Decreased insulin action and insulin secretion predict the development of impaired glucose tolerance

Haffner, S M; Miettinen, Heikki; Gaskill, Sarah J.; Stern, Michael P.

doi:10.1007/bf02658507

Cited by 113 publications

(79 citation statements)

References 41 publications

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“…Insulin resistance found in men who further developed isolated IGT is consistent with the increased adiposity found in these men and is concordant with other studies [7,8]. In contrast, men who developed isolated IFG were not characterised by increased insulin resistance at baseline but rather by decreased early insulin secretion.…”

Section: Observationssupporting

confidence: 91%

Predictors of the development of impaired fasting glucose versus impaired glucose tolerance are partly different in men: a 6-year follow-up study

et al. 2004

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ObservationsPredictors of the development of impaired fasting glucose versus impaired glucose tolerance are partly different in men: a 6-year follow-up study To the Editor: Some studies have confirmed that impaired glucose tolerance and Type 2 diabetes share common aetiological factors such as obesity, abdominal obesity, insulin resistance, impaired insulin secretion, family history of diabetes, age and sedentariness [1,2]. As for IGT, impaired fasting glucose is considered as an intermediate metabolic state between normal and diabetic glucose homeostasis. The aetiology of IFG, however, remains unclear. Several studies have suggested that IGT and IFG are two classes of glucose homeostasis disorders, which could describe two distinct populations with differing cardiovascular risk [2,3].Our aim was to examine factors potentially related to the development of impaired glucose regulation in a sample of men tested over a 6-year follow-up who all had a normal glucose tolerance at baseline. No study has yet documented the respective contribution of regional body-fat distribution as measured by computed tomography (CT) and of indices of plasma glucose-insulin homeostasis to the development of IFG in men. Therefore, as a specific objective, we compared isolated IFG to isolated IGT in terms of their metabolic and anthropometric predictors.The study was conducted in men (20-62 years of age at baseline) recruited through media advertising in the Quebec City metropolitan area. All subjects were healthy and were not under treatment for coronary heart disease, diabetes, dyslipidaemias or endocrine disorders. At baseline, all men involved in this study had a NGT. At follow-up (mean follow-up: 6.4±1.1 year), some men developed a deteriorated glucose tolerance state whereas others remained with a NGT. A total of 71 men had a NGT at baseline and kept a NGT at follow-up whereas 24 developed an impaired glucose regulation state (did not remain NGT). Among the 24 men who developed impaired glucose regulation, 8 developed isolated IFG and 12 developed isolated IGT. The American Diabetes Association diagnostic criteria (1997) were used to determine the glucose tolerance status [4]. All participants signed an informed consent document before entering the study, which was approved by the Laval University Medical Ethics Committee.Height, body weight, waist and hip circumferences as well as body fat mass were measured using standardised procedures Diabetologia (2004) Men who developed isolated IFG had at baseline body composition and body-fat distribution variables that were not significantly different from men who remained NGT throughout the follow-up (Table 1). In contrast, men who developed isolated IGT during the follow-up had significantly higher BMI, waist circumference and waist-to-hip ratio than men who remained NGT and tended (p=0.09) to have higher visceral AT accumulation.Men who developed isolated IFG during the follow-up had, at baseline, higher FPG concentrations and lower insulin secretion as evaluated by Stumvoll 1st phas...

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Section: Observationssupporting

confidence: 91%

Predictors of the development of impaired fasting glucose versus impaired glucose tolerance are partly different in men: a 6-year follow-up study

et al. 2004

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“…Model C was as model B but was also adjusted for serum phosphate and serum creatinine. All models evaluating the relationship between EIR and serum calcium were also adjusted for M/I, as previous studies have shown that EIR does not seem to provide clinically relevant information except when adjusted for insulin sensitivity [22,23]. Apart from using the whole cohort (n=961) for our analyses, we also used the following prespecified subgroups: 1, normal fasting glucose and glucose tolerance (n=442); 2, normal fasting glucose and glucose tolerance and serum calcium in the normal range (n=413).…”

