Demonstration of insulin resistance in untreated adult onset diabetic subjects with fasting hyperglycemia.
Demonstration of insulin resistance in untreated adult onset diabetic subjects with fasting hyperglycemia.
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在未经治疗的患有空腹高血糖的成年糖尿病受试者中证明胰岛素抵抗。
DOI：
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发表时间：
1975
影响因子：
15.9
通讯作者：
G. Reaven
中科院分区：
文献类型：
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作者：
H. Ginsberg;G. Kimmerling;J. Olefsky;G. Reaven
我们使用连续静脉输注葡萄糖（6 mg/kg/min）、胰岛素（80 mU/min）、肾上腺素（6 μg/min）和普萘洛尔（0.08 mg/min）来直接评估 14 名未经治疗的成年发病糖尿病患者的胰岛素抵抗，这些患者的平均（正负 SE）空腹血糖水平为 217 ± 17 mg/100 ml。输注过程中，内源性胰岛素分泌受到抑制，90 分钟后血浆葡萄糖和胰岛素水平达到稳态。由于所有受试者都达到相似的血浆胰岛素稳态水平，因此在稳态期间观察到的血浆葡萄糖浓度是个体胰岛素抵抗的量度。在这些条件下，14名糖尿病患者的平均（正负SE）稳态血浆葡萄糖水平为350正负16毫克/100毫升，而12名正常受试者的平均稳态血浆葡萄糖水平为121正负4毫克/100毫升。还进行了其他研究，其中对照受试者和糖尿病患者在接受葡萄糖、胰岛素、肾上腺素和普萘洛尔的基本输注混合物之前，其空腹血糖水平急剧升高或降低至相当水平。这些研究的结果表明，初始血浆葡萄糖水平的差异不能解释两组对基础输注的不同葡萄糖反应。最后，在五名继发于慢性胰腺炎的空腹高血糖患者（平均正负SE，142正负12毫克/100毫升）的相同基础输注过程中观察到的平均（正负SE）稳态血浆葡萄糖水平为104正负17毫克/100毫升，这表明慢性高血糖和低胰岛素血症本身都不一定导致胰岛素抵抗。这些结果表明，患有空腹高血糖的成年糖尿病患者存在明显的胰岛素抵抗。由于之前的研究已经证明化学性糖尿病患者存在胰岛素抵抗，因此胰岛素抵抗可能是成人发病糖尿病的特征。
We have used a continuous intravenous infusion of glucose (6 mg/kg/min), insulin (80 mU/min), epinephrine (6 mug/min), and propranolol (0.08 mg/min) to directly assess insulin resistance in 14 untreated adult onset diabetics with a mean (plus or minus SE) fasting plasma glucose level of 217 plus or minus 17 mg/100 ml. During the infusion endogenous insulin secretion is inhibited and steady-state plasma glucose and insulin levels are achieved after 90 min. Since similar steady-state levels of plasma insulin are achieved in all subjects, the plasma glucose concentration observed during the steady-state period is a measure of an individual's insulin resistance. Under these conditions, the mean (plus or minus SE) steady-state plasma glucose level of the 14 diabetic patients was 350 plus or minus 16 mg/100 ml, while that of 12 normal subjects was 121 plus or minus 4 mg/100 ml. Additional studies were performed in which control subjects and patients with diabetes had their fasting plasma glucose levels acutely raised or lowered to comparable levels before receiving the basic infusion mixture of glucose, insulin, epinephrine, and propranolol. The results of these studies indicated that differences in initial plasma glucose levels could not account for the different glucose responses of the two groups to the basic infusion. Finally, the mean (plus or minus SE) steady-state plasma glucose level of 104 plus or minus 17 mg/100 ml observed during the same basic infusion in five patients with fasting hyperglycemia (mean plus or minus SE, 142 plus or minus 12 mg/100 ml) secondary to chronic pancreatitis suggested that neither chronic hyperglycemia nor hypoinsulinemia per se necessarily lead to insulin resistance. These results demonstrate that marked insulin resistance exists in adult onset diabetics with fasting hyperglycemia. Since previous studies have documented the presence of insulin resistance in patients with chemical diabetes, the possibility exists that insulin resistance may be characteristic of adult onset diabetes mellitus.