Obesity, defined by the WHO as BMI > 30, is considered as one of the major preventable causes of death worldwide and is characterized by a positive disequilibrium between energy intake and energy expenditure . It is directly involved in the pathogenesis of insulin resistance, atherosclerosis, dyslipidemia, hypertension and degenerative joint disease . Research conducted in the past few decades has revealed the pleiotropic effects of adipose tissue on every aspect of bodily functions and homeostasis, including immunity, metabolism and aging .
Mesenteric fat can be accurately and reliably assessed by ultrasonography, using the methodology described by Liu et al.. This method requires significant training by experienced physicians . However, if properly trained, the intra- and inter- operator variability is low [13, 15–17]. The presence of obesity does not negatively affect the reliability of the imaging modality, since increased adipose tissue accumulation renders mesenteric leaves readily visible .
The estimation of MFT ultrasonographically is one of the newest additions to the array of available imaging techniques for adipose tissue estimation. MFT has demonstrated positive associations with indices of insulin resistance (ie fasting blood glucose, HOMA-IR index, fasting serum insulin) [13, 17, 19] and subclinical atherosclerosis (carotid intima-media thickness) [13, 15]. Increased MFT has been proposed as a significant prognostic factor for polycystic ovary syndrome and fatty liver, conditions directly linked to insulin resistance, the metabolic syndrome, as well as atherosclerosis [16, 19].
Even though MFT has been correlated to LDL and HDL serum concentrations [13, 17], no studies have been carried out regarding the relationship between MFT and lipoprotein subfractions or serum concentrations. To our knowledge, this is the first available study to investigate the correlation of MFT to a large array of apolipoproteins.
Much attention has been devoted to the effect of apolipoproteins on the progression of atherosclerosis . They act as cofactors for enzymes involved in lipid metabolism, ligands for receptors or mediators of reverse cholesterol transport. Assessment of apolipoprotein levels is useful in predicting risk of cardiovascular disease .
Mesenteric fat may have a significant effect on serum lipoproteins by modulating liver function. It is the only adipose tissue depot that drains to the portal circulation, thus directly affecting liver metabolism and biosynthetic activity. It promotes liver fat accumulation and insulin resistance, which in turn leads to elevated hepatic glucose production and increased release of free fatty acids (FFAs) from adipose tissue [20, 21].
Abdominal fat cell weight has been previously reported to negatively correlate with plasma apoAI concentration . However, in our study we did not observe a statistically significant relationship of MFT with apoAI levels. On the other hand, MFT measurements correlated linearly with apoAII serum concentrations. This correlation may reflect the role of mesenteric fat as a significant source of triglycerides in the fasting state. A study investigating the impact of weight loss on HDL apoAII kinetics in the metabolic syndrome reported a significant correlation between changes in apoAII fractional catabolic rate and visceral adipose tissue mass, indicating a potential role for adiposity in the regulation of apoAII catabolism .
In our study, we also observed a significant correlation between MFT and apoB levels, the major component of LDL lipoproteins. FFAs released by mesenteric fat have been shown to increase apoB production and VLDL release. VLDL is transformed into IDL and LDL, a process, which results in the production of atherogenic LDL lipoproteins containing apoB [24–26]. Mesenteric adipose tissue may be a significant source of FFAs in both the fasting and fed period, given its relative resistance to the lipotrophic effects of insulin and its sensitivity to the lipolytic effects of catecholamines [4, 27]. These effects may be exaggerated in individuals with increased mesenteric adipose tissue depots.
As far as the other secretory products of mesenteric fat are concerned, interleukin- 6 and tumor necrosis factor alpha have been shown to increase apoB and VLDL production by hepatocytes in both clinical and experimental studies [25, 28–31].
On the other hand, no statistically significant correlations were observed between mesenteric fat thickness and components of VLDL lipoproteins, such as apoCII or apoCIII. This lack of association may be attributed to the design of the study. During the fasting state, VLDL lipoprotein levels tend to be diminished, and this may interfere with the possible relationship between mesenteric adipose tissue and liver lipoprotein production. In a previous study and in accordance to our results, serum apoE levels did not differ between obese and non-obese individuals . However, visceral fat accumulation significantly correlated with serum apoE concentration in middle-aged non-obese Japanese men .
The role of mesenteric fat on inflammation and oxidative damage in vascular tissue and the correlation of its thickness with cardiovascular disease risk are documented in literature . Trying to extend the existing knowledge, our study showed that MFT significantly correlates with apoB and apoAII levels. The correlation with apoB confirms the close association between MFT and atherosclerotic risk, observed in a significant number of previous studies. The correlation of MFT with apoAII may reflect the role of mesenteric fat as a significant source of triglycerides in the fasting state.