Section: Statistical Analysesmentioning

confidence: 99%

Serum calcium is independently associated with insulin sensitivity measured with euglycaemic–hyperinsulinaemic clamp in a community-based cohort

et al. 2006

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Aims/hypothesis Diabetes mellitus type 2 is associated with altered calcium metabolism. Moreover, in diseases with supranormal serum calcium levels, such as primary hyperparathyroidism, the prevalence of diabetes is increased. Relatively little is known about the relationship between serum calcium concentration and the underlying causes of diabetes-insulin resistance and defective insulin secretionin the normocalcaemic general population. Materials and methods We investigated associations between serum calcium concentration and insulin sensitivity and secretion in a population-based cohort of elderly men (Uppsala Longitudinal Study of Adult Men, n=961). Insulin sensitivity index (M/I; glucose disposal rate [M] divided by mean insulin concentration [I]) was assessed using euglycaemic-hyperinsulinaemic clamp, and insulin secretion was estimated from the early insulin response (EIR) during an OGTT.Results In a multivariable linear regression model adjusting for BMI, physical activity, smoking, consumption of tea, alcohol, coffee and dietary calcium, serum phosphate and serum creatinine, 1 SD increase in serum calcium was associated with 0.17 mg kg −1 min −1 (mU/l) −1 × 100 (0.024 mg kg −1 min −1 [pmol/l] −1 ×100) decrease in M/I (p=0.01). The results remained robust in individuals with normal fasting glucose, normal glucose tolerance and serum calcium within the normal range (n=413, regression coefficient for 1 SD increase −0.45, p=0.001). Serum calcium was not associated with EIR. Dietary intake of calcium was not independently associated with insulin sensitivity or EIR. Conclusion/interpretation Our data support the notion that endogenous calcium may be involved early in the development of diabetes and that this effect is mediated mainly through effects on insulin sensitivity rather than defective insulin secretion. Dietary intake of calcium does not seem to influence insulin sensitivity.

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“…Serum cholesterol and triglycerides were measured by enzymatic methods. Early insulin secretion was calculated using the ratio of the 0-to 30-min incremental insulin values to the 0-to 30-min incremental glucose (4,14).…”

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confidence: 99%

Reduced insulin secretion in offspring of African type 2 diabetic parents.

et al. 2000

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OBJECTIVE -To determine the early biochemical predictors of increased susceptibility to develop diabetes in offspring of African type 2 diabetic parents.RESEARCH DESIGN AND METHODS -A total of 69 offspring (case subjects) of 26 families in Cameroon with at least one type 2 diabetic parent were studied, and 62 offspring (control subjects) from 25 families in Cameroon with no parent with type 2 diabetes underwent an oral glucose tolerance test. Early insulin secretion was calculated using the ratio of the 0-to 30-min incremental insulin values to the 0-to 30-min incremental glucose. Anthropometric parameters were also measured.RESULTS -Of the case subjects, 23% were glucose intolerant (4% with diabetes and 19% with impaired glucose tolerance [IGT]) compared with 6.5% (all with IGT) of control subjects (P = 0.02). There was also an increasing prevalence of glucose intolerance, especially IGT with increasing number of glucose-intolerant parents. Fasting serum insulin levels were not different in the two groups; however, at 30 min, the case subjects had lower insulin levels than the control subjects (P Ͻ 0.006). Case subjects with IGT had lower 30-min insulin concentration, early insulin secretion, and 2-h insulin levels than those with normal glucose tolerance (NGT) (F = 4.1, P Ͻ 0.05; F = 4.1, P Ͻ 0.04; and F = 5.1, P Ͻ 0.03, respectively). Furthermore, case subjects with NGT and IGT had lower early insulin secretion than control subjects (F = 4.1, P Ͻ 0.03). These differences remained after adjustment for BMI and regardless of the status of parental diabetes. Two-hour insulin concentration showed a positive association (odds ratio = 0.95 CI 0.90-0.99, P = 0.039) with IGT in the case subjects.CONCLUSIONS -Diabetes and IGT are more prevalent in the offspring of African type 2 diabetic parents, and this may be due to an underlying degree of ␤-cell impairment marked by reduced early-phase insulin secretion.

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Decreased insulin action and insulin secretion predict the development of impaired glucose tolerance

Cited by 113 publications

References 41 publications

Predictors of the development of impaired fasting glucose versus impaired glucose tolerance are partly different in men: a 6-year follow-up study

Predictors of the development of impaired fasting glucose versus impaired glucose tolerance are partly different in men: a 6-year follow-up study

Serum calcium is independently associated with insulin sensitivity measured with euglycaemic–hyperinsulinaemic clamp in a community-based cohort

Reduced insulin secretion in offspring of African type 2 diabetic parents.

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