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

¹ Department of Radiology, Leiden University Medical Center, Leiden, the Netherlands
² Department of Endocrinology, Leiden University Medical Center, Leiden, the Netherlands
³ Department of Clinical Chemistry, Leiden University Medical Center, Leiden, the Netherlands
⁴ Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands
⁵ Department of Endocrinology, VU University Medical Center, Amsterdam, the Netherlands

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

Abbreviations: AMARES, Advanced Magnetic RESonance; ECG, electrocardiogram; HEP, high-energy phosphate; jMRUI, Java-based magnetic resonance user interface; LV, left ventricular; MR, magnetic resonance; MRI, MR imaging; MRS, MR spectroscopy; NEFA, nonesterified fatty acid; TR, repetition time; VLCD, very low–calorie diet

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 x 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.

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