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

Abstract

Background. Adipocytes contribute to inflammation and the innate immune response through expression of inflammatory mediators. High levels of these mediators have been related to chronic inflammation state and insulin resistance, cardiovascular diseases and diabetes type 2, among other disorders. 3-octadecylglycerol (batyl alcohol) has been described as an inflammatory agent, whereas Conjugated Linoleic Acid (CLA) is considered effective against obesity. In this study we examined the anti-inflammatory activity and mechanisms of modified alkoxyglycerols. Tumor necrosis factor (TNF-α) activated mature adipocytes were used as cellular model of inflammation. Secreted levels and gene expressions of some inflammatory mediators, such as the adipokines, interleukin (IL)-β1, IL-6 and IL-10; and the levels of leptin and adiponectin hormones were quantified in presence and absence of alkoxyglycerols and when human adipocyte cells were or not activated by TNF-α. The aim of this study is to describe the effects of nonesterified alkoxyglycerols, CLA and diesterified alkoxyglycerols with CLA (DEA-CLA) and check if they present beneficial properties using an in vitro model of some chronic diseases related to the inflammatory process, such as obesity, using human mature adipocytes activated with TNF-α. Results. 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-β10). 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. Conclusions. CLA and DEA-CLA modify adipocyte inflammatory mediators and also could play a role on energy homeostasis through depletion of leptin levels. © 2010 Ocaña et al; licensee BioMed Central Ltd.