Aims While the disposition index provides a useful measure of B-cell function, its calculation requires the performance of a frequently sampled intravenous glucose tolerance test (FSIVGTT). Recently, the demonstration of a hyperbolic relationship between indices of insulin secretion and insulin sensitivity derived from the oral glucose tolerance test (OGTT) has led to the introduction of two novel OGTT-based measures of B-cell function analogous to the disposition index: (i) the insulin secretion-sensitivity index-2 (ISSI-2) (defined as the ratio of the area-under-the-insulin-curve to the area-under-the-glucose curve, multiplied by the Matsuda index) and (ii) insulinogenic index (IGI)/fasting insulin. However, neither of these two measures has been directly compared with the disposition index. Methods Two hundred and thirteen non-diabetic children (122 boys, 91 girls) underwent both OGTT and FSIVGTT, allowing for the calculation of ISSI-2, IGI/fasting insulin and the disposition index. Results ISS1-2 and IGI/fasting insulin were strongly correlated with each other (r = 0.82, P < 0.0001). Both measures correlated with the disposition index, with ISSI-2 showing a modestly stronger association (ISSI-2: r = 0.24, P = 0.0003; IGI/fasting insulin: r = 0.21, P = 0.0022). Standardized linear regression analyses confirmed that the relationship between log ISSI-2 and the disposition index (standardized regression coefficient = 0.224, P = 0.001) was stronger than that between log IGI/fasting insulin and the disposition index (standardized regression coefficient = 0.166, P = 0.015). Conclusions The OGTT-derived measures ISSI-2 and IGI/fasting insulin exhibit modest correlations with the disposition index. These relationships require further assessment in other patient populations.
OBJECTIVETo examine cross-sectional associations of serum vitamin D [25-hydroxyvitamin D, 25(OH)D] concentration with insulin resistance (IR) and β-cell dysfunction in 712 subjects at risk for type 2 diabetes.RESEARCH DESIGN AND METHODSSerum 25(OH)D was determined using a chemiluminescence immunoassay. Insulin sensitivity/resistance were measured using the Matsuda insulin sensitivity index for oral glucose tolerance tests (ISOGTT) and homeostasis model assessment of insulin resistance HOMA-IR. β-Cell function was determined using both the insulinogenic index (IGI) divided by HOMA-IR (IGI/IR) and the insulin secretion sensitivity index-2 (ISSI-2).RESULTSLinear regression analyses indicated independent associations of 25(OH)D with ISOGTT and HOMA-IR (β = 0.004, P = 0.0003, and β = −0.003, P = 0.0072, respectively) and with IGI/IR and ISSI-2 (β = 0.004, P = 0.0286, and β = 0.003, P = 0.0011, respectively) after adjusting for sociodemographics, physical activity, supplement use, parathyroid hormone, and BMI.CONCLUSIONSVitamin D may play a role in the pathogenesis of type 2 diabetes, as 25(OH)D concentration was independently associated with both insulin sensitivity and β-cell function among individuals at risk of type 2 diabetes.
OBJECTIVE -The purpose of this study was to test the hypothesis that any degree of abnormal glucose homeostasis detected on antepartum screening for gestational diabetes mellitus (GDM) should be associated with an increased risk of postpartum pre-diabetes or diabetes.RESEARCH DESIGN AND METHODS -In this prospective cohort study, 487 women underwent 1) antepartum GDM screening by a glucose challenge test (GCT) and a diagnostic oral glucose tolerance test (OGTT) and 2) postpartum metabolic characterization by OGTT at 3 months after delivery. Four baseline glucose tolerance groups were defined on the basis of the antepartum GCT/OGTT: 1) GDM (n ϭ 137); 2) gestational impaired glucose tolerance (GIGT) (n ϭ 91); 3) abnormal GCT with normal glucose tolerance on an OGTT (abnormal GCT NGT) (n ϭ 166); and 4) normal GCT with NGT on an OGTT (normal GCT NGT) (n ϭ 93).RESULTS -The prevalence of postpartum glucose intolerance (pre-diabetes or diabetes) increased across the groups from normal GCT NGT (3.2%) to abnormal GCT NGT (10.2%) to GIGT (16.5%) to GDM (32.8%) (P trend Ͻ 0.0001). On logistic regression analysis, all three categories of abnormal glucose homeostasis in pregnancy independently predicted postpartum glucose intolerance: abnormal GCT NGT odds ratio (OR) 3.6 (95% CI 1.01-12.9); GIGT OR 5.7 (1.6 -21.1); and GDM OR 14.3 (4.2-49.1). Furthermore, both in pregnancy and at 3 months postpartum, insulin sensitivity (IS OGTT ) and pancreatic -cell function (insulinogenic index/ homeostasis model assessment of insulin resistance) progressively decreased across the groups from normal GCT NGT to abnormal GCT NGT to GIGT to GDM (all P trend Ͻ 0.0001).CONCLUSIONS -Any degree of abnormal glucose homeostasis in pregnancy independently predicts an increased risk of glucose intolerance postpartum.
