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Brief Reports

Myocardial Uptake of Circulating Triglycerides in Nondiabetic Patients With Heart Disease

  1. Robert H. Nelson1,
  2. Abhiram Prasad2,
  3. Amir Lerman2 and
  4. John M. Miles1
  1. 1Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota
  2. 2Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota
  1. Address correspondence and reprint requests to John M. Miles, MD, Endocrine Research Unit, Mayo Clinic, 200 First St. SW, Rochester, MN 55905. E-mail: miles.john{at}mayo.edu
Diabetes 2007 Feb; 56(2): 527-530. https://doi.org/10.2337/db06-1552
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Abstract

Animal studies indicate that oversupply of fatty acids derived from the action of cardiac lipoprotein lipase (LPL) on plasma lipoproteins may contribute to myocardial dysfunction. However, the contribution of circulating triglycerides to myocardial fatty acid supply in humans is not known. Six postabsorptive nondiabetic subjects who were scheduled for diagnostic coronary angiography were studied. 14C oleate and a lipid emulsion labeled with 3H triolein were infused to assess myocardial uptake of free fatty acids (FFAs) and triglycerides, as well as myocardial spillover of LPL-generated fatty acids. Six paired blood samples were taken from the femoral artery and the coronary sinus. Coronary sinus concentrations of unlabeled triglycerides were slightly, but not significantly, lower than arterial (P = 0.12), whereas labeled triglyceride concentrations were significantly lower in the coronary sinus than in the artery (P < 0.05; extraction fraction ≅11%). Triglycerides and FFAs accounted for ∼17% and ∼83%, respectively, of myocardial fatty acid uptake. Systemic and myocardial fractional spillover of LPL-generated fatty acids was 49.0 ± 7% and 34.7 ± 13%, respectively. The myocardium was a minor contributor to systemic triglyceride uptake (∼3%) and a trivial contributor to systemic FFA production (∼0.5%). These results indicate that circulating triglycerides may be a significant source of fatty acids for myocardial respiration.

  • FFA, free fatty acid
  • LPL, lipoprotein lipase
  • LPLc, myocardial LPL

It has been suggested that free fatty acids (FFAs) are the primary energy source for the myocardium (1). However, the heart contains a considerable amount of lipoprotein lipase (LPL) (2), and studies in animals have found significant triglyceride uptake by the myocardium. It has been suggested recently that circulating triglycerides are actually the primary lipid fuel for this tissue (3). Very little information on the role of triglycerides in human myocardial metabolism is available, however. The present study was therefore undertaken to determine whether significant uptake of triglycerides occurs in the heart and also to determine the relative role of triglycerides and FFAs in the provision of lipid fuel to that tissue.

RESEARCH DESIGN AND METHODS

Informed written consent was obtained from six Caucasian subjects (three male, three female; average age 65 years, weight 91.3 kg, BMI 30.9 kg/m2) scheduled for diagnostic coronary angiography. Individuals with diabetes, significant hypertriglyceridemia (>2.26 mmol/l), congestive heart failure, unstable angina, recent stroke, previous myocardial infarction or angioplasty, left ventricular ejection fraction <45%, or significant endocrine, hepatic, or renal disorders were excluded. Five of the six subjects proved to have coronary artery disease; four of these underwent percutaneous stent placement. One subject had valve replacement surgery for aortic stenosis.

Subjects were studied according to a protocol approved by the Mayo Institutional Review Board. On the morning of the study (after an overnight fast and after obtaining informed consent), a catheter was placed in a forearm vein for isotope infusion. Infusions of tracer amounts of [9,10-3H]triolein (∼1.2 μCi/min) and [1-14C]oleate (∼0.3 μCi/min) were started 90 and 60 min, respectively, before blood sampling; the isotope infusions were continued until blood sampling had been completed as previously described (4). After transfer to the catheterization laboratory, a sheath was placed in the right femoral artery, and a catheter was advanced to the coronary sinus via either the right femoral vein or the right internal jugular vein. After the catheters were positioned, six paired arterial and coronary sinus blood samples were taken at 4-min intervals for measurement of plasma triglyceride concentration and radioactivity, FFA concentration and specific activity, and glucose concentration. Blood gas analysis was also performed to assess the position of the coronary sinus catheter. Heparin was not administered to the subjects until blood sampling was complete.

Analyses.

Blood samples were collected in chilled 10-ml EDTA tubes containing paraoxon (5) and kept on ice until centrifugation at 4°C. Plasma triglyceride concentrations were determined on a Cobas Mira Plus centrifugal analyzer (4).

