Myocardial fatty acid oxidation in patients with impaired glucose tolerance

Citation
J. Knuuti et al., Myocardial fatty acid oxidation in patients with impaired glucose tolerance, DIABETOLOG, 44(2), 2001, pp. 184-187
Citations number
10
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
DIABETOLOGIA
ISSN journal
0012186X → ACNP
Volume
44
Issue
2
Year of publication
2001
Pages
184 - 187
Database
ISI
SICI code
0012-186X(200102)44:2<184:MFAOIP>2.0.ZU;2-T
Abstract
Aims/hypothesis. Fatty acids are an important source of energy in the myoca rdium. Abnormal myocardial fatty acid metabolism could contribute to the de terioration of cardiac function frequently observed in patients with Type I I (non-insulin-dependent) diabetes mellitus. In our previous study, myocard ial total uptake of non-esterified fatty acid (NEFA) was measured in patien ts with impaired glucose tolerance and found to be normal. This study aimed to investigate the subsequent metabolic steps and beta -oxidation of NEFA. Methods. A total of 6 men with impaired fasting glucose (age 50 +/- 2 years , BMI 29 +/- 1 kg/m(2), means +/- SEM) and 6 healthy men (50 +/- 1 years, 2 5 +/- 1 kg/ m(2)) were studied in the fasting state. Myocardial blood flow was measured with [O-15]H2O and positron emission tomography and myocardial NEFA metabolism with [C-11]palmitic acid. Results. Myocardial blood flow was normal and not different between the imp aired glucose tolerance and the control group (78 +/- 6 vs 73 +/- 13 ml/100 g/ min, NS). The [C-11]palmitic acid uptake indices were similar between t he groups (10.4+/-0.5 vs 11.2 +/- 0.8 ml/100 g/min, respectively, NS). The clearance of [C-11]-palmitate from the myocardium, an index of NEFA beta -o xidation, was similar between the groups (half-times of activity 17.6 +/- 1 .6 vs 19.5 +/- 2.3 min, respectively, NS) Conclusion/interpretation. The results indicate that myocardial NEFA uptake and beta -oxidation are not altered in patients with IGT. Thus, it is not likely that altered NEFA metabolism contributes to the deterioration of the cardiac function in patients with IGT or Type II diabetes.