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LDs were stained by incubating cells with BODIPY 493/503 (Invitrogen) for 30?min and were fixed and processed for immunofluorescence as described above. Images from cells were acquired with a Laser Scanning Confocal microscope (A1R VAAS with �� 60/numerical aperture 1.49 oil-immersion lens, Nikon, Melville, NY) along with NIS-Elements find more AR software (Nikon). In all experiments, approximately 30 cells per sample were counted, and triplicate samples were counted per experimental condition. Quantification for autophagy was performed in deconvoluted and threshold-limited images using the ��Analyze Particle�� function in ImageJ software (NIH). For quantification of colocalizations, the ImageJ JACoP plug-in (Bolte and Cordeli��res, 2006) was used to calculate the percentage of colocalization from Manders's overlapping coefficients (fraction of red overlapping green) (Manders et?al., 1992). The data are presented as mean?�� SEM. Differences between the means of the individual groups were assessed by one-way ANOVA with Dunnett's multiple comparison test; differences were considered significant at p value?FDA-approved Drug Library Florida, for help with the Affymetrix microarray and confocal imaging analysis, respectively. This work was supported in part by NIH grant HL48044 to T.F.O. and NSF grant DBI-0846218 to X.X. J.B. and H.K.C. were supported by NIH/NLM bioinformatics training grant T1507443. ""The metabolic defects of obesity and type 2 diabetes, characterized by insulin resistance, nonalcoholic fatty liver disease, and dyslipidemia, lead to an increased risk of cardiovascular disease (Semenkovich, 2006). Sterol regulatory element binding protein (SREBP) is a key lipogenic transcription factor that is nutritionally Enol regulated by glucose and insulin (Horton et?al., 2002?and?Goldstein and Brown, 2008). SREBP-1c preferentially regulates the lipogenic process by activating genes involved in fatty acid and triglyceride synthesis, whereas SREBP-2 primarily controls cholesterol homeostasis by activating genes required for cholesterol synthesis and uptake. Both SREBP-1c and -2 isoforms are synthesized as precursor proteins that are inserted into the endoplasmic reticulum (ER) membrane. The precursor of SREBP migrates from the ER to the Golgi and undergoes sequential proteolytic processing to release the transcriptionally active N-terminal basic-helix-loop-helix (bHLH)-Zip domain.