Plasma FFA concentration and specific activity (6) and plasma triglyceride radioactivity (4) were determined as previously described. Plasma glucose concentrations were measured using a Beckman Glucose Analyzer II. Arterial blood gasses were determined using a Radiometer America OSM3 Hemoximeter, and hematocrit was determined on an Abbott I-STAT 1 Analyzer.

Calculations.

All calculations were made using steady-state assumptions. Systemic FFA turnover was calculated using the equations of Steele (7). Global coronary blood flow was estimated to be 120 ml/min in all subjects, based on magnetic resonance estimates of blood flow (8), and an estimated left ventricular plus interventricular septal mass of 158 g (9). Plasma flow was estimated from estimated blood flow and hematocrit. The contribution of the heart to whole-body triglyceride disappearance was calculated by dividing myocardial uptake of labeled triglyceride by the infusion rate of 3H triolein. Systemic and myocardial FFA and triglyceride kinetics, as well as LPL-generated fatty acid spillover (i.e., escape of fatty acids into the venous effluent from the tissue), were calculated as previously described in a study of forearm metabolism (4).

Mean arterial and coronary sinus values were calculated by averaging results from the six samples taken from each site. Comparisons between arterial and coronary sinus values in the group of subjects were analyzed by a paired t test. Paired t tests (arterial vs. coronary sinus) were performed on triglyceride data in each subject to determine whether significant myocardial uptake was detected.

RESULTS

Coronary sinus oxygen saturation was <42% in five of the six subjects; it was 67% in one subject, indicating some dilution of the coronary sinus sample with mixed venous blood. Because hematocrit was significantly higher in the coronary sinus compared with arterial blood (36.5 ± 1.3 vs. 35.9 ± 1.4%, respectively; P = 0.024), coronary sinus concentrations were corrected for hemoconcentration in each subject.

Arterial and coronary sinus triglyceride concentrations and radioactivity are shown in Figs. 1 and 2, respectively. In the six subjects, triglyceride concentrations were slightly, but not significantly, lower in the coronary sinus than in arterial plasma (0.946 ± 0.26 vs. 0.959 ± 0.25 mmol/l, respectively; P = 0.12). In a within-subject analysis, coronary sinus concentrations of unlabeled triglyceride were significantly lower than arterial (P < 0.05) in three of six subjects. Coronary sinus 3H triglyceride concentrations were significantly lower than arterial concentrations (2,640 ± 442 vs. 3,009 ± 553 dpm/ml; P < 0.05). Myocardial arteriovenous differences of labeled triglyceride were statistically greater than zero in five of six subjects. Myocardial fractional extraction was greater for labeled triglyceride compared with unlabeled triglyceride (10.8 ± 3.3 vs. 2.8 ± 1.6%; P = 0.035, data not shown).

FIG. 1.
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FIG. 1.

Arterial and coronary sinus plasma triglyceride concentrations.

FIG. 2.
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FIG. 2.

Concentrations of 3H triglyceride in arterial and coronary sinus plasma.

Table 1 shows plasma oleate and total FFA concentrations, together with plasma 14C and 3H specific activities. Coronary sinus concentrations of both oleate and total FFA were significantly lower than arterial (P < 0.001). Coronary sinus 14C oleate specific activities were also lower than arterial (P = 0.033). In contrast, 3H oleate specific activity was not different in coronary sinus and arterial plasma (P = 0.17). There was a strong negative correlation between 14C oleate fractional extraction (34 ± 5%) and plasma oleate concentration (R = 0.973, P < 0.01, data not shown).

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TABLE 1

Plasma oleate and total FFA concentrations and plasma oleate specific activities

Systemic and myocardial triglyceride and FFA kinetics are shown in Table 2. Uptake of triglycerides averaged 17% of total myocardial fatty acid uptake. Systemic and myocardial fractional spillover of LPL-generated fatty acids was 49 and 34.7%, respectively. Coronary sinus glucose concentration (data not shown) was lower than arterial (4.80 ± 0.31 vs. 5.15 ± 0.21 mmol/l; P = 0.025).

