{'fraction_non_alphanumeric': 0.027632561613144136, 'fraction_numerical': 0.01194921583271098, 'mean_word_length': 5.7, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Rapamycin attenuates palmitate-induced lipid aggregation by up-regulating sirt-1 signaling in AML12 hepatocytes.

Rapamycin (Rap), a specific inhibitor of the mTOR signaling, has been shown to affect lipid metabolism in vitro and in vivo. Sirt-1, an NAD+ dependent deacetylase, regulates a variety of cellular processes, including aging, lifespan extension and glucose and lipid metabolism. Herein, we applied a cellular steatosis model to investigate whether rapamycin's role in lipid metabolism is sirt 1-associated. Cells were exposed to palmitate stimulation for 48 h with or without rapamycin treatment. Lipid droplets in AML12 cells were observed by oil red O staining, and the intracellular lipid content was measured. We found that rapamycin treatment, at a relatively low concentration, significantly attenuated lipid aggregation, whereas knockdown of sirt-1 by siRNA abrogated rapamycin's effect on ameliorating lipid accumulation. Moreover, rapamycin exposure increased the expression levels of sirt-1 and AMPK, and enhanced sirt-1 deacetylase activity in steatotic AML12 hepatocytes. This is the first report demonstrating that rapamycin ameliorates lipid accumulation through upregulating sirt-1 signaling supporting the hypothesis that rapamycin may positively influence sirt-1 signaling in maintaining metabolic homeostasis.