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Objective: To investigate the effects of berberine(BBR) and cinnamic acid(CA), the main active components in Jiaotai Pill(交泰丸, JTP), on palmitic acid(PA)-induced intracellular triglyceride(TG) accumulation in NIT-1 pancreatic β cells. Methods: Cells were incubated in culture medium containing PA(0.25 mmol/L) for 24 h. Then treatments with BBR(10 μmol/L), CA(100 μmol/L) and the combination of BBR and CA(BBR+CA) were performed respectively. Intracellular lipid accumulation was assessed by Oil Red O staining and TG content was measured by colorimetric assay. The expression of adenosine monophosphate-activated protein kinase(AMPK) protein and its downstream lipogenic and fatty acid oxidation genes, including fatty acid synthase(FAS), acetyl-co A carboxylase(ACC), phosphorylation acetyl-co A carboxylase(p ACC), carnitine acyl transferase 1(CPT-1) and sterol regulating element binding protein 1c(SREBP-1c) were determined by Western blot or real time polymerase chain reaction. Results: PA induced an obvious lipid accumulation and a significant increase in intracellular TG content in NIT-1 cells. PA also induced a remarkable decrease in AMPK protein expression and its downstream targets such as p ACC and CPT-1. Meanwhile, AMPK downstream lipogenic genes including SREBP-1c m RNA, FAS and ACC protein expressions were increased. Treatments with BBR and BBR+CA, superior to CA, significantly reversed the above genes changes in NIT-1 pancreatic β cells. However, the synergistic effect of BBR and CA on intracellular TG content was not observed in the present study. Conclusion: It can be concluded that in vitro, BBR and BBR+CA could inhibit PA-induced lipid accumulation by decreasing lipogenesis and increasing lipid oxidation in NIT-1 pancreatic β cells.