Abstract
Aquaglyceroporins—aquaporin membrane channels (AQP) that conduct glycerol and other small neutral solutes in addition to water—play major roles in obesity. In adipocytes, aquaglyceroporins mediate glycerol uptake and release across the plasma membrane, which are two key steps for triacylglycerols (TAGs) synthesis (lipogenesis) and hydrolysis (lipolysis). The aim of this study was to assess both glycerol permeability and metabolism in undifferentiated 3T3-L1 cells (UDCs) as well as in untreated (CTL-DCs) versus lipopolysaccharide (LPS-DCs)-treated differentiated 3T3-L1 adipocytes. Glycerol release, TAGs content and whole membrane glycerol permeability were significantly increased in DCs as compared to UDCs. Moreover, in DCs, LPS treatment significantly increased TAGs content and decreased glycerol permeability. In addition, a significant reduction in whole membrane glycerol permeability was observed in LPS-DCs as compared to CTL-DCs. The relative contributions of AQP3, AQP7 and AQP9 (facilitated diffusion), as well as that of the phospholipid bilayer (simple diffusion), to the whole membrane glycerol permeability, were estimated biophysically in UDCs, CTL-DCs and LPS-DCs, using selective AQP inhibitors. Further studies will be required to determine if modifications in either subcellular localization and/or activity of aquaglyceroporins could account for the data herein. Nevertheless, our findings provide novel insights in understanding the LPS-induced adipocyte hypertrophy that accompanies obesity.
Highlights
Obesity is characterized by increased adipose tissue mass resulting from both an increase in size of individual adipocytes and the generation of new adipocytes [1]
Adipocytes are made up of more than 95% triacylglycerols (TAGs) that are hydrolyzed to fatty acids and glycerol during lipolysis [2]
Glycerol Release and Triacylglycerols (TAGs) Content in Undifferentiated 3T3-L1 Cells (UDCs), 2U.1n. tGrelaytceedro3lTR3e-lLe1asCe ealnlsdDTrififaecryelngtliyacterdolisnt(oTAAGdisp)oCcyotnetsen(Ct TinL-UDnCdsif)fearnedntLiaipteodpo3lTys3a-cLc1hCareildlse-(tUreDatCeds)3, T3-L1 UCnetlrlseaDteidffe3rTe3n-tLia1teCdeilnlstoDAiffdeirpeonctyiatteesd(LinPtSo -ADdCipso)cytes (CTL-DCs) and Lipopolysaccharide-treated 3T3-L1 Cells Differentiated into Adipocytes (LPS-DCs)
Summary
Obesity is characterized by increased adipose tissue mass resulting from both an increase in size of individual adipocytes and the generation of new adipocytes [1]. Adipocytes are made up of more than 95% triacylglycerols (TAGs) that are hydrolyzed to fatty acids and glycerol during lipolysis [2]. Glycerol plays a major role in energy homeostasis, as it represents the carbon backbone of TAGs and is the major substrate for hepatic gluconeogenesis during fasting [3,4,5]. Circulating plasma glycerol results from its release from adipocyte TAGs during lipolysis and its reabsorption by kidney proximal tubules [5,6]. Adipocytes play a central role in whole-body energy homeostasis as they supply energy during starvation. Over-nutrition and lack of exercise result in over-accumulation of fat that can lead to obesity [7]
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