Hyperinsulinaemia in offspring of Type 2 diabetic patients: impaired response of carbohydrate metabolism, but preserved cardiovascular response

被引:4
作者
Frontoni, S [1 ]
Pellegrinotti, M [1 ]
Bracaglia, D [1 ]
Farrace, S [1 ]
Caselli, A [1 ]
Baroni, A [1 ]
De Angelis, C [1 ]
Menzinger, G [1 ]
Gambardella, S [1 ]
机构
[1] Univ Roma Tor Vergata, Ctr Diabetol, I-00133 Rome, Italy
关键词
autonomic nervous system; blood pressure; hyperinsulinaemia; offspring; spectral analysis;
D O I
10.1046/j.1464-5491.2000.00349.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Aims To investigate the effects of endogenous insulin on haemodynamics in nine offspring of Type 2 diabetic patients (P), compared with 18 subjects without family history of diabetes (C), all with normal glucose tolerance. Methods All subjects underwent a 180-min oral glucose tolerance test with continuous blood pressure and ECG recording. Low-to-high frequency ratio (LF/HF), an index of the sympatho-vagal balance, was calculated by heart rate spectral analysis. Results At baseline, LF/HF correlated with fasting plasma insulin (r = 0.44, P < 0.03) and with insulin/glucose ratio (r = 0.46, P < 0.03). Plasma insulin, basally similar in the two groups, was significantly increased in P (342 +/- 34.2) when compared to C (177.6 +/- 25.2 pmol/l), P < 0.005 from time 30 min onward. Blood glucose, also similar at baseline, remained not significantly different in P (5.74 +/- 0.25) vs. C (5.08 +/- 0.27 mmol/l), throughout the study. Diastolic blood pressure significantly decreased in P, but not in C during the first hour of the study. Finally, LF/HF ratio significantly increased in P (2.5 +/- 0.4 vs. C, 1.7 +/- 0.2) during the first hour. Conclusions In conclusion, the offspring of Type 2 diabetic patients with normal glucose tolerance display an increased insulin secretion; however, they are not resistant to the haemodynamic effects of insulin, as suggested by the reduction of diastolic blood pressure. This, in turn, may determine a chronic sympathetic activation, which could be involved in the pathogenesis of Type 2 diabetes mellitus.
引用
收藏
页码:606 / 611
页数:6
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