lower after meals rich in palmitate or oleate than after a low

64 However, adipose tissue fat storage after meals was substantially depressed in the obese men

65 ease in portal and peripheral levels of S-28 after meals, with minimal changes in S-14.

66 s was observed in all patients 15 to 120 min after meals, with the CAP peak value at 60 min and the m