ライフサイエンスコーパス: pre-diabetes

1 ntrations and size in 2993 participants with pre-diabetes.

2 is known to be disrupted in mouse models of pre-diabetes.

3 dy outcome, signifying potential diabetes or pre-diabetes.

4 throcytes of human subjects with diabetes or pre-diabetes.

5 Association criteria to define diabetes and pre-diabetes.

6 ar pattern over time, and 13% had persistent pre-diabetes.

7 echanism also underlies cardiac apoptosis in pre-diabetes.

8 trials in an attempt to alter the course of pre-diabetes.

9 cts developed type 2 diabetes, 40% never had pre-diabetes, 47% had intermittent pre-diabetes with no

10 n mice fed a high-fat diet (HFD), a model of pre-diabetes and alimentary obesity.

11 Pre-diabetes and diabetes are a global epidemic, and the

12 d in erythrocytes from both individuals with pre-diabetes and diabetes compared with normal control s

13 n tumor metastasis in vivo in the setting of pre-diabetes and endogenous hyperinsulinemia.

14 d in erythrocytes from both individuals with pre-diabetes and individuals with less well-controlled d

15 sed to investigate associations of diabetes, pre-diabetes and metabolic syndrome and its separate com

16 he mechanisms whereby obesity predisposes to pre-diabetes and metabolic syndrome are incompletely und

17 k factor for polyneuropathy, but the role of pre-diabetes and metabolic syndrome remains unclear.

18 For both pre-diabetes and metabolic syndrome, the desirable appro

19 Similar to human subjects with pre-diabetes and obesity, HFD-fed mice develop periphera

20 Hyperinsulinemia, a key factor in obesity, pre-diabetes and T2D, has been associated with decreased

21 P = 0.021) and a significant interaction of pre-diabetes and time on IAAT (greater increase over tim

22 glucose regulation (AGR) (i.e. diabetes and pre-diabetes) and its associated factors among people ag

23 ndings among adults with insulin resistance (pre-diabetes) and obese children with type 2 diabetes, y

24 ant aspects of the genetics and diagnosis of pre-diabetes, and both current and future clinical trial

25 Volunteers with normal condition, pre-diabetes, and diabetes were recruited through a Nati

26 ed measures, S(i) deteriorated regardless of pre-diabetes, and there was a significant effect of pre-

27 s compound in an animal model of obesity and pre-diabetes as well as the lack of relevant actions in

28 Pre-diabetes can be identified as either impaired fastin

29 Pre-diabetes carries some predictive power for macrovasc

30 Pre-diabetes commonly associates with the metabolic synd

31 epGFP transgenic mice that develop prolonged pre-diabetes due to proinsulin dysmaturation and ER-crow

32 At baseline, those with persistent pre-diabetes had lower BCF and higher IAAT.

33 ntion of microvascular disease starting with pre-diabetes has not been evaluated.

34 Pre-diabetes has only a minor impact on microvascular di

35 Subjects with dietary obesity and pre-diabetes have an increased risk for developing both

36 ears is 13%; and 3) children with persistent pre-diabetes have lower BCF, due to a lower AIR, and inc

37 tunity to identify unrecognized diabetes and pre-diabetes in dental patients and refer them to a phys

38 nt 'advances' geared toward the detection of pre-diabetes, including genome wide association studies

39 children at high risk of type 2 diabetes, 1) pre-diabetes is highly variable from year to year; 2) th

40 egulation of O-GlcNAcase in individuals with pre-diabetes may eventually have diagnostic utility.

41 ss the dysglycemia spectrum as normal (39%), pre-diabetes mellitus (31%), or diabetes mellitus (30%)

42 The prevalence of pre-diabetes mellitus and its consequences in patients w

43 Individuals with diabetes mellitus and pre-diabetes mellitus are at particularly high risk of i

44 ejection fraction, dysglycemia is common and pre-diabetes mellitus is associated with a higher risk o

45 derly individuals with diabetes mellitus and pre-diabetes mellitus is not well known.

46 Patients with pre-diabetes mellitus were also at higher risk (hazard r

47 agnosed diabetes mellitus and 2103 (25%) had pre-diabetes mellitus.

48 [< 42 mmol/mol], 6.0%-6.4% [42-47 mmol/mol; pre-diabetes mellitus], and >/= 6.5% [>/= 48 mmol/mol; d

49 In this study, a mouse model of pre-diabetes (MKR mouse) was used to investigate the mec

50 betes, and there was a significant effect of pre-diabetes on AIR (42% lower in pre-diabetes; P = 0.01

51 non-white, and had never been told they have pre-diabetes or diabetes.

52 reduce metastases in patients with obesity, pre-diabetes or T2D.

53 rtance in younger patients who may also have pre-diabetes or the metabolic syndrome and who are likel

54 ear to year; 2) the prevalence of persistent pre-diabetes over 3 years is 13%; and 3) children with p

55 effect of pre-diabetes on AIR (42% lower in pre-diabetes; P = 0.01) and disposition index (34% lower

56 = 0.01) and disposition index (34% lower in pre-diabetes; P = 0.021) and a significant interaction o

57 AT (greater increase over time in those with pre-diabetes; P = 0.034).

58 biomarkers of predicting the transition from pre-diabetes (pre-DM) to normal glucose regulation (NGR)

59 Pre-diabetes represents an elevation of plasma glucose a

60 Middle-aged and older individuals with the pre-diabetes state of IFG do not exhibit abnormal proxim

61 ent-induced insulin secretion is impaired in pre-diabetes, subjects with impaired or normal fasting g

62 ss or treatment of glucose intolerance (from pre-diabetes to diabetes).

63 as 7.4% (95%CI 6.1-8.8), while prevalence of pre-diabetes was 8.6% (95%CI 7.3-10.2) using WHO criteri

64 spirin to high-risk individuals, controlling pre-diabetes, weight reduction in obese individuals, low

65 never had pre-diabetes, 47% had intermittent pre-diabetes with no clear pattern over time, and 13% ha