用小檗碱对脂肪肝进行治疗，结果显示：肝指数降低，肝组织学病变减轻，脂代谢、胰岛素抵抗明显改善，提示小檗碱可有效地用于脂肪肝的治疗。其机制可能为改善胰岛素抵抗，减轻“第一次打击”，从而减少了脂肪在肝细胞中的沉积。有文献表明，小檗碱可促进胰岛β细胞的修复，抑制糖异生和促进糖酵解，而产生降糖作用；降低交感神经活性，抑制肾上腺皮质的功能，使糖原异生减少，胰岛素代谢缓慢，且周围组织对胰岛素敏感性增加；增加胰岛素生物活性，减轻糖耐量损伤。由于小檗碱改善胰岛素抵抗作用，从而可调节脂代谢，降低血及肝组织中TG，抑制外源性TG的吸收，加速TG排泄，减少肝脏合成TG；抑制VLDL的合成，促进HLDL的合成。脂质代谢的改善又可减轻氧应激，加上小檗碱所具有的抗氧化作用，可以抑制脂质过氧化反应，使SOD明显升高，MDA则显著降低，可减轻最终的组织损伤，阻止脂肪肝的进一步发展。The results of treating fatty liver with berberine showed that: the liver index was decreased, liver histological lesions alleviated and the lipid metabolism and insulin resistance significantly improved, indicating that berberine could be used for the treatment of fatty liver in an effective way. Its mechanism may relieve the “first-strike” due to improvement of insulin resistance, thereby reducing the fat deposition in liver cells. Literatures demonstrated that berberine could promote the repair of islet β-cells, inhibit gluconeogenesis and promote glycolysis and therefore, the hypoglycemic effect can be produced. At the same time, it can reduce sympathetic activity, inhibit the function of the adrenal cortex, reduce gluconeogenesis, slow down the insulin metabolism, and increase the sensitivity of surrounding tissues to insulin, thus, increase the biological activity of insulin and reduce sugar tolerance injury. The effect of improving insulin resistance with berberine can regulate lipid metabolism, decrease TG in the blood and liver tissue, inhibit exogenous TG absorption, accelerate TG excretion, reduce liver TG synthesis, inhibit VLDL synthesis and promote HLDL synthesis. The improvement in lipid metabolism also reduces the oxidative stress, coupled with the anti-oxygenation that berberine possessed, the lipid peroxidation can be inhibited and SOD significantly increases, also, MDA can be significantly reduced. Thus, the final tissue damage can be reduced and further development of fatty liver can be prevented.