Both GDM and mild glucose intolerance in pregnancy predict an increased likelihood of metabolic syndrome at 3 months postpartum, supporting the concept that women with gestational dysglycemia may have an underlying latent metabolic syndrome.
OBJECTIVEBoth gestational diabetes mellitus (GDM) and mild glucose intolerance in pregnancy identify women at increased risk of future type 2 diabetes. In this context, we queried whether metabolic changes that occur in the 1st year postpartum vary in relation to gestational glucose tolerance status.RESEARCH DESIGN AND METHODSThree-hundred-and-ninety-two women underwent glucose challenge test (GCT) and oral glucose tolerance test (OGTT) in pregnancy followed by repeat OGTT at both 3 months' postpartum and 12 months' postpartum. The antepartum testing defined four gestational glucose tolerance groups: GDM (n = 107); gestational impaired glucose tolerance (GIGT) (n = 75); abnormal GCT with normal glucose tolerance (NGT) on OGTT (abnormal GCT NGT) (n = 137); and normal GCT with NGT on OGTT (normal GCT NGT) (n = 73).RESULTSThe prevalence of dysglycemia progressively increased across the groups from normal GCT NGT to abnormal GCT NGT to GIGT to GDM at both 3 months' postpartum (2.7% to 10.2% to 18.7% to 34.6%, P < 0.0001) and 12 months' postpartum (2.7% to 11.7% to 17.3% to 32.7%, P < 0.0001). Between 3 and 12 months' postpartum, the groups did not differ with respect to changes in waist circumference, weight, or insulin sensitivity. Importantly, however, they exhibited markedly different changes in β-cell function (Insulin Secretion-Sensitivity Index-2 [ISSI-2]) (P = 0.0036), with ISSI-2 declining in both the GDM and GIGT groups. Furthermore, on multiple linear regression analysis, both GDM (t = −3.06, P = 0.0024) and GIGT (t = −2.18, P = 0.03) emerged as independent negative predictors of the change in ISSI-2 between 3 and 12 months' postpartum.CONCLUSIONSWomen with GDM and GIGT exhibit declining β-cell function in the 1st year postpartum that likely contributes to their future diabetic risk.
Aims/hypothesis The postpartum phase following gestational diabetes (GDM) is characterised by subtle metabolic defects, including the beta cell dysfunction that is believed to mediate the increased future risk of type 2 diabetes in this patient population. Low circulating levels of adiponectin and increased leptin and C-reactive protein (CRP) have recently emerged as novel diabetic risk factors, although their relevance to GDM and subsequent diabetes has not been characterised. Thus, we sought to determine whether adiponectin, leptin and CRP levels during pregnancy relate to the postpartum metabolic defects linking GDM with type 2 diabetes.Methods Metabolic characterisation, including oral glucose tolerance testing, was undertaken in 487 women during pregnancy and at 3 months postpartum. Based on the antepartum OGTT, there were 137 women with GDM, 91 with gestational impaired glucose tolerance and 259 with normal glucose tolerance. Results Adiponectin levels were lowest (p<0.0001) and CRP levels highest (p=0.0008) in women with GDM. Leptin did not differ between the glucose tolerance groups (p = 0.4483). Adiponectin (r = 0.41, p < 0.0001), leptin (r= −0.36, p <0.0001) and CRP (r = −0.30, p < 0.0001) during pregnancy were all associated with postpartum insulin sensitivity (determined using the insulin sensitivity index of Matsuda and DeFronzo [IS OGTT ]). Intriguingly, adiponectin levels were also related to postpartum beta cell function (insulinogenic index/HOMA of insulin resistance; r=0.16, p=0.0009). Indeed, on multiple linear regression analyses, adiponectin levels during pregnancy independently predicted both postpartum insulin sensitivity (t=3.97, p<0.0001) and beta cell function (t=2.37, p=0.0181), even after adjustment for GDM. Furthermore, adiponectin emerged as a significant negative independent determinant of postpartum fasting glucose (t=−3.01, p=0.0027). Conclusions/interpretation Hypoadiponectinaemia during pregnancy predicts postpartum insulin resistance, beta cell dysfunction and fasting glycaemia, and hence may be relevant to the pathophysiology relating GDM with type 2 diabetes.
These findings suggest that standard, clinically relevant hematological variables may be related to the underlying pathophysiological changes associated with type 2 diabetes mellitus.
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