In vitro study of the effect of diesterified alkoxyglycerols with conjugated linoleic acid on adipocyte inflammatory mediators

Our data suggest that DEA-CLA, product of the esterification between the CLA and batyl alcohol, present beneficial effects on adipocytes close to observed and described for CLA (i.e. decrease of IL-1β) and no adverse effects as observed for batyl alcohol (i.e. decrease of IL-10). In addition, DEA-CLA presented similar activity to CLA showing a trend to increase the secreted levels of adiponectin and decreasing the secreted levels of leptin.CLA and DEA-CLA modify adipocyte inflammatory mediators and also could play a role on energy homeostasis through depletion of leptin levels.Obesity and its pathological complications, including atherosclerosis, hypertension, and insulin resistance, have increased to reach epidemic dimensions nowadays [1]. Some important factors for the development of these disorders are excessive accumulation of abdominal fat, which is known to play an important role in development of chronic inflammation; deposition of lipids into non-adipose tissues such as liver and muscles; atherosclerosis and chronic inflammation that increase risk in cardiovascular disorders and diabetes [2]. Adipose tissue is not just a site of energy storage but also behaves as a dynamic endocrine organ [3], it also plays an important role in energy expenditure, both as depot for energy-rich triglycerides as a source for metabolic hormones as well [4,5]. Adipocytes produce a large number of so-called adipokines, such as leptin, adiponectin, interleukin (IL)-1β, IL-6 and tumor necrosis factor-alpha (TNF-α). Some of these molecules affect energy metabolism and insulin sensitivity in other tissues such as muscle and liver [6]. During obesity, lipid storage in adipocytes is increased, which triggers the release of adipokines [7,8]. During inflammation, the mature adipocytes of the adipose tissue are responsible for increasing production of pro-inflammatory adipokines [9], including mentioned TNF-α, IL-1β, IL-6. That disregulation contributes to obesity and chronic inflammation