Lipid droplet structural remodeling in adipose tissue upon caloric excess

Abstract

Excess calories are stored as triacylglycerols (TAG) and cholesteryl esters (CE) in lipid droplets (LD), and during obesity, LD expansion occurs. X-ray scattering of adipose tissue uncovered that LDs comprise two TAG packing domains: a disordered core and a multilamellar shell. The number of TAG layers increases upon diet-induced obesity and is adipose depot-specific. Further, collagen was highly oriented in brown but randomly dispersed in white fat. We discovered that the bodys surfactant, bile acids (BAs) stimulate remodeling of LD size. Deleting the BA receptor, Farnesoid X receptor (FXR) reduced a hydrophilic BA, {beta} muricholic acid ({beta}-MCA), and enlarged the adipocytes. BA composition is a critical determinant of overall hydrophobicity index and solubilization ability. Accordingly, we found that the obesogenic diet reduced a hydrophobic BA, chenodeoxycholic acid (CDCA). Taken together, these findings implicate that BAs, tissue niches, and diet influence LD structural remodeling. SummaryLipid droplets (LDs) pack triacylglycerols (TAGs) with altered dimensions and exhibit distinct collagen orientation between the white and brown fat depots and are remodeled by bile acids (BAs) such that deletion of BA-receptor, Farnesoid X receptor (FXR) results in adipocyte hypertrophy.