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Short-Term Caloric Restriction Induces Accumulation of Myocardial Triglycerides and Decreases Left Ventricular Diastolic Function in Healthy Subjects

  1. Rutger W. van der Meer12,
  2. Sebastiaan Hammer2,
  3. Johannes W.A. Smit2,
  4. Marijke Frölich3,
  5. Jeroen J. Bax4,
  6. Michaela Diamant5,
  7. Luuk J. Rijzewijk5,
  8. Albert de Roos1,
  9. Johannes A. Romijn2 and
  10. Hildo J. Lamb1
  1. 1Department of Radiology, Leiden University Medical Center, Leiden, the Netherlands
  2. 2Department of Endocrinology, Leiden University Medical Center, Leiden, the Netherlands
  3. 3Department of Clinical Chemistry, Leiden University Medical Center, Leiden, the Netherlands
  4. 4Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands
  5. 5Department of Endocrinology, VU University Medical Center, Amsterdam, the Netherlands
  1. Address correspondence and reprint requests to R.W. van der Meer, MD, Department of Radiology, C2S, Leiden University Medical Center, P.O. Box 9600, 2300 RC Leiden, Netherlands. E-mail: r.W.van_der_meer{at}lumc.nl

Abstract

OBJECTIVE—Diabetes and obesity are associated with increased plasma nonesterified fatty acid (NEFA) levels, myocardial triglyceride accumulation, and myocardial dysfunction. Because a very low–calorie diet (VLCD) also increases plasma NEFA levels, we studied the effect of a VLCD on myocardial triglyceride content and cardiac function in healthy subjects.

RESEARCH DESIGN AND METHODS—Fourteen healthy nonobese men underwent 1H-magnetic resonance spectroscopy (MRS) to determine myocardial and hepatic triglyceride content, 31P-MRS to assess myocardial high-energy phosphate (HEP) metabolism (phosphocreatine/ATP), and magnetic resonance imaging of myocardial function at baseline and after a 3-day VLCD.

RESULTS—After the dietary intervention, plasma NEFA levels increased compared with those at baseline (from 0.5 ± 0.1 to 1.1 ± 0.1 mmol/l, P < 0.05). Concomitantly, myocardial triglyceride content increased by ∼55% compared with that at baseline (from 0.38 ± 0.05 to 0.59 ± 0.06%, P < 0.05), whereas liver triglyceride content decreased by ∼32% (from 2.2 ± 0.5 to 1.5 ± 0.4%, P < 0.05). The VLCD did not change myocardial phosphocreatine-to-ATP ratio (2.33 ± 0.15 vs. 2.33 ± 0.08, P > 0.05) or systolic function. Interestingly, deceleration of the early diastolic flow across the mitral valve decreased after the VLCD (from 3.37 ± 0.20 to 2.91 ± 0.16 ml/s2 × 10−3, P < 0.05). This decrease in diastolic function was significantly correlated with the increase in myocardial triglyceride content.

CONCLUSIONS—Short-term VLCD induces accumulation of myocardial triglycerides. In addition, VLCD decreases left ventricular diastolic function, without alterations in myocardial HEP metabolism. This study documents diet-dependent physiological variations in myocardial triglyceride content and diastolic function in healthy subjects.

Footnotes

  • Published ahead of print at http://diabetes.diabetesjournals.org on 23 August 2007. DOI: 10.2337/db07-0768.

    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.

    • Accepted August 21, 2007.
    • Received June 6, 2007.
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This Article

  1. Published online before print August 23, 2007, doi: 10.2337/db07-0768 Diabetes December 2007 vol. 56 no. 12 2849-2853
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