Title: Effects of leptin on the content of triglyceride and the expression of peroxisome proliferator activated receptor α and carnitine palmitoyltransferase-I in human hepatocytes with fatty degeneration
Abstract: AIM: To the inf luence of lept in on l ipid degeneration of hepatocytes and its mechanism. METHODS: The model of hepatocyte fatty degeneration was prepared using human L-02 liver cells. This experiment included the following groups: normal hepatocytes group, fatty degeneration model group, positive control group (treated with gemfibrozil), and leptin treatment groups I, II and III (using 10, 10 and 10 mol/L leptin, respectively). After 24-hour incubation, cell morphology and the formation of intracellular lipid droplets were observed by oil red O staining and the content of intracellular triglyceride (TG) was detected through high performance liquid chromatography (HPLC). Besides, the mRNA expression levels of peroxisome proliferator activated receptor α (PPARα) and its target gene carnitine palmitoyltransferase-I (CPT-I) were detected by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The intracellular lipid droplets were increased in the model group and leptin group I as compared with those in the other groups. The contents of intracellular TG were 1.063 ± 0.146, 0.648 ± 0.023 and 0.553 ± 0.045 mmol/g protein respectively when leptin was used at concentrations of 10, 10 and 10 mol/L. In comparison with that in the positive control group, the mRNA expression of PPARα was increased significantly in the leptin groups II or III (P < 0.01); but PPARα mRNA expression was not remarkably different between the leptin group I and the positive control group. There was no marked difference between the model group and the normal group in CPT-I mRNA expression, but it was significantly elevated after leptin treatments (P < 0.01). CONCLUSION: Leptin decreases the content of TG in human L-02 hepatocytes with fatty degeneration in a dose-dependent manner, and its mechanism may be related to the up-regulation of PPARα and its target genes.