ライフサイエンスコーパス: pre-diabetes

1 ve therapeutic strategies in obesity-related pre-diabetes.

2 echanism also underlies cardiac apoptosis in pre-diabetes.

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

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

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

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

7 Association criteria to define diabetes and pre-diabetes.

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

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

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

11 95% CI: 1.41 to 1.54) but not for those with pre-diabetes (adjHR: 0.98; 95% CI: 0.92 to 1.03).

12 Half (53%) had pre-diabetes and 92% a reduction in insulin sensitivity.

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

14 d-1) was associated with lower incidences of pre-diabetes and diabetes (pooled IRs: 0.84; 95% CI: 0.8

15 of carbohydrates revealed increased risks of pre-diabetes and diabetes (pooled IRs: 1.04; 95% CI: 1.0

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

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

18 nt-based, and animal protein and the risk of pre-diabetes and diabetes in 4 population-based studies

19 ic incidence ratios (IRs) were estimated for pre-diabetes and diabetes, adjusting for general charact

20 1 . d-1) was associated with a lower risk of pre-diabetes and diabetes.

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

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

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

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

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

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

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

28 fibrillation (NVAF). The association between pre-diabetes and risk of ischemic stroke has not been st

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

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

31 abolism contributes to the high incidence of pre-diabetes and type 2 diabetes.

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

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

34 h beta-cell loss in mice and humans such as (pre-)diabetes, and hemipancreatectomy.

35 ormoglycemic individuals, 1.40 in those with pre-diabetes, and 2.15 in those with diabetes.

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

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

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

39 ng and further reveals that individuals with pre-diabetes are associated with lower levels of HCA spe

40 Such conditions, termed pre-diabetes, are characterized by fasting plasma glucos

41 f Cardiology guidelines chose not to include pre-diabetes as a treatment target for atherosclerotic c

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

43 referred for clinical applications to treat (pre)diabetes at any stage.

44 Pre-diabetes can be identified as either impaired fastin

45 Pre-diabetes carries some predictive power for macrovasc

46 Pre-diabetes commonly associates with the metabolic synd

47 n all pre-diabetes groups and even below the pre-diabetes cut-off (HbA1c 5.5% to 5.6% odds ratio: 1.3

48 In pre-diabetes, delta cells undergo morphological changes

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

50 we examine this in 10,873 individuals with (pre)diabetes from two ethnically distinct cohorts.

51 The association was significant in all pre-diabetes groups and even below the pre-diabetes cut-

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

53 There is little doubt that pre-diabetes has important prognostic implications, espe

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

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

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

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

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

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

60 urpose of this study was to evaluate whether pre-diabetes is associated with increased risk of stroke

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

62 It is disputed, however, whether pre-diabetes is itself an actionable disease entity, in

63 ed with reduced insulin resistance and other pre-diabetes markers, lower hepatic fat (as determined b

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

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

66 Pre-diabetes mellitus (DM) is associated with proteinuri

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

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

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

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

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

72 erotic vascular disease or diabetes mellitus/pre-diabetes mellitus), longer time from enrollment to d

73 auses by therapeutic area (diabetes mellitus/pre-diabetes mellitus, stable atherosclerosis, atrial fi

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

75 [< 42 mmol/mol], 6.0%-6.4% [42-47 mmol/mol; pre-diabetes mellitus], and >/= 6.5% [>/= 48 mmol/mol; d

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

77 normal glucose-obese, prediabetes-obese and pre-diabetes-non obese were not associated with CVD inci

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

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

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

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

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

83 Pre-diabetes overlaps with the components of the 'metabo

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

85 = 0.01) and disposition index (34% lower in pre-diabetes; P = 0.021) and a significant interaction o

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

87 n sensitive (IS), IR normoglycaemic (IR-NG), pre-diabetes (PD) and T2D) is still poorly understood.

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

89 Pre-diabetes represents an elevation of plasma glucose a

90 beta cell function are often abnormal during pre-diabetes stage, well before frank diabetes.New, cons

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

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

93 compared 3 groups of individuals: those with pre-diabetes, those with diabetes, and normoglycemic pat

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

95 wn that over-nutritional obesity may lead to pre-diabetes, type 2 diabetes and cognitive decline.

96 nical development of ABA in the treatment of pre-diabetes, type 2 diabetes and metabolic syndrome.

97 es include insulin resistance, inflammation, pre-diabetes, Type 2 diabetes, MASH, hypertension, CKD,

98 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

99 n both univariate and multivariate analyses, pre-diabetes was associated with an increased risk of st

100 this cohort of patients with incident NVAF, pre-diabetes was associated with an increased risk of st

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

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