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  • 1
    ISSN: 1432-0428
    Keywords: Insulin secretion ; Type 2 (non-insulin-dependent) diabetes mellitus ; glucagon secretion ; C-peptide ; arginine ; dexamethasone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have compared insulin responses to L-arginine before and during dexamethasone treatment in healthy subjects, previously classified as subjects with either high or low insulin response according to a standardized glucose infusion test. Arginine stimulation was administered as a 150 mg/kg bolus followed by 10 mg·kg−1·min−1 to six subjects with high insulin response and to seven subjects with low insulin response. Before dexamethasone treatment the incremental insulin level during 0–10 min of arginine was higher in subjects with high (36.5±6.8 μU/ml) than in subjects with low response (14.5±2.3 μU/ml), p〈0.01 for difference. Dexamethasone treatment (6 mg/day for 60 h) markedly enhanced the insulin response to arginine in subjects with high response (+99% 0–30 min) but failed to affect the subjects with low response (+4% 0–30 min). The C-peptide response to arginine exhibited similar differences between groups. Decreased responsiveness to arginine in subjects with low insulin response, especially during dexamethasone treatment, suggests a Beta-cell capacity defect although a decreased potentiating-sensing effect of glucose cannot be completely ruled out.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Keywords Glucose tolerance ; insulin secretion ; insulin resistance ; obesity ; genetics of diabetes.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have investigated the association of a family history of diabetes with glucose tolerance in a population of Swedish men. All men 35–54 years of age in 1992 and living in four different local municipalities of the outer Stockholm area were screened by questionnaire. From 10 236 completed questionnaires 1622 men, selected for presence of such a history but without known diabetes, as well as 1507 men without a family history underwent an oral glucose tolerance test. Diabetes (2 h-plasma glucose levels 〉 11.0 mmol/l) was detected in 55 and impaired glucose tolerance (plasma glucose levels 7.8–11.0 mmol/l) in 172 subjects. The odds ratio of diabetes, associated with a family history, was 4.1, confidence interval 2.1–8.3 and for impaired glucose tolerance 1.6, confidence interval 1.2–2.3. Influence of a family history was measurable also within the range of normal 2-h glucose concentrations: compared to 2-h glucose levels 〈 3.8 mmol/l; the odds ratio associated with a family history was 1.4, confidence interval 1.1–1.7 and 1.3, confidence interval 1.1–1.6 for concentrations 4.8–5.7 mmol/l and 5.8–7.7 mmol/l respectively. The odds ratio of diabetes and impaired glucose tolerance among men with a family history increased with number and closeness of relatives with diabetes but was not affected by the gender of the family member. Overweight (BMI 〉 25.0 kg/m2) increased the odds ratio of diabetes in subjects with a family history, the odds ratio being 24, confidence interval 3–177, when both conditions were present. In subjects with Type II (non-insulin-dependent) diabetes mellitus discovered during the investigation, the presence of a family history of diabetes was associated with decreased insulin secretion rather than insulin resistance as assessed by fasting insulin, homeostasis model assessment, and the 2-h insulin response to the oral glucose tolerance test. We conclude that a family history of diabetes strongly but independently of gender associates with decreased glucose tolerance. Furthermore, the results are compatible with a major role for low insulin secretion in the diabetogenic influence of a family history of diabetes in middle-aged Swedish men. Lastly, the very high risk for diabetes in middle-aged men with both a family history of diabetes and obesity indicates that such people should, for the purpose of therapeutic intervention, be identified in the general population. [Diabetologia (1999) 42: 15–23]
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-5233
    Keywords: Insulin secretion ; Type 2 diabetes ; Gestational diabetes ; Glucagon secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The relationship between insulin responses to glucose and to arginine was studied in non-obese women with previous gestational diabetes (PGD). One group,n=10, had normal glucose tolerance (NGT) by WHO criteria and another,n=8, had impaired glucose tolerance (IGT). A third group of women without PGD,n=12, was also studied. A hyperglycaemic clamp (blood glucose level 11 mM) and an arginine stimulation test (150 mg/kgl-arginine followed by 10 mg/kg · min) were performed on separate days. The ratios of arginine to glucose responses 0–10 min differed: they were 1.00 for non-PGD, 1.29 for NGT and 1.46 for IGT (P〈0.02 vs non-PGD). A further difference between groups was the ratio between first- and second-phase glucose-induced insulin secretion, which was significantly decreased in IGT, 0.72, compared with NGT, 0.98 (P〈0.01), and non-PGD, 1.05 (P〈0.005). However, within each group insulin responses 0–10 min to glucose and arginine were strongly correlated: for NGT (r=0.75,P〈0.05), for IGT (r=0.85,P〈0.01) and for women without PGD (r=0.69,P〈0.05). Insulin sensitivity, as assessed by the M/I ratio, was non-significantly decreased in IGT (0.18±0.03 mg/kg·min per mU/l vs 0.26 ±0.03 in NGT and 0.28±0.03 in non-PGD,P〈0.1). Conclusions are: (1) insulin responses to glucose and arginine are linked both in PGD and non-PGD women, but (2) the relative potency of these secretagogues as well as the time-dynamics of glucose-induced insulin secretion may be altered in PGD with IGT.
    Type of Medium: Electronic Resource
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