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Two days after adding insulin (green), the hormone is present in fat-free cells but absent from cells that contain fat (white); red represents CARS signals from membrane lipids.
Subtle differences in the way identical cells process insulin lead to large differences in the amount of fat those cells store, according to researchers at Purdue University (PLoS ONE, DOI: 10.1371/journal.pone.0005189). These findings could help elucidate how nongenetic factors contribute to fat storage in individual cells. Ji-Xin Cheng and Thuc T. Le profiled lipid accumulation in individual mouse fibroblast cells, which can differentiate into fat cells, by using coherent anti-Stokes Raman scattering (CARS) microscopy. Cheng and Le also analyzed expression of fat-associated genes, insulin signaling, and the import of glucose into the cells from the culture medium. All the cells in the cultures expressed genes associated with fat cells, but not all of the cells accumulated lipids. Although the cells were genetically identical, some stored practically no fat while others stored large amounts. By tracking fluorescently labeled insulin, Cheng and Le found a correlation between insulin degradation and fat accumulation, with lipid-rich cells degrading insulin much faster than lipid-poor ones.