Fatty acid uptake in normal human myocardium.

Vyska, K.; Meyer, W.; Stremmel, Wolfgang; Notohamiprodjo, G.; Minami, Kazutomo; Machulla, H.-J.; Gleichmann, U.; Meyer, Hans; Körfer, Reiner

doi:10.1161/01.res.69.3.857

Cited by 29 publications

(13 citation statements)

References 32 publications

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“…Myocardial palmitate extraction in the current study was similar to others reporting 40 -74% isotopically measured fractional extraction in resting human myocardium (18,40,44). Fractional extraction of FFA has been reported to be unchanged during atrial pacing (34) and to either not change (22) or decrease during whole body exercise (18,22).…”

Section: Discussionsupporting

confidence: 89%

Myocardial FFA metabolism during rest and atrial pacing in humans

Bergman¹,

Tsvetkova²,

Lowes³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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Bergman BC, Tsvetkova T, Lowes B, Wolfel EE. Myocardial FFA metabolism during rest and atrial pacing in humans. Am J Physiol Endocrinol Metab 296: E358 -E366, 2009. First published December 9, 2008 doi:10.1152/ajpendo.90747.2008.-There is limited in vivo data in humans evaluating myocardial fat utilization during increased heart work. This study was done to determine myocardial free fatty acid (FFA) metabolism during rest and atrial pacing, which increases cardiac work without changing arterial substrate concentration. We studied seven healthy men and women (age ϭ 49.7 Ϯ 3.9 yr, BMI ϭ 23.4 Ϯ 1.1 kg/m 2 , V O2max ϭ 35.5 Ϯ 3.0 ml ⅐ kg Ϫ1 ⅐ min Ϫ1 , ejection fraction ϭ 68 Ϯ 3%). After 3 days of dietary control, coronary sinus, femoral arterial and venous, and peripheral venous catheters were placed. Subjects received [13 C]bicarbonate followed by a continuous infusion of [1-13 C]palmitate through the end of the study. Arterial and coronary sinus blood sampling and measurements of resting coronary sinus blood flow were made during rest and atrial pacing to 120 beats/min. MV O2 increased (P Ͻ 0.05) from rest to atrial pacing. Coronary sinus FFA concentration was significantly lower than arterial through rest and atrial pacing (P ϭ 0.007). Isotopically measured myocardial palmitate uptake increased significantly from rest to atrial pacing (P ϭ 0.03). Approximately one-third of palmitate delivery was extracted by the myocardium during rest and atrial pacing. Myocardial V 13 CO2 production and palmitate oxidation increased significantly from rest (P Ͻ 0.01) to atrial pacing. Net glycerol balance was significantly greater than zero during rest (P ϭ 0.04) but not different from zero during atrial pacing (P ϭ 0.13). These data suggest that myocardial lipid uptake and oxidation increase with greater heart work during atrial pacing, with a similar relative proportion of fat oxidation to total myocardial energy expenditure. free fatty acid; stable isotopes; myocardial substrate utilization MYOCARDIAL SUBSTRATE UTILIZATION can influence myocardial energy efficiency (8), tissue survival during ischemia (19), and cardiac efficiency (30). Additionally, alteration of myocardial substrate utilization has been reported and may be implicated in decreased ventricular performance in heart failure (2, 36), obesity (30), and type 1 (4) and type 2 diabetes (35). Therefore, understanding myocardial substrate utilization is important to elucidate potential derangements in myocardial metabolic control that may contribute to disease states.Much of the knowledge on myocardial free fatty acid (FFA) utilization comes from studies on isolated heart preparations. It is well established that the majority of myocardial energy supply in the resting state comes from the oxidation of FFAs (6, 38), with arterial substrate concentration influencing myocardial uptake (32). Some data indicate that the isolated working heart increases reliance on carbohydrate-derived fuels more than ␤-oxidation (15), whereas others have suggested increased reliance on circ...

