Abnormal myocardial kinetics of 123 I-heptadecanoic acid in subjects with impaired glucose tolerance

Turpeinen, Anu; Kuikka, Jyrki T.; Vanninen, Esko; Uusitupa, Matti

doi:10.1007/s001250050713

Cited by 19 publications

(18 citation statements)

References 34 publications

(57 reference statements)

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“…The defect was not detected, however, in patients with Type II diabetes in that study [4]. [8] and those limitations could have been the reason for the finding of reduced myocardial NEFA uptake and b-oxidation in IGT in that study.…”

Section: Discussionmentioning

confidence: 53%

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Myocardial fatty acid oxidation in patients with impaired glucose tolerance

et al. 2001

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On the basis of both experimental and human studies, it has been shown that diabetes could be associated with alterations in the myocardial glucose and the non-esterified fatty acid (NEFA) metabolism, which could further contribute to the deterioration of cardiac function [1]. The results of the recent studies with positron emission tomography (PET) have, however, shown that myocardial glucose uptake during euglycaemic hyperinsulinaemia both in patients with Type I (insulin-dependent) and II (non-insulin-dependent) diabetes is normal during controlled metabolic conditions (euglycaemic hyperinsulinaemia), confirming that the heart is not insulin-resistant in diabetes [2,3].Studies on myocardial NEFA metabolism are sparse. A study with [ ]HDA) and single-photon emission tomography (SPET) found myocardial NEFA uptake and b-oxidation to be reduced in patients with impaired glucose tolerance (IGT) [4]. Surprisingly, the same study found that NEFA metabolism was normal in patients with Type II diabetes. We recently measured the myocardial uptake of NEFA in patients with IGT Diabetologia (2001) Abstract Aims/hypothesis. Fatty acids are an important source of energy in the myocardium. Abnormal myocardial fatty acid metabolism could contribute to the deterioration of cardiac function frequently observed in patients with Type II (non-insulin-dependent) diabetes mellitus. In our previous study, myocardial total uptake of non-esterified fatty acid (NEFA) was measured in patients with impaired glucose tolerance and found to be normal. This study aimed to investigate the subsequent metabolic steps and b-oxidation of NEFA.

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Section: Discussionmentioning

confidence: 53%

“…A study with [ ]HDA) and single-photon emission tomography (SPET) found myocardial NEFA uptake and b-oxidation to be reduced in patients with impaired glucose tolerance (IGT) [4]. Surprisingly, the same study found that NEFA metabolism was normal in patients with Type II diabetes.…”

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confidence: 99%

Myocardial fatty acid oxidation in patients with impaired glucose tolerance

et al. 2001

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“…Although the impact of plasma levels of FFAs on the level of myocardial fatty acid uptake was not determined, a negative correlation between myocardial glucose uptake and plasma fatty acid levels is consistent with our data. Measurements of MFAO and %MFAO were not performed in these earlier studies, but measurements of myocardial fatty acid metabolism using single-photon emission computed tomography and the fatty acid analogue 123 I-hepadecanoic acid have suggested reduced beta-oxidation in patients with T2DM (38). Interestingly, measurements of myocardial clearance of 11 Cpalmitate (an estimate of beta-oxidation) did not differ between normal subjects and patients with insulin resistance (39).…”

Section: Discussionmentioning

confidence: 94%

Increased Myocardial Fatty Acid Metabolism in Patients With Type 1 Diabetes Mellitus

Herrero

Peterson

McGill

et al. 2006

Journal of the American College of Cardiology

231

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“…In three smaller PET studies in involving older men, there were no differences in myocardial FFA uptake and oxidation or a decrease in FFA uptake and oxidation between normal volunteers and subjects with impaired glucose tolerance [32][33][34]. Differences in sex, age, sample size, endogenous substrate availability, and PET tracers may have contributed to differences in results between these studies and the PET study in young women described above [29••].…”

Section: Effects On Myocardial Metabolismmentioning

confidence: 89%

Obesity and insulin resistance: Effects on cardiac structure, function, and substrate metabolism

Peterson

2006

Current Science Inc

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It is widely recognized that obesity and insulin resistance can contribute to an increased risk of coronary disease, but it has also become increasingly apparent that they may contribute directly to cardiac dysfunction even in the absence of significant coronary disease. Recently, obesity, which is frequently accompanied by insulin resistance, has been independently related to clinically diagnosed heart failure. Thus, there is renewed interest in the pathophysiology of myocardial disease related to obesity and insulin resistance, as well as in the specific cellular mechanisms by which obesity may cause detrimental cardiac structural and functional changes. Alterations in hemodynamics, plasma volume, neurohormonal status, and myocardial substrate metabolism all appear to contribute to these changes. Improving our understanding of cardiac dysfunction related to obesity and insulin resistance may provide clues for new strategies to prevent and treat this alarmingly prevalent condition.

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Abnormal myocardial kinetics of 123 I-heptadecanoic acid in subjects with impaired glucose tolerance

Cited by 19 publications

References 34 publications

Myocardial fatty acid oxidation in patients with impaired glucose tolerance

Myocardial fatty acid oxidation in patients with impaired glucose tolerance

Increased Myocardial Fatty Acid Metabolism in Patients With Type 1 Diabetes Mellitus

Obesity and insulin resistance: Effects on cardiac structure, function, and substrate metabolism

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