Impact of chronic dietary aflatoxin B1 intake on rumen fermentation, hepatic health, oxidative stress, inflammation, and glucose-lipid metabolism in fat-tailed ewes.

Chronic dietary exposure to aflatoxin B₁ (AFB₁) is a major threat to ruminant health, but its integrated effects on rumen fermentation, hepatic function, inflammatory-oxidative status, and glucose-lipid metabolism in fat-tailed sheep remain insufficiently characterized. This study evaluated the effects of high-level chronic AFB₁ exposure in twenty non-pregnant, non-lactating multiparous Ghezel ewes assigned to either a control diet or the same basal diet supplemented with AFB₁-contaminated rice culture providing 500 µg AFB₁/kg dry matter for 40 d. Individual dry matter intake was not measured; however, all animals consumed the full daily ration, ensuring uniform nutrient intake. AFB₁ reduced ruminal total volatile fatty acid concentration by approximately 16% (P = 0.011), with lower acetate (P = 0.014) and propionate (P = 0.017), and increased ruminal ammonia nitrogen (P = 0.018) and lipopolysaccharide (P = 0.009). Plasma activities of aspartate aminotransferase, γ-glutamyl transferase, and glutamate dehydrogenase increased approximately 2.2-, 2.9-, and 2.8-fold, respectively (all P < 0.001), while albumin and total protein decreased. AFB₁ increased TNF-α, IL-6, IL-1β, nitric oxide, and protein carbonyls, and decreased IL-10, IFN-γ, glutathione, superoxide dismutase, and catalase. During intravenous glucose tolerance testing, AFB₁-exposed ewes had lower basal glucose, higher peak glucose, greater incremental glucose area under the curve, prolonged glucose half-life, higher basal non-esterified fatty acids, and attenuated NEFA suppression. These findings indicate that chronic high-level AFB₁ exposure disrupts coordinated rumen-liver-immune-metabolic function and reduces glucose-lipid metabolic flexibility in fat-tailed ewes.