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Section: Discussionsupporting

confidence: 89%

Myocardial FFA metabolism during rest and atrial pacing in humans

Bergman¹,

Tsvetkova²,

Lowes³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

show abstract

“…There is evidence that indicates that fatty acids enter cells by simple diffusion (51) and/or via a carrier-mediated process. Proteins that function as fatty acid transporters have been reported to exist on the plasma membrane of a number of cell types (52,53). It is possible that these mechanisms are not mutually exclusive.…”

Section: Resultsmentioning

confidence: 99%

Stimulation of p38 Phosphorylation and Activity by Arachidonic Acid in HeLa Cells, HL60 Promyelocytic Leukemic Cells, and Human Neutrophils

Hii¹,

Huang²,

Bilney³

et al. 1998

Journal of Biological Chemistry

100

101

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Although it is well appreciated that arachidonic acid, a second messenger molecule that is released by ligandstimulated phospholipase A 2 , stimulates a wide range of cell types, the mechanisms that mediate the actions of arachidonic acid are still poorly understood. We now report that arachidonic acid stimulated the appearance of dual-phosphorylated (active) p38 mitogen-activated protein kinase as detected by Western blotting in HeLa cells, HL60 cells, human neutrophils, and human umbilical vein endothelial cells but not Jurkat cells. An increase in p38 kinase activity caused by arachidonic acid was also observed. Further studies with neutrophils show that the stimulation of p38 dual phosphorylation by arachidonic acid was transient, peaking at 5 min, and was concentration-dependent. The effect of arachidonic acid was not affected by either nordihydroguaiaretic acid, an inhibitor of the 5-, 12-, and 15-lipoxygenases or by indomethacin, an inhibitor of cyclooxygenase. Arachidonic acid also stimulated the phosphorylation and/or activity of the extracellular signal-regulated protein kinase and of c-jun N-terminal kinase in a cell-typespecific manner. An examination of the mechanisms through which arachidonic acid stimulated the phosphorylation/activity of p38 and extracellular signal-regulated protein kinase in neutrophils revealed an involvement of protein kinase C. Thus, arachidonic acid stimulated the translocation of protein kinase C ␣, ␤I, and ␤II to a particulate fraction, and the effects of arachidonic acid on mitogen-activated protein kinase phosphorylation/activity were partially inhibited by GF109203X, an inhibitor of protein kinase C. This study is the first to demonstrate that a polyunsaturated fatty acid causes the dual phosphorylation and activation of p38.

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“…Other potential explanations linking hyperglycemia and poor outcome after acute myocardial infarction, are reduction of nitric oxide availability and endothelial dysfunction and oxidative stress related to hyperglycemia [22]. Another possible mechanism which could link hyperglycemia with adverse outcome in patients with acute myocardial infarction is a shift from glucose metabolism toward fatty acid metabolism which is more energy demanding [23] and antagonizing the myocardial uptake of glucose, lactate and pyruvate [24]. On the other hand, elevated levels of free fatty acids have been associated with impaired ventricular function in animal models [25] and increased risk of arrhythmias, post-infarct angina, infarct extension, heart failure and death in patients with MI [26].…”

Section: Pathophysiological Impact Of Hyperglycemia During Acute Myocmentioning

confidence: 99%

Hyperglycemia during acute myocardial infarction in patients who are treated by primary percutaneous coronary intervention: Impact on long-term prognosis

Lavi

Kapeliovich

Gruberg

et al. 2008

International Journal of Cardiology

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Fatty acid uptake in normal human myocardium.

Abstract: Fatty acid binding protein has been found in rat aortic endothelial cell membrane. It has been identified to be a

Cited by 29 publications

References 32 publications

Myocardial FFA metabolism during rest and atrial pacing in humans

Myocardial FFA metabolism during rest and atrial pacing in humans

Stimulation of p38 Phosphorylation and Activity by Arachidonic Acid in HeLa Cells, HL60 Promyelocytic Leukemic Cells, and Human Neutrophils

Hyperglycemia during acute myocardial infarction in patients who are treated by primary percutaneous coronary intervention: Impact on long-term prognosis

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