Endocrine Abstracts

Obesity, characterized by excess intra-abdominal adipose tissue, is closely associated with a cluster of metabolic disorders such as type 2 diabetes mellitus (T2DM). Our previous study revealed significant associations between interleukin 4 (IL4) genotypes and T2DM, as well as IL4 genotypes and high density lipoprotein-cholesterol levels. Our most recent study results reveal that IL4 has anti-hyperglycemic function by improving insulin sensitivity and glucose tolerance. In addition, IL4 is also involved in lipid metabolism by regulating serum levels of adipokines and free fatty acids. Taking the above results together, it strongly suggests that IL4 involves in the regulation of lipid and glucose metabolism. The aim of the present study is to identify differentially expressed proteins in 3T3-L1 adipocytes under IL4 treatment for further elucidating roles of IL4 in adipocyte metabolism. Differentially expressed proteins in mature 3T3-L1 adipocytes under IL4 treatment were identified by proteomic strategy. Levels of ATP synthase δ chain, cytochrome c reductase, pyrophsphatase and vimentin are increased, whereas levels of alpha-enolase, gelsolin, vinculin and valosin are down-regulated in the presence of IL4 stimulus. IL4 tends to potentiate the elevation of intracellular ATP levels and promote metabolism in adipocytes by up-regulating expression levels of proteins accelerating ATP synthesis. Our results suggest that metabolism of adipocytes is deviated to catabolism with an unfavorable condition for lipid storage by IL4. The lipids in adipocytes might either be released into periphery or metabolized intracellularlly, which in turn influence the systemic energy metabolism of other insulin-targeted organs.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.