Aflatoxin B1 (AFB1) is a stable and highly toxic toxin that causes multi-organ toxicity with sustained ingestion, most typically in the duck liver. Previous research has shown that AFB1 can bring about endoplasmic reticulum stress (ERS) in animals, and ERS is strongly associated with lipid metabolism. However, the relationship between AFB1-induced duck liver toxicity and ERS and lipid metabolism is currently unclear. Great attention has been paid to the prevention and treatment of AFB1 because of its great harm. Curcumin, a natural polyphenol, is notable for its powerful anti-inflammatory and antioxidant properties. Studies have shown curcumin to be protective against afb1-induced avian multi-organ toxicity. However, the effects of curcumin on the liver of ducks exposed to AFB1 are largely unknown. In the present study, we aimed to investigate whether AFB1 exposure induces ERS and lipid metabolism disorders in duck liver, while exploring the positive role of curcumin in it. One-day-old ducks (n = 80) were randomly divided in four groups: control group, AFB1 group (0.1 mg / kg.bw AFB1), Cur group (400 mg/kg curcumin), and AFB1 + Cur group (0.1 mg/kg.bw AFB1 + 400 mg/kg curcumin), and blood and liver were collected for the study after 21 days of continuous administration. Our research has found that AFB1 exposure significantly increases the levels of liver function indicators ALP, AST, and ALT in ducks' serum (P <
0.05). Duck liver undergoes fatty degeneration under the influence of AFB1. Under the effect of curcumin, AFB1-induced structural damage in duck liver was somewhat controlled. Further experimental results showed that AFB1 treatment significantly increased the expression of glucose-regulated protein 78 (P <
0.001), and activated the endoplasmic reticulum stress pathway. Meanwhile, AFB1 inhibited the LKB1-AMPK signaling pathway and disrupted lipid metabolic homeostasis. And curcumin treatment effectively reversed these changes. Overall, our results suggest that curcumin attenuates AFB1-induced hepatotoxicity in ducks by inhibiting ERS and lipid metabolism disorders.