Very-Low-Calorie Diet Increases Myocardial Triglyceride Content and Decreases Diastolic Left Ventricular Function in Type 2 Diabetes With Cardiac Complications

In healthy subjects and patients with uncomplicated type 2 diabetes, short-term very-low-calorie diet (VLCD) increases myocardial triglyceride (TG) content and decreases diastolic cardiac function (1). We hypothesized that in diabetic patients with cardiac complications, the adaptive capacity of the heart to adjust myocardial TG content, depending on the metabolic context, is diminished or lost. We aimed to assess the effects of a short-term VLCD in type 2 diabetic patients with cardiac complications on myocardial TG content and cardiac function.

Therefore, 14 type 2 diabetic patients were included in this study (7 men, mean age 57 ± 3 years, 10 insulin users). Cardiac complications were defined as 1) obstructive coronary artery disease on multislice computed tomography angiography (≥50% luminal narrowing) and/or 2) myocardial perfusion defect on single photon emission computed tomography (summed stress score ≥3) (2). Exclusion criteria were age <18 years, thiazolidinedione use, congenital cardiac disease, or contraindications for magnetic resonance imaging. Written informed consent was obtained from all patients. This study was approved by the medical ethics committee of the Leiden University Medical Center and performed according to the Declaration of Helsinki.

Patients were studied on two separate study days. Three days before the first study day, patients used their regular diet. The second study day was after a 3-day VLCD (471 kcal/day, Modifast Intensive; Nutrition & Santé Benelux, Vilvorde, Belgium). Glucose-lowering therapy was adjusted during the VLCD to maintain comparable glucose levels before both study days. The acquisition and postprocessing of myocardial and hepatic proton spectroscopy, magnetic resonance imaging of the heart and abdominal fat, and the assays used for the biochemical parameters have previously been described (1,3,4).

For statistical analysis, within-group changes were assessed using paired sample t tests and nonparametric tests for normally and nonnormally distributed variables, respectively, using SPSS (version 17.0; SPSS, Chicago, IL). Data are expressed as means ± SE or, if nonnormally distributed, as median (interquartile range). P < 0.05 was considered statistically significant.

Of the 14 included type 2 diabetic patients, 6 had coronary artery disease on computed tomography angiography and 11 had myocardial perfusion defects, of whom 3 had both. Table 1 shows all parameters at baseline and after the VLCD.

Plasma nonesterified fatty acid (NEFA) levels increased significantly after the VLCD compared with baseline. Myocardial TG increased by ∼30% after the 3-day VLCD (baseline: 0.66 ± 0.08 to 0.89 ± 0.08%, P = 0.021). The other measured fat compartments did not significantly change (Table 1).

Several parameters of diastolic heart function decreased after the 3-day VLCD (Table 1). Main parameters are the E/A ratio (early diastolic filling phase/diastolic atrial contraction) (1.03 ± 0.06 to 0.92 ± 0.06, P = 0.004) and E deceleration peak (3.1 ± 0.2 to 2.4 ± 0.2 mL/s² ⋅ 10⁻³, P < 0.001), whereas estimated filling pressures remained unchanged after the 3-day VLCD.

In conclusion, the current study in type 2 diabetic patients with cardiac complications shows that only 3 days of VLCD increased plasma NEFA levels and myocardial TG content considerably, associated with a decrease in diastolic cardiac function. The observations suggest that type 2 diabetic patients with cardiac complications have preserved flexibility of myocardial TG stores, at least in response to short-term caloric restriction.