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  • 1
    ISSN: 1432-0428
    Keywords: Insulin-dependent diabetes ; autonomic neuropathy ; graded exercise ; heart rate ; blood pressure ; cardiac output ; cardiac stroke volume ; plasma volume ; hepato-splanchnic blood flow ; body temperature ; plasma catecholamines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Haemodynamic variables were measured during supine rest and during ergometer cycle exercise at two work loads (50 W and 100 W) in normal subjects (n = 7), in insulin-dependent diabetic subjects without neuropathy (n = 8), in insulin-dependent diabetic subjects with slight autonomic neuropathy (decreased beat-to-beat variation in heart rate, which is considered due to a cardiac parasympathetic defect; n = 8), and in insulin-dependent diabetic subjects with severe autonomic neuropathy, including orthostatic hypotension (n = 7). Compared with normal subjects, cardiac stroke volume was lower in the diabetic subjects with autonomic neuropathy, both at rest and during exercise (p 〈 0.025), whereas intermediate values were found in the diabetic subjects without neuropathy. The increase in cardiac output in response to exercise was smaller (p 〈 0.05) in both diabetic groups with autonomic neuropathy compared with the normal and diabetic subjects without autonomic neuropathy. The increase in hepato-splanchnic vascular resistance was smaller in the diabetic subjects with severe autonomic neuropathy than in the normal subjects and the diabetic subjects without autonomic neuropathy (p 〈 0.025), whereas intermediate values were found in the diabetic subjects with slight autonomic neuropathy. We conclude that, in diabetic patients with severe autonomic neuropathy, the responses of the heart and the splanchnic resistance vessels to exercise are impaired. While sympathetic neuropathy may be responsible for impaired function of splanchnic resistance vessels, both cardiac sympathetic neuropathy and diabetic cardiomyopathy may be involved in the impaired cardiac response to exercise in diabetic subjects with autonomic neuropathy.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Gestational diabetes ; glucose metabolism ; insulin secretion ; intravenous glucose tolerance test ; minimal model ; pregnancy ; stable isotope
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Gestational diabetes affects 2–3% of pregnant women and is associated with foetal complications including macrosomia and an increased likelihood of developing diabetes in later life. We have therefore studied seven women with gestational diabetes and five control women both during the third trimester of pregnancy and again 2–3 months post-partum, using the minimal model analysis of the frequently sampled labelled ([6, 6-2H2]-glucose) intravenous glucose tolerance test. Glucose tolerance (glucose Kd) was significantly reduced in the women with gestational diabetes compared with the normal pregnant women both in pregnancy (1.16±0.11 vs 1.78±0.23%/min; p〈0.05) and post-partum (1.47±0.22 vs 2.59±0.43%/min; p〈0.05) and increased significantly in the control women after delivery (p〈0.05). Glucose effectiveness was not significantly different between the women with gestational diabetes and the control group either during or after pregnancy. Insulin sensitivity was significantly lower during pregnancy than after delivery in the women with gestational diabetes (p〈0.05). There was no significant difference in basal insulin secretion in the two groups during pregnancy or post-partum. However, during pregnancy the control subjects significantly increased (p〈0.001) their insulin secretion over a period of 20 min in response to an intravenous glucose tolerance test (96.2±42.7 pmol/kg) compared with post-partum values (58.3±25.2 pmol/kg) while in the women with gestational diabetes insulin secretion was similar in pregnancy (65.5±9.3 pmol/kg) and after delivery (57.7±15.7 pmol/kg). These data suggest that the glucose intolerance in gestational diabetes compared to normal pregnancy is due to reduced insulin sensitivity and an impaired ability in gestational diabetes to increase insulin secretion in response to glucose.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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