MYOCARDIAL-METABOLISM IN TYPE-1 DIABETIC-PATIENTS WITHOUT CORONARY-ARTERY DISEASE

被引：27

作者：

DORIA, A ^{[1
]}

NOSADINI, R ^{[1
]}

AVOGARO, A ^{[1
]}

FIORETTO, P ^{[1
]}

CREPALDI, G ^{[1
]}

机构：

[1] UNIV PADOVA POLICLIN,IST MED INTERNA,VIA GIUSTINIANI 2,I-35128 PADUA,ITALY

来源：

DIABETIC MEDICINE | 1991年 / 8卷

关键词：

DIABETES MELLITUS; KETONE BODIES; LACTATE; CARDIAC METABOLISM;

D O I：

10.1111/j.1464-5491.1991.tb02168.x

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Myocaridal exchange of metabolic substrates was investigated in eight Type 1 diabetic patients with angiographically normal coronary arteries and seven normal control subjects, after an overnight fast. Simultaneous samples of arterial and coronary sinus blood were collected for analysis of the major metabolic substrates. Myocardial blood flow was measured by the thermodilution technique. Although the Type 1 patients were hyperglycaemic (10.0 +/- 2.0 (+/- SE) mmol 1(-1)) myocardial glucose uptake was lower than in control subjects (27 +/- 6 vs 42 +/- 5-mu-mol min-1 1.73 m-2, p < 0.05). The net balance of lactate and pyruvate across the myocardium showed a net release in Type 1 patients (13.4 +/- 2.7-mu-mol min-1 1.73 m-2 and 1.3 +/- 0.2-mu-mol min-1 1.73 m-2, respectively) and a net uptake in control subjects (2.2 +/- 0.7-mu-mol min-1 1.73 m-2 and 3.5 +/- 0.3-mu-mol min-1 1.73 m-2, both p < 0.01). Myocardial uptake of ketone bodies was significantly higher in diabetic patients (37.0 +/- 6.3) mu-mol min-1 1.73 m-2) than in control subjects (10.1 +/- 3.4-mu-mol min-1 1.73 m-2, p < 0.01). Non-esterified fatty acid (NEFA) uptake was significantly greater in the diabetic patients than in control subjects (44.1 +/- 7.0) vs 24.1 +/- 5.1-mu-mol min-1 1.73 m-2, p < 0.01). Net balance of glucose, lactate, and pyruvate across the myocardium was inversely and significantly related to that of NEFAs and ketone bodies (p < 0.01). Myocardial carbohydrate uptake is markedly impaired in Type 1 diabetic patients with angiographically intact coronary vessels. Ketones and NEFA represent the major fuel for the diabetic myocardium. Thus, in diabetes, myocardial lactate metabolism may be profoundly altered independently of coronary artery disease.

引用

页码：S104 / S107

页数：4

共 24 条

[11]

Lloyd B., Burrin J., Smythe P., Alberti KGMM., Simple automated enzymatic fluorimetric assays for glucose, lactate, pyruvate, alanine, glycerol and 3‐hydroxybutyrate, Clin Chem, 24, pp. 1724-1729, (1978)

[12]

Price C., Lloyd B., Alberti KGMM., A kinetic spectrophotometric assay for rapid determination of acetoacetate on blood, Clin Chem, 23, pp. 1893-1897, (1977)

[13]

Parker JD, Chiong MA, West RO, Case RB., Sequential alterations in myocardial lactate metabolism S‐T segments and left ventricular function during angina induced by atrial pacing, Circulation, 40, pp. 113-131, (1969)

[14]

Mudge GH, Millis RM, Taegtmeyer H., Gorlin R., Lesch M., Alterations of myocardial amino acid metabolism in chronic ischaemic heart disease, J Clin Invest, 58, pp. 1185-1192, (1976)

[15]

Lassers BW, Wahlquist ML, Kaijser L., Carlson LA., Relationship in man between plasma free fatty acids and myocardial metabolism of carbohydrate substrates, Lancet, 1, pp. 448-450, (1971)

[16]

Gertz EW, Wisneski JA, Neese R., Bristow JD, Searle GL, Hanlon JT., Myocardial lactate metabolism: evidence of lactate release during net chemical extraction in man, Circulation, 63, pp. 1273-1279, (1981)

[17]

Wisneski JA, Gertz EW, Neese RA, Gruenke LD, Morris LD, Craig JC., Metabolic fate of extracted glucose in normal human myocardium, J Clin Invest, 76, pp. 1819-1827, (1985)

[18]

Richarson PJ, Livesly B., Oram S., Olden EGJ, Armstrong P., Angina pectoris with normal coronary arteries. Transvenous myocardial biopsy in diagnosis, Lancet, 2, pp. 677-680, (1974)

[19]

Mosseri M., Yaron R., Gotsman MS, Hasin Y., Histologic evidence for small vessel coronary artery disease in patients with angina pectoris and patent large coronary arteries, Circulation, 74, pp. 964-972, (1986)

[20]

Greenberg MA, Gross RM, Neuberger N., Silverman R., Strain JE, Cohen M., Impaired coronary vasodilatatory responsiveness as a cause of lactate production during pacing induced ischaemia in patients with angina pectoris and normal coronary arteries, J Am Coll Cardiol, 9, pp. 743-751, (1987)

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