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TABLE 2

Kinetic data

DISCUSSION

The present study demonstrates that the myocardium metabolizes circulating triglycerides in humans and establishes for the first time that the majority of the fatty acids generated by this process are transported into the heart. Previous reports (10,11) suggested triglyceride hydrolysis by the heart, presumably by myocardial LPL (LPLc), but did not determine whether the fatty acids generated were taken up by the myocardium or whether they spilled over into the systemic circulation. The extraction of unlabeled triglyceride in the present study was significant in 3 of 6 subjects, but not for the group (P = 0.12), consistent with a previous report in which significant uptake of unlabeled triglyceride was observed in 9 of 17 subjects (11); this is likely a reflection of the difficulty in detecting very small arteriovenous concentration differences. The extraction of labeled triglyceride in our study, on the other hand, was significant in five of six subjects and for the group as a whole (P < 0.05). These observations indicate a significant potential role for circulating triglycerides as a source of fuel for myocardial metabolism. It has been suggested that measurements in subjects with heart disease may generally reflect normal myocardial metabolism in the absence of heart failure or active ischemia, since myocardial FFA uptake, glucose uptake, and lactate balance in individuals with coronary artery disease is not different than that observed in young healthy volunteers (12). Nonetheless, caution should be exercised in extrapolating our findings in a small group of individuals with heart disease to other populations.

Studies in mice indicate that circulating triglycerides actually contribute the majority of fatty acids for myocardial respiration (3). Our results are consistent with previous work, suggesting that FFAs are the majority contributor in humans, at least under postabsorptive conditions (11–13). Triglyceride fractional extraction was 2.8% in our study, similar to the findings of Lassers et al. (11). It should be acknowledged that secretion of triglyceride-containing lipoproteins by the heart, which has been reported in rodents (14), would result in an underestimate of myocardial uptake of circulating triglycerides.

Measurement of arterial-coronary sinus concentration differences of labeled or unlabeled triglyceride could overestimate myocardial uptake of triglyceride fatty acids if there were spillover of LPLc-generated fatty acids. The spillover phenomenon has previously been demonstrated in the forearm (4,15) and in adipose tissue (15). Myocardial uptake of an exogenously labeled triglyceride tracer has not previously been investigated in humans. The present study estimates fractional spillover of LPLc-generated fatty acids from a chylomicron-like particle to be ∼35%. We found fractional extraction of the labeled emulsion to be ∼11% or approximately fourfold higher than the extraction of unlabeled triglyceride. This indicates a preference by LPLc for larger chylomicron-sized particles, as has been previously observed in forearm (4) and adipose tissues (16). In contradistinction to chylomicrons, systemic spillover from VLDL triglyceride appears to be negligible (17).

It is possible that dietary fat is a major direct source of myocardial fatty acid uptake. No data on myocardial uptake of meal fat is available in humans, but the amount of triglyceride fatty acids traversing the circulation in subjects consuming high-fat diets is similar to the amount of FFA released in a 24-h period, ∼100 g/day in a 70-kg individual (4).

The release of unlabeled FFA into the coronary sinus in the present study presumably derives from the action of hormone-sensitive lipase in epicardial fat. This is trivial in systemic terms, however, accounting for only ∼0.5% of whole-body FFA appearance. It is unlikely that the triglyceride uptake observed in the present study occurred in epicardial fat, in view of the low spillover of LPLc-generated fatty acids observed. We found an average fractional spillover of ∼35%, much lower than previously reported for adipose tissue, which is ∼80% several hours after meal ingestion (15).

The present study provides the first available estimates of the contribution of the heart to whole-body FFA and triglyceride metabolism. When heterozygous LPL knockout mice were crossbred with mice possessing human LPLc to create a mouse with LPLc activity only, the animals had near-normal circulating triglyceride levels and normal HDL levels in spite of the absence of LPL in adipose tissue and skeletal muscle (18). This suggests that LPLc may be an important contributor to whole-body LPL activity. Our data indicate that only ∼2% of whole-body triglyceride disappearance and ∼3% of systemic FFA uptake occurs in the heart in postabsorptive humans. This is the case in spite of the fact that most myocardial ATP production is derived from FFA oxidation after an overnight fast (19). Although no data are available on myocardial metabolism during meal absorption, the heart readily switches to carbohydrate oxidation during infusion of insulin and glucose (20).

It is not known with certainty whether myocardial uptake of triglyceride fatty acids from blood is essential for optimal myocardial energetics, but animals deficient in LPLc apparently have normal cardiac function (21). The fact that the heart can take up and oxidize large amounts of carbohydrate when deprived of FFA (20), together with the avid extraction of FFA from blood as shown in the present and previous studies, would suggest that circulating triglycerides are not an essential fuel for this tissue.

On the other hand, LPLc may represent a route for oversupply of fatty acids to the myocardium. Expression of an abnormal LPLc on the surface of cardiomyocytes in mice leads to increased intracardiomyocellular lipid accumulation and a cardiomyopathy (22). Increased triglyceride accumulation in cardiac muscle has been shown in humans (23,24), although the relative contributions of FFAs and circulating triglycerides to this phenomenon are not known. This accumulation of lipid may be a major contributor to contractile dysfunction and even nonischemic cardiomyopathy (25). Additional research will be required to assess myocardial uptake of circulating triglycerides during meal absorption.

