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Rice is one of the most significant food crops for human sustenance. Every year, many countries around the world hoard enormous amounts of rice to avert emergencies and guarantee food security and sufficiency. As a result, the inventory of aged rice is growing as the number of inventory years rises. Aged rice stored over three years loses its nutritional value and is no longer suitable for human consumption. There is a pressing need to find a solution to effectively utilize aged brown rice produced from aged rice after dehulling. Developing and utilizing aged brown rice as feed is economical and efficient due to its massive resources and rich nutritional content, which will also lessen food waste while resolving the problem of excessive hoarding of aged rice. This review mainly summarizes the nutritional value, application in feed, and nutritional limiting factors of aged brown rice. It provides a theoretical basis for solving the overstock of aged brown rice and the feasibility of using aged brown rice as feed in a cost-effective way. [ABSTRACT FROM AUTHOR]

Simple Summary: Aflatoxin B1 (AFB1) is widely present in animal feed as a mycotoxin, and it poses a serious threat to human and animal health. Curcumin (CUR) as a feed additive has been well documented for its antimicrobial, anti-inflammatory, antioxidant, and antiviral activities. The present experiment was designed to investigate the mitigating effect of CUR on the growth performance, liver, and intestinal health of broilers fed AFB1-contaminated diets. The results showed that CUR alleviated liver and intestinal damage in broilers caused by feeding AFB1-contaminated diets, and this damage was associated with the Nrf2 pathway. Notably, CUR also mitigated the changes in intestinal permeability caused by AFB1, which may be closely related to liver health (via the gut–liver axis). These results provide new ideas for future research on the therapeutic mechanism of CUR in alleviating AFB1 poisoning in broilers. This experiment aimed to investigate the mitigating effect of CUR on the growth performance and liver and intestinal health of broilers fed AFB1-contaminated diets. In this study, 320 one-day-old healthy male Arbor Acres (AA) broilers were randomly divided into four groups, including the Control group (fed the basal diet), the AFB1 group (fed the AFB1-contaminated diet containing 1 mg/kg AFB1), the AFB1+CUR group (fed the AFB1-contaminated diet with 500 mg/kg CUR), and the CUR group (fed the basal diet containing 500 mg/kg CUR), with eight replicates of ten animals per group and a 28 d experimental period. In terms of the growth performance, the addition of 500 mg/kg CUR significantly improved AFB1-induced significant reductions in the final body weight on day 28 and mean daily gain (p < 0.05) and increased the ratio of the mean daily feed intake to mean daily weight gain in broilers (p < 0.05). In terms of liver health, significant improvements in liver histological lesions occurred in broilers in the AFB1+CUR group compared to the AFB1 group, with significantly higher glutathione peroxidase (GSH-Px), catalase (CAT), and total superoxide dismutase (T-SOD) activities (p < 0.05) and significantly higher levels of nuclear factor erythroid 2-related factor 2 (Nrf2), Kelch-like ECH-associated protein 1 (Keap-1), heme oxygenase 1 (HO-1), and NAD(P)H quinone oxidoreductase 1 (NQO-1) gene expression (p < 0.05). In terms of intestinal health, CUR addition significantly increased the relative length of ileum (p < 0.05), significantly elevated the height of ileal villi (p < 0.05), significantly reduced D-Lactate (D-LA) and diamine oxidase (DAO) activities in broiler serum (p < 0.05), significantly increased GSH, CAT, and T-SOD activities in ileal tissues (p < 0.05), and significantly elevated the expression of Nrf2, HO-1, and NQO-1 genes (p < 0.05) compared to the AFB1 group. In conclusion, CUR showed a protective effect against damage to the liver and intestine caused by AFB1 in broilers through the Nrf2 signaling pathway, thereby improving the growth performance of broilers exposed to AFB1. [ABSTRACT FROM AUTHOR]