Endocrine Abstracts

Background: Although it has been conceived that type 2 diabetes mellitus (DM2) is associated with increased myocardial triglyceride (TG) accumulation, it is unknown whether this can be influenced by modifying plasma non-esterified fatty acids (NEFA) levels. We therefore determined in uncomplicated DM2 whether modifications in plasma NEFA influence myocardial TG content and myocardial function.

Research design and methods: Myocardial TG content and left ventricular (LV) function were determined using proton magnetic resonance spectroscopy and MRI respectively at 1.5 T (Gyroscan ACS/NT15, Philips) in 11 subjects with uncomplicated DM2 (mean age±S.D.: 59.8±5.4 years, BMI 26.2±0.9 kg/m², HbA1c: 6.0±0.2%) before and after 3 days of a very low calorie diet (VLCD, 473 kcal/day, to increase plasma NEFA levels) and after 3 days of a VLCD complemented with the administration of acipimox (4×250 mg during the last day of caloric restriction, to decrease NEFA levels). The percentage (%) of myocardial TG was calculated as TG/water×100. Myocardial function was calculated as ejection fraction (EF) for systolic function, and the ratio between early and atrial filling phase (E/A ratio) for diastolic function.

Results: A VLCD increased plasma levels of NEFA, from (mean±S.E.M.) 0.50±0.08 mmol/l (baseline) to 0.91±0.15 (P=0.023), associated with myocardial TG accumulation (from 0.66±0.09% (baseline) to 0.98±0.16% (P=0.028), and a decrease in E/A ratio (from 1.00±0.05 (baseline) to 0.90±0.06 (P=0.002). After the VLCD with acipimox, plasma NEFA levels decreased (to 0.24±0.05 mmol/l, P=0.002) and myocardial TG content and diastolic function returned to baseline values.

Conclusion: A short-term VLCD induces myocardial TG accumulation in patients with uncomplicated DM2, and is associated with changes in diastolic function. Administration of acipimox during the VLCD reduced myocardial TG accumulation together with plasma NEFA level in conjunction with diastolic heart function. These data stress the relation between plasma NEFA levels and myocardial TG accumulation in DM2.