Quiønones Galvan A, Natali A, Muscelli E, Ciociaro D, Pecori N, Camici P G, Ferrannini E
Metabolism Unit, National Research Council (CNR), Institute of Clinical Physiology, Pisa, Italy.
J Intern Med. 1996 Mar;239(3):241-7. doi: 10.1046/j.1365-2796.1996.448802000.x.
To test whether cardiological syndrome X is an insulin-resistant state. SETTING, DESIGN AND SUBJECTS: The coronary care unit of a referral centre for angina pectoris in Pisa, Italy. A case-control study, involving 10 patients with unequivocal (angiographycally proven) cardiological syndrome X, but normal glucose tolerance, blood pressure and lipid levels, and 13 matched healthy subjects.
Insulin sensitivity and pattern of substrate oxidation (assessed by the euglycaemic insulin clamp technique in combination with indirect calorimetry).
Fasting plasma glucose and insulin levels were 5.05 +/- 0.11 versus 4.88 +/- 0.11 mmol l-1 and 68 +/- 10 versus 56 +/- 6 pmol l-1, respectively (controls versus patients, ns). During the insulin clamp, glucose disposal rate was nearly identical in patients and controls (25.9 +/- 1.8 and 27.2 +/- 1.8 mumol kg-1 min-1, respectively. P = 0.88). Non-oxidative glucose disposal accounted for similar proportions of total glucose uptake (59 versus 53%, patients versus controls, ns). Resting energy expenditure (13.7 +/- 0.6 versus 13.8 +/- 0.8 cal kg-1 min-1, ns) and insulin-induced thermogenesis were similar in the two groups. Fasting plasma NEFA concentrations (0.64 +/- 0.09 and 0.64 +/- 0.06 mmol l-1, patients and controls, ns) fell in a similar time-course and to virtually identical nadirs (0.13 +/- 0.02 and 0.14 +/- 0.02 mmol l-1) after insulin infusion. Fasting plasma potassium was similar in patients and controls (3.99 +/- 0.10 and 4.16 +/- 0.04 mmol l-1, ns), and insulin induced equivalent hypokalaemia (-14 versus -19%).
None of the in vivo actions of insulin were impaired in patients with 'pure' syndrome X when compared to matched controls. Therefore, we conclude that cardiological syndrome X is not an insulin resistant state per se, and that any decrease in insulin sensitivity found in this condition is likely to be secondary.
检测心脏X综合征是否为胰岛素抵抗状态。
设置、设计及研究对象：意大利比萨一家心绞痛转诊中心的冠心病监护病房。一项病例对照研究，纳入10例明确诊断（经血管造影证实）为心脏X综合征但糖耐量、血压及血脂水平正常的患者，以及13例匹配的健康受试者。
胰岛素敏感性及底物氧化模式（通过正常血糖胰岛素钳夹技术结合间接测热法评估）。
空腹血糖和胰岛素水平分别为5.05±0.11与4.88±0.11 mmol/L以及68±10与56±6 pmol/L（对照组与患者组，无显著差异）。在胰岛素钳夹期间，患者和对照组的葡萄糖处置率几乎相同（分别为25.9±1.8和27.2±1.8 μmol·kg-1·min-1，P = 0.88）。非氧化葡萄糖处置占总葡萄糖摄取的比例相似（患者组与对照组分别为59%与53%，无显著差异）。两组的静息能量消耗（13.7±0.6与13.8±0.8 cal·kg-1·min-1，无显著差异）和胰岛素诱导的产热相似。空腹血浆游离脂肪酸浓度（患者组和对照组分别为0.64±0.09和0.64±0.06 mmol/L，无显著差异）在胰岛素输注后下降的时间过程相似，且降至几乎相同的最低点（0.13±0.02和0.14±0.02 mmol/L）。患者和对照组的空腹血浆钾相似（3.99±0.10和4.16±0.04 mmol/L，无显著差异），胰岛素诱导的低钾血症程度相当（-14%与-19%）。
与匹配的对照组相比，“单纯”X综合征患者胰岛素的任何体内作用均未受损。因此，我们得出结论，心脏X综合征本身并非胰岛素抵抗状态，在这种情况下发现的胰岛素敏感性降低可能是继发性的。
