Aflatoxin is a toxin produced by Aspergillus species of fungi. The main route of aflatoxin exposure is through the diet. Indeed, long-term aflatoxin exposure is linked to the development of hepatocellular carcinoma (HCC). Aflatoxin causes aflatoxicosis, which can be affected by several factors and is prevalent in many developing Asian and African countries. This mini-review discusses the effects of carbohydrate, fat and protein on aflatoxicosis based on findings from animal and human studies. It was found that high carbohydrate intake enhanced aflatoxicosis occurrence, while low ingestion of carbohydrate with caloric restriction slowed the symptoms associated with aflatoxicosis. Additionally, diets with low protein content worsened the symptoms related to HCC due to aflatoxin exposure. Nevertheless, a study reported that a high-protein diet favored detoxification of aflatoxin in vivo. There were also conflicting results on the influence of dietary fat, as high ingestion of fat enhanced aflatoxicosis development as compared with a low-fat diet. Moreover, the type of fat also plays a significant role in influencing aflatoxin toxicity. In regard to food safety, understanding the influence of macronutrients toward the progression of aflatoxicosis can improve preventive measures against human and animal exposure to aflatoxin. © 2017 Society of Chemical Industry.

Probiotic Lactobacillus casei Shirota (LcS) is a potential decontaminating agent of aflatoxin B1 (AFB1). However, few studies have investigated the influence of diet, especially a high protein (HP) diet, on the binding of AFB1 by probiotics. This research was conducted to determine the effect of HP diet on the ability of LcS to bind AFB1 and reduce aflatoxin M1 (AFM1) in AFB1-induced rats. Sprague Dawley rats were randomly divided into three groups: A (HP only), B (HP + 108 CFU LcS + 25 μg AFB1/kg BW), and C (HP + 25 μg AFB1/kg BW). Levels of AST and ALP were higher in all groups but other liver function's biomarkers were in the normal range, and the liver's histology showed no structural changes. The urea level of rats in group B (10.02 ± 0.73 mmol/l) was significantly lower (p < 0.05) than that of rats in group A (10.82 ± 0.26 mmol/l). The presence of carcinoma in the small intestine and colon was more obvious in group C than in group B. Moreover, rats in group B had significantly (p < 0.05) lower AFM1 concentration (0.39 ± 0.01 ng/ml) than rats in group C (5.22 ± 0.28 ng/ml). Through these findings, LcS supplementation with HP diet alleviated the adverse effects of AFB1 by preventing AFB1 absorption in the small intestine and reducing urinary AFM1.