Modulation of Adipogenesis by Oxylipins ? Differential Effects on Lipid Droplet Formation and Adipokine Production
Modulation of Adipogenesis by Oxylipins ? Differential Effects on Lipid Droplet Formation and Adipokine Production
Year: 2014
Authors: Aukema, H.M.
Publication Name: ISSFAL International Congress, Stockholm, Sweden June 28 – July 1
Publication Details: ID # Monday S2.06
Abstract:
It has been generalized that oxylipins derived from n6 fatty acids promote inflammation while those derived from n3 fatty acids suppress inflammation. However, these generalizations have been based on oxylipins derived from 20 and 22carbon fatty acids, while those derived from 18carbon fatty acids are generally present at higher levels. Thus, to investigate whether oxylipins, including those derived from 18carbon fatty acids, contribute to inflammation by modulating the production of inflammatory mediators from adipose tissue, we examined the effect of select oxylipins derived from linoleic acid (LA), alpha linolenic acid (ALA) and arachidonic acid (ARA) on lipid accumulation and adipokine production by 3T3L1 adipocytes. Individual oxylipins were added to the culture medium of preadipocytes after stimulating adipogenesis. After 8 days of differentiation, lipid accumulation was determined by oil Red O staining, while Western blotting was used to measure levels of proteins associated with lipid metabolism (perilipin, fatty acid synthase (FAS), adipose triglyceride lipase (ATGL)), adipokines (adiponectin, leptin) and adipocyte differentiation (PPARγ and C/EBPalpha ). Addition of 30 nM of all oxylipins tested was sufficient to significantly decrease lipid accumulation, and higher levels completely blocked lipid production. In parallel, perilipin levels were reduced, but not FAS and ATGL. These data suggest that formation of lipid droplets and not triglyceride synthesis
is the primary target. In contrast, adiponectin levels were lowered by some ARA and LA derived oxylipins, but not by oxylipins from ALA. Leptin was unchanged by any of the oxylipins. These effects were not due to suppression of adipogenesis, since the transcription factors PPARγ and C/EBPalpha were unaffected by oxylipin treatment. These results suggest inflammation could be modulated by 18carbon fatty acidderived oxylipins via their actions on adipose tissue function, specifically through regulatory pathways associated with both adiponectin production and lipid droplet formation.(Authors abstract)