In summary, the present study confirms that the myocardium takes up fatty acids from circulating triglycerides in humans. The magnitude of postprandial triglyceride fatty acid uptake is unknown. Studies in postabsorptive hypertriglyceridemic subjects and after ingestion of a mixed meal are needed to improve our understanding of the contribution of circulating lipids to myocardial energy supply.

Acknowledgments

This study was supported by U.S. Public Health Service Commissioned Corps Grants HL67933, HL63911, HL69840, and RR00585, as well as grants from the Kogod Foundation and the Mayo Foundation.

We thank J. Roesner and K. Sagdalen for technical assistance.

Footnotes

  • The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

  • Received July 28, 2006.
  • Accepted November 9, 2006.
  • DIABETES

REFERENCES

  1. ↵
    Ballard FB, Danforth WH, Naegle S, Bing RJ, Kako K, Choudhury JD: Myocardial metabolism of fatty acids. J Clin Invest 39 : 717 –723,1960
    OpenUrlCrossRefPubMedWeb of Science
  2. ↵
    Korn E: Clearing factor, a heparin-activated lipoprotein lipase. I. Isolation and characterization of the enzyme from normal rat heart. J Biol Chem 215 : 1 –14,1955
    OpenUrlFREE Full Text
  3. ↵
    Augustus AS, Kako Y, Yagyu H, Goldberg IJ: Routes of FA delivery to cardiac muscle: modulation of lipoprotein lipolysis alters uptake of TG-derived FA. Am J Physiol 284 : E331 –E339,2003
    OpenUrlCrossRef
  4. ↵
    Miles J, Park Y, Walewicz D, Russell-Lopez C, Windsor S, Isley W, Coppack S, Harris W: Systemic and forearm triglyceride metabolism: fate of lipoprotein lipase-generated glycerol and free fatty acids. Diabetes 53 : 521 –527,2004
    OpenUrlAbstract/FREE Full Text
  5. ↵
    Miles JM, Glasscock R, Aikens J, Gerich JE, Haymond MW: A microfluorometric method for the determination of free fatty acids in plasma. J Lipid Res 24 : 96 –99,1983
    OpenUrlAbstract
  6. ↵
    Miles JM, Ellman MG, McClean KL, Jensen MD: Validation of a new method for determination of free fatty acid turnover. Am J Physiol 252 : E431 –E438,1987
  7. ↵
    Steele R, Wall JS, DeBodo RC, Altszuler N: Measurement of size and turnover rate of body glucose pool by the isotope dilution method. Am J Physiol 18 : 15 –24,1956
    OpenUrl
  8. ↵
    Schwitter J, DeMarco T, Kneifel S, von Schulthess GK, Jorg MC, Arheden H, Ruhm S, Stumpe K, Buck A, Parmley WW, Luscher TF, Higgins CB: Magnetic resonance-based assessment of global coronary flow and flow reserve and its relation to left ventricular functional parameters: a comparison with positron emission tomography. Circulation 101 : 2696 –2702,2000
  9. ↵
    Reiner L, Amazzoleni A, Rodriguez F, Freudenthal R: The weight of the human heart. I. “Normal” cases. Arch Pathol 68 : 58 –73,1959
    OpenUrl
  10. ↵
    Carlson LA, Kaijser L, Lassers BW: Myocardial metabolism of plasma triglycerides in man. J Mol Cell Cardiol 1 : 467 –475,1970
    OpenUrlPubMed
  11. ↵
    Lassers BW, Kaijser L, Carlson LA: Myocardial lipid and carbohydrate metabolism in healthy, fasting men at rest: studies during continuous infusion of 3H-palmitate. Eur J Clin Invest 2 : 348 –358,1972
    OpenUrlCrossRefPubMedWeb of Science
  12. ↵
    Wisneski JA, Gertz EW, Neese RA, Mayr M: Myocardial metabolism of free fatty acids: studies with 14C-labelled substrates in humans. J Clin Invest 79 : 359 –366,1987
    OpenUrlCrossRefPubMedWeb of Science
  13. ↵
    Most AS, Brachfeld N, Gorlin R, Wahren J: Free fatty acid metabolism of the human heart at rest. J Clin Invest 48 : 1177 –1188,1969
    OpenUrlCrossRefPubMed
  14. ↵
