Ten-year Follow-up of Subjects with Impaired Glucose Tolerance: Prevention of Diabetes by Tolbutamide and Diet Regulation

Ten-year Follow-up of Subjects with Impaired Glucose Tolerance: Prevention of Diabetes by Tolbutamide and Diet Regulation
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糖耐量受损受试者的十年随访:通过甲苯磺丁脲和饮食调节预防糖尿病

DOI:
10.2337/diab.29.1.41
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发表时间:
1980
期刊:
影响因子:
7.7
通讯作者:
G. Persson
G. Persson
中科院分区:
医学1区
文献类型:
--
作者:
G. Sartor;B. Scherstén;S. Carlström;A. Melander;Å. Nordén;G. Persson

文献摘要

被引文献

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在1962年至1965年间进行的一项糖尿病检测调查中,228,883名受试者中有2477人(1.1%)在富含碳水化合物的午餐后出现了clinistix阳性的血糖。在这2477人中,578人表现出口服葡萄糖耐受性受损,但没有明显的糖尿病。从该组中,267名男性分为5组,并进行以下治疗和对照:(a)饮食调节和0.5 g tolbuamide t.i.d (N = 49),每年口服葡萄糖耐量试验(OGTT);(b)饮食调节和1片安慰剂,每日1次(N = 48),每年OGTT;(c)仅调节饮食(N = 50),年OGTT;(d)未治疗(N = 61),年度OGTT;(e)未治疗,随访时OGTT(随访时N = 59)。另外,对照组包括OGTT正常的男性(N = 52)。在随访中,29%没有饮食调节和药物治疗的患者(e组,N = 59)发展为糖尿病。在饮食调节但没有积极药物治疗的患者中(b组加c组,N = 98), 13%患有糖尿病。没有维持甲磺丁胺和饮食调节的个体(N = 23)进展为糖尿病。在这一组中,80%后来接受检查的患者(N = 11)血清tolbuamide浓度在治疗范围内。最初OGTT正常的个体没有发展成糖尿病或OGTT受损。研究结果表明,正常的口服糖耐量意味着进展为糖耐量受损和明显糖尿病的风险很小,而糖耐量受损与进展为糖尿病的高风险相关。此外,饮食调节治疗,结合甲苯磺丁胺,可能预防或延缓糖耐量受损进展为明显的糖尿病。
In a diabetes detection survey carried out between 1962 and 1965, 2477 (1.1%) of 228,883 subjects had Clinistix-positive glucosuria after a carbohydrate-rich luncheon meal. Of these 2477, 578 displayed impaired tolerance to oral glucose without having manifest diabetes. From this group, 267 men were divided into five groups and subjected to the following treatments and controls: (a) diet regulation and 0.5 g tolbutamide t.i.d. (N = 49), annual oral glucose tolerance test (OGTT); (b) diet regulation and one placebo tablet t.i.d. (N = 48), annual OGTT; (c) diet regulation only (N = 50), annual OGTT; (d) no treatment (N = 61), annual OGTT; and (e) no treatment, OGTT at follow-up (N = 59 at follow-up). In addition, a control group was included comprised of men with normal OGTT (N = 52). At follow-up, 29% of those without diet regulation and medication (group e; N = 59) had developed diabetes. Of those on diet regulation, but without active medication (group b plus group c, N = 98), 13% had diabetes. No individual maintaining tolbutamide and diet regulation (N = 23) had progressed to diabetes. In this group, 80% of those later examined (N = 11) had serum tolbutamide concentrations in the therapeutic range. No individual with initially normal OGTT developed diabetes or impaired OGTT. The findings suggest that normal oral glucose tolerance signifies little risk of progress to impaired glucose tolerance and manifest diabetes, whereas impaired glucose tolerance is associated with a high risk of progression to diabetes. In addition, it seems possible that treatment with diet regulation, in combination with tolbutamide, may prevent or postpone progression from impaired glucose tolerance to manifest diabetes.