Comparison of Diagnostic Criteria of IGT, Borderline, and GDM: Blood Glucose Curve and IRI Response

Omori, Yasue; Minei, Satomi; Uchigata, Yasuko; Shimizu, Meimi; Sanaka, Mayumi; Honda, Masashi; Hirata, Yoshihiro

doi:10.2337/diab.40.2.s30

Cited by 4 publications

(2 citation statements)

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“…Diagnosis of IDDM and NIDDM was made based on the World Health Organization criteria [10]. Of 46 pregnant women with abnormal glucose tolerance, 12 were diagnosed as having gestational diabetes mellitus (GDM) using the criteria of the Japanese Society of Obstetrics and Gynecology [11,29] (Table 1), the remaining 34 women with abnormal glucose tolerance were diagnosed as "borderline" [12] ( Table 1). Their mean ages were 30.3 + 3.6 years during pregnancy.…”

Section: Patients Our Diabetes Center At the Tokyo Women's Medicalmentioning

confidence: 99%

“…There were no sex differences for this mutation and no differences of lifestyle in this mutation rate [8]. To our knowledge, the most frequent gene mutation in Japanese non-insulin-dependent diabetes mellitus (NIDDM) patients is the 3243 bp mito- (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) Borderline 34 30.3+3.6 31.4+3.7 29% 2(5.9%) (22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) GDM exceeds two points of fasting blood glucose 5.5 mmol/1, 1-h blood glucose level 10 mmol/1, or 2-h blood glucose 8.3 mmol/1, and borderline is defined as a glucose tolerance test result of 1-h blood glucose /> 8.9 mmol/l and 2-h blood glucose f> 8.3 mmol/1 and < 11.1 mmol/l [29]. ~ Percentage of diabetic first-degree relatives Fig.1.…”

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confidence: 91%

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Mutation in the mitochondrial tRNAleu at position 3243 and spontaneous abortions in Japanese women attending a clinic for diabetic pregnancies

Yanagisawa¹,

Uchigata

Sanaka

et al. 1995

Diabetologia

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SummaryMitochondrial DNA is exclusively maternally inherited. We recently found the prevalence of diabetic patients with an A to G transition at position 3243 of leucine tRNA (3243 base pair (bp) mutation) to be nearly 1% in randomly selected Japanese subjects. Here, we report the higher prevalence of diabetic patients with the 3243 bp mutation in a specific Japanese population of women attending a diabetic pregnancy clinic. Of 102 patients with non-insulin-dependent diabetes mellitus 6 (5.9 %) were positive for the mutation, 1 (8.3 %) of 12 patients with gestational diabetes and 2 (5.9 %) out of 34 borderline diabetic patients. In contrast, none of 64 patients (0 %) with insulin-dependent diabetes mellitus had the 3243 bp mutation. Moreover, there was a difference in the prevalence of spontaneous abortions between patients with and without this mutation (27.3 vs 12.4%). Among nine probands with the mutation, four had a history of one spontaneous abortion (p = 0.0518) and two had a history of two abortions (p = 0.0479). Two probands had a spontaneous abortion even while under strict diabetic metabolic control. The 3243 bp mutation thus may cause spontaneous abortion during pregnancy. [Diabetologia (1995) 38: 809-815] Key words Mitochondrial DNA mutation, insulin-dependent diabetes mellitus, non-insulin-dependent diabetes mellitus, gestational diabetes mellitus.It is well-known that one of the main causes of spontaneous abortion is an abnormality in the fetus rather than a problem in the mother [1]. The prevalence of abortion in diabetic women is higher in the high-titre HbAI: group during the first trimester [2,3]. Pre-pregnancy education courses are available in diabetic pregnancy clinics in Japan, and diabetic mothers are instructed to keep postprandial blood

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Section: Patients Our Diabetes Center At the Tokyo Women's Medicalmentioning

confidence: 99%

mentioning

confidence: 91%

Mutation in the mitochondrial tRNAleu at position 3243 and spontaneous abortions in Japanese women attending a clinic for diabetic pregnancies

Yanagisawa¹,

Uchigata

Sanaka

et al. 1995

Diabetologia

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Infant nutrition and subsequent risk of Type 2 (non-insulin-dependent) diabetes mellitus

Dowse

Zimmet

Alberti³

1993

Diabetologia

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] have pieced together a number of disparate observations to provide a fascinating and novel hypothesis on the aetiology of Type 2 (non-insulin-dependent) diabetes mettitus. Central to their hypothesis is the notion that beta-cell function is diminished as a result of under-nutrition at a critical point in the development of the islets of Langerhans during fetal and early infant life.We are unable to reconcile this hypothesis to observations of increased insulin levels (in relation to Caucasian populations) in normal, glucose intolerant and diabetic individuals in developing populations, such as Pacific islanders According to Hales and Barker [1], these populations (or the individuals within them) are at increased risk of developing glucose intolerance with modernization, presumably because early under-nutrition resulting in beta-cell damage has left the pancreas unable to cope with the increased insulin requirements of the diet, obesity and reduced activity levels of a modern lifestyle.However, the very populations with the greatest susceptibility to Type 2 diabetes, are those with the highest beta-cell function, based on their total immunoreactive insulin levels. Hales and colleagues [1,6] claim that much of this "immunoreactive" insulin is biologically less active proinsulin and des 31,32-split proinsulin. This appeared to be the case in newly diagnosed Type 2 diabetic patients, particularly 30 min after an oral glucose load [6], but is not the case in mild non-insulin-dependent diabetes [7]. If a high proportion of insulin in susceptible populations could be shown to be composed of physiologically inactive proinsulin and its split products, then the Hales and Barker hypothesis of relative insulin deficiency might still hold. To date, there is no confirmation that population differences in total insulin levels can be explained by differences in concentrations of true insulin compared to proinsufins.Within populations, the Hales and Barker hypothesis also runs into difficulties. In several populations it has been shown that increased (not decreased) insulin levels (fasting, 2-h, etc.), predict deterioration in glucose tolerance from normal to impaired or to Type 2 diabetes [8][9][10][11]. While admittedly these studies need to be repeated measuring true insulin, they suggest that the beta cells of individuals with deteriorating glucose tolerance tend to have increased (but possibly still "abnormal") rather than decreased function. If it is only first phase secretion [12] that needs to be diminished to provide the susceptibility (and this is not outside the bounds of possibility), it is not clear that the "thrifty phenotype" hypothesis relating infant nutrition to pancreatic development adequately explains such a specific lesion.Furthermore, we should point out that Hales and Barker have misinterpreted our data showing a recent decline in the incidence of glucose intolerance in the high prevalence Nauruan population [13]. We certainly did not attribute the recently observed changes in prevalence and incidence t...

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Management of diabetic pregnancy

Littley¹

1994

Postgraduate Medical Journal

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Comparison of Diagnostic Criteria of IGT, Borderline, and GDM: Blood Glucose Curve and IRI Response

Cited by 4 publications

References 0 publications

Mutation in the mitochondrial tRNAleu at position 3243 and spontaneous abortions in Japanese women attending a clinic for diabetic pregnancies

Mutation in the mitochondrial tRNAleu at position 3243 and spontaneous abortions in Japanese women attending a clinic for diabetic pregnancies

Infant nutrition and subsequent risk of Type 2 (non-insulin-dependent) diabetes mellitus

Management of diabetic pregnancy

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