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It is well known that obesity is an established risk factor for cardiovascular complications. There are large-scale epidemiologic studies clearly demonstrating that accumulation of excessive amounts of adipose tissue in the body may lead to type 2 diabetes mellitus, hypertension and coronary artery disease – disorders associated with myocardial damage (1, 2). It has also become clear that not every fat location is equally morbid. Both histopathologic studies and clinical observations point to the visceral fat depot with inflammatory infiltration as the most metabolically active one and carrying major responsibility for deleterious effects of increased body weight (3). However, it has been shown that triglyceride (TG) content in obese individuals increases not only in adipose tissue but also ectopically in organs such as the liver, pancreas, skeletal muscles and the heart (4, 5). Lipid accumulation in non-adipose tissues may impair organs’ function and further explain mechanisms underlying detrimental effects of overweight and obesity. The introduction and validation of a reproducible method of in vivo myocardial TG content quantification – proton magnetic resonance spectroscopy (1HMRS) (1), enabled researchers to carry out studies on myocardial lipid accumulation in humans and thus a new fascinating area of clinical research seems to have been opened. A recently published article on the issue at hand is summarized below and followed by a brief contextual comment.
The study by Hammer et al. investigates whether prolonged caloric restriction can change myocardial TG content and influence left ventricular function. To answer these questions, 12 obese patients (7 men, mean age 48.3 ± 2.3 yrs) with insulin treated type 2 diabetes mellitus (T2DM) were put on a very-lowcalorie diet (VLCD; 450 kcal/day) for a 16-week time interval. To assess the effects of prolonged caloric restriction in these patients, myocardial TG content (MR spectroscopy), myocardial function (MRI), plasma hemoglobin A1C and body mass index (BMI) were measured 1 week before and directly after the dietary intervention.
Additionally, to evaluate the tissue-specific effects of caloric restriction further, liver TG content was examined during both of the MR studies. As the result of VLCD, the patients’ BMI decreased from 35.6 kg/m2 to 27.5 kg/m2 (p < 0.001) and considerable improvements in glucoregulation and lipid profile were noted. MR spectroscopy showed that prolonged caloric restriction was associated with significant reduction in TG content in the myocardium (from 0.88% at baseline to 0.64% after the intervention, p < 0.019) and even more notably in the liver (from 21.2% to 3.0%, resp., p < 0.001). Interestingly, the diet modification led to improvements in myocardial function with a significant decrease in LV mass (from 118±7g to 99±6g after the VLCD, p<0.001) and improved diastolic function (E/A ratio increased from 1.02±0.08 at baseline to 1.18±0.06 after the VLCD). These data show that myocardial TG stores in obese patients with T2DM are flexible and respond to therapeutic intervention by caloric restriction.
The summarized paper is the latest report concerning the issue of TG accumulation in the myocardium and shows that myocardial TG stores in obese patients with T2DM are flexible and amenable to dietary intervention (caloric restriction). Previous investigations demonstrated that myocardial TG content increases with older age, in patients with impaired glucose tolerance, type 2 diabetes mellitus and in subjects with visceral obesity (4, 6, 7). Furthermore, clinical observations linked excessive heart TG
accumulation to increased left ventricular (LV) mass and impaired LV function (4, 6, 7).
These data are in agreement with extensive evidence stemming from basic sciences. Experiments in rodents showed that obesity and T2DM led to excessive fatty acids uptake and, in consequence, to an increase in myocardial TG pool, generation of lipotoxic fatty acid intermediates and free radicals. The shift in metabolism causes
apoptosis of cardiac myocytes, increased oxidative stress and eventually non-ischeamic cardiomyopathy (8). Importantly, this pathogenic process could be interrupted, thus preventing or even reversing the development of LV dysfunction (9, 10). It is plausible that at least some of these mechanisms may work in a similar fashion in obese humans.
The paper by Hammer et al. is the first one to demonstrate the capability of a dietary intervention to decrease myocardial TG content. Furthermore, the study suggests that LV function in obese patients with T2DM is related to myocardial TG accumulation. However, it remains unknown whether this relationship was independent of other metabolic and hemodynamic changes induced by VLCD. Of interest, Sharma et al. showed with analysis of myocardial lipid staining (oil red O) that intramyocardial lipid overload was present in 30% (9 of 27) of non-ischemic failing human hearts.
The highest levels of lipid staining were observed in patients with diabetes and obesity (BMI>30) (11). The potential associations of increased myocardial TG content with heart failure development remain to be elucidated.
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