    Bjorkegren J, Veniant M, Kim SK, Withycombe SK, Wood PA, Hellerstein MK, Neese RA, Young SG: Lipoprotein secretion and triglyceride stores in the heart. J Biol Chem 276 : 38511 –38517,2001
    OpenUrlAbstract/FREE Full Text
  15. ↵
    Evans K, Burdge GC, Wootton SA, Clark ML, Frayn KN: Regulation of dietary fatty acid entrapment in subcutaneous adipose tissue and skeletal muscle. Diabetes 51 : 2684 –2690,2002
    OpenUrlAbstract/FREE Full Text
  16. ↵
    Coppack SW, Fisher RM, Gibbons GF, Humphreys SM, McDonough MJ, Potts JL, Frayn KN: Postprandial substrate deposition in human forearm and adipose tissues in vivo. Clin Sci 79 : 339 –348,1990
  17. ↵
    Gormsen LC, Jensen MD, Nielsen S: Measuring VLDL-triglyceride turnover in humans using ex vivo-prepared VLDL tracer. J Lipid Res 47 : 99 –106,2006
    OpenUrlAbstract/FREE Full Text
  18. ↵
    Levak-Frank S, Hofmann W, Weinstock PH, Radner H, Sattler W, Breslow JL, Zechner R: Induced mutant mouse lines that express lipoprotein lipase in cardiac muscle, but not in skeletal muscle and adipose tissue, have normal plasma triglyceride and high-density lipoprotein-cholesterol levels. Proc Natl Acad Sci U S A 96 : 3165 –3170,1999
    OpenUrlAbstract/FREE Full Text
  19. ↵
    Kako KJ, Vasdev SC, Narbaitz R: Lipid metabolism, contractility, and ultrastructure of heats of rats fed a mustard seed oil diet. In Advances in Myocardiology. 2nd ed. Tajuddin M, Bhatia B, Siddiqui HH, Rona G, Eds. Baltimore, MD, University Park Press,1980 , p. 61 –69
  20. ↵
    Ferrannini E, Santoro D, Bonadonna R, Natali A, Parodi O, Camici PG: Metabolic and hemodynamic effects of insulin on human hearts. Am J Physiol 264 : E308 –E315,1993
  21. ↵
    Augustus A, Yagyu H, Haemmerle G, Bensadoun A, Vikramadithyan RK, Park SY, Kim JK, Zechner R, Goldberg IJ: Cardiac-specific knock-out of lipoprotein lipase alters plasma lipoprotein triglyceride metabolism and cardiac gene expression. J Biol Chem 279 : 25050 –25057,2004
    OpenUrlAbstract/FREE Full Text
  22. ↵
    Yagyu H, Chen G, Yokoyama M, Hirata K, Augustus A, Kako Y, Seo T, Hu Y, Lutz EP, Merkel M, Bensadoun A, Homma S, Goldberg IJ: Lipoprotein lipase (LpL) on the surface of cardiomyocytes increases lipid uptake and produces a cardiomyopathy. J Clin Invest 111 : 419 –426,2003
    OpenUrlCrossRefPubMedWeb of Science
  23. ↵
    Szczepaniak LS, Dobbins RL, Metzger GJ, Sartoni-D’Ambrosia G, Arbique D, Vongpatanasin W, Unger R, Victor RG: Myocardial triglycerides and systolic function in humans: in vivo evaluation by localized proton spectroscopy and cardiac imaging. Magn Reson Med 49 : 417 –423,2003
    OpenUrlCrossRefPubMedWeb of Science
  24. ↵
    McGavock JM, Victor RG, Unger RH, Szczepaniak LS: Adiposity of the heart, revisited. Ann Intern Med 144 : 517 –524,2006
    OpenUrlCrossRefPubMedWeb of Science
  25. ↵
    Unger RH: Minireview: weapons of lean body mass destruction: the role of ectopic lipids in the metabolic syndrome. Endocrinology 144 : 5159 –5165,2003
    OpenUrlCrossRefPubMedWeb of Science
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Myocardial Uptake of Circulating Triglycerides in Nondiabetic Patients With Heart Disease
Robert H. Nelson, Abhiram Prasad, Amir Lerman, John M. Miles
Diabetes Feb 2007, 56 (2) 527-530; DOI: 10.2337/db06-1552

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Myocardial Uptake of Circulating Triglycerides in Nondiabetic Patients With Heart Disease
Robert H. Nelson, Abhiram Prasad, Amir Lerman, John M. Miles
Diabetes Feb 2007, 56 (2) 527-530; DOI: 10.2337/db06-1552
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Keywords

FFA, free fatty acid
LPL, lipoprotein lipase
LPLc, myocardial LPL

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