Burge M R, Zeise T M, Sobhy T A, Rassam A G, Schade D S
Department of Medicine/Endocrinology, University of New Mexico Health Sciences Center, Albuquerque 87131, USA.
Diabetes Care. 1999 Dec;22(12):2037-43. doi: 10.2337/diacare.22.12.2037.
It has previously been demonstrated that the risk of hypoglycemia is low among otherwise healthy elderly fasted patients with type 2 diabetes taking oral sulfonylurea medications. Nevertheless, these agents do cause hypoglycemia in clinical practice, suggesting that accompanying factors must typically be present for hypoglycemia to occur. Ethanol is one putative risk factor that has not been evaluated as a mechanism for low blood glucose among sulfonylurea users. We hypothesized that low concentrations of ethanol would reduce blood glucose concentrations in elderly type 2 diabetic patients receiving sulfonylureas during a short-term fast.
A total of 10 type 2 diabetic patients, aged 68 +/- 3 years and receiving 20 mg glyburide daily, participated in a prospective double-blind placebo-controlled in-patient study consisting of two 24-h fasts at least 1 week apart. During hours 14 and 15 of the fasting studies, subjects received intravenous infusions of either 4.35 mmol.kg-1.h-1 ethanol (equivalent to one or two alcoholic beverages) or saline placebo in random order. Ethanol, plasma glucose, insulin, and counterregulatory hormones were assessed very 30-60 min during the final 10 h of the fast.
Blood ethanol levels peaked at 17 +/- 2 mmol/l (the lower legal limit of intoxication in New Mexico) during the ethanol study. Plasma glucose concentrations did not differ at baseline (placebo 8.5 +/- 1.8 vs. ethanol 8.7 +/- 1.7 mmol/l; P = 0.50), but nadir plasma glucose was lower after the ethanol infusion compared with placebo (4.4 +/- 1.2 vs. 5.0 +/- 1.4 mmol/l; P = 0.01), and the absolute decline in plasma glucose was also greater during the ethanol study than the placebo study (4.7 +/- 0.9 vs. 3.6 +/- 1.2 mmol/l; P = 0.01). Counterregulatory hormone levels were increased during the ethanol study and nonesterified fatty acid concentrations were suppressed compared with the placebo study.
Low doses of ethanol predispose fasted elderly type 2 diabetic patients to low blood glucose during a short-term fast. This may be one of several mechanisms by which sulfonylurea-induced hypoglycemia occurs in elderly patients.
先前已有研究表明,在口服磺脲类药物的健康老年2型糖尿病空腹患者中,低血糖风险较低。然而,在临床实践中这些药物确实会导致低血糖,这表明低血糖的发生通常必有伴随因素。乙醇是一种尚未被评估为磺脲类药物使用者低血糖发生机制的潜在风险因素。我们推测,低浓度乙醇会降低短期禁食期间接受磺脲类药物治疗的老年2型糖尿病患者的血糖浓度。
共有10名年龄为68±3岁、每日服用20mg格列本脲的2型糖尿病患者参与了一项前瞻性双盲安慰剂对照住院研究,该研究包括两次间隔至少1周的24小时禁食。在禁食研究的第14和15小时,受试者随机接受静脉输注4.35 mmol·kg-1·h-1乙醇(相当于一杯或两杯酒精饮料)或生理盐水安慰剂。在禁食的最后10小时内,每30 - 60分钟评估一次乙醇、血糖、胰岛素和反调节激素水平。
在乙醇研究中,血液乙醇水平在17±2 mmol/l时达到峰值(这是新墨西哥州的较低法定醉酒限度)。血浆葡萄糖浓度在基线时无差异(安慰剂组为8.5±1.8 mmol/l,乙醇组为8.7±1.7 mmol/l;P = 0.50),但与安慰剂相比,乙醇输注后血浆葡萄糖最低点更低(4.4±1.2 mmol/l对5.0±1.4 mmol/l;P = 0.01),并且在乙醇研究期间血浆葡萄糖的绝对下降幅度也大于安慰剂研究(4.7±0.9 mmol/l对3.6±1.2 mmol/l;P = 0.01)。与安慰剂研究相比,乙醇研究期间反调节激素水平升高,非酯化脂肪酸浓度受到抑制。
低剂量乙醇使禁食的老年2型糖尿病患者在短期禁食期间易发生低血糖。这可能是老年患者磺脲类药物诱导低血糖发生的几种机制之一。