[Effect of chitooligosaccharide on hepatic triglyceride metabolism and related mechanisms].

OBJECTIVE: To investigate the effect of chitooligosaccharide (COS) on hepatic triglyceride (TG) metabolism and related mechanisms.

METHODS: The LO2 cells treated by 1 mmol/L fatty acid were used as model group, the cells treated by 1 mmol/L fatty acid and 0.5 mg/ml COS were used as COS group, and the untreated cells were used as control group. The TG content in cells was measured. RT-PCR and Western blot were used to measure the mRNA and protein expression of sterol regulatory element binding protein-1c (SREBP-1c), fatty acid synthase (FAS), and carnitine palmityl transferase 1A (CPT1A) in each group. Male C57BL/6J mice were randomized into control group, high-fat group, and COS group to receive different treatments. Sixteen weeks later, the liver was harvested for HE and oil red O staining to measure the content of TG in the liver. The t-test or one-way analysis of variance was used for comparison of data between groups, and the SNK method was used for comparison of data between any two groups.

RESULTS: The LO2 cells in the model group had an increased number of lipid droplets and an increased TG content, and after COS treatment, the TG content was low. The COS group had significantly lower relative mRNA expression of SREBP-1c and FAS compared with the model group (1.135 ± 0.177 vs 2.322 ± 0.198,F= 60.457,P< 0.01; 1.226 ± 0.150 vs 1.801 ± 0.159,F= 24.753,P< 0.01), while compared with the control group, the COS group had significantly higher mRNA expression of CPT1A (1.254 ± 0.156 vs 1.908 ± 0.087,F= 31.734,P< 0.01). The COS group had significantly lower protein expression of SREBP-1c and FAS than the model group (0.161 ± 0.081 vs 0.351±0.016,F= 188.920,P< 0.01; 0.332 ± 0.023 vs 1.238 ± 0.051,F= 624.069,P< 0.01), and significantly higher protein expression of CPT1A than the model group (1.014 ± 0.033 vs 0.561 ± 0.046,F= 193.793,P< 0.01). COS reduced the TG content in the liver in rats on high-fat diet.

CONCLUSION: COS can reduce the accumulation of TG in the hepatocyte model of nonalcoholic fatty liver disease and in the liver in rats on high-fat diet, and the possible mechanism may be related to inhibiting the expression of SREBP-1c and downstream FAS, reducing the synthesis of TG, increasing the expression of CPT1A, and accelerating the breakdown of TG.