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In order to explore the effect of dietary supplementation of Clostridium butyricum on the volatile flavor substances in the meat of small-tailed Han sheep during postmortem aging and its possible mechanism, the Longissimus dorsi muscle of small-tailed Han sheep slaughtered at the age of six months was taken for postmortem maturation at 4 ℃, and then the volatile flavor substances, the contents of lipid metabolism-related enzymes including adenosine monophosphate activated protein kinase (AMPK), acetyl CoA carboxylase (ACC) and carnitine lipoyltransferase 1 (CPT1) were measured on days 0, 1, 2, 3, 4 and 5. The results of electronic nose test showed that the contents of alkanes, hydroperoxide and nitrogen oxides in the C. butyricum supplementation group were higher than in the control group without C. butyricum supplementation. According to the results of gas chromatography-mass spectrometry (GC-MS), the types of aldehydes, alcohols and ketones in the C. butyricum group were more than in the control group, while the contents of fatty oxidation products such as octanal, nonanal, decanal and heptaldehyde were obviously reduced. The key flavor substances common to both groups, as determined by relative odor activity value (ROAV), included octanal, nonanal, trans-2-decenal and 1-octen-3-ol, nonanal being the greatest contributor to the flavor of lamb meat. Compared with the control group, the contents of AMPK and CPT1 in the C. butyricum group decreased significantly during postmortem aging (P < 0.05), while the contents of ACC in the C. butyricum group were significantly higher than those in the control group at 0, 1, 3 and 5 days postmortem (P < 0.05). The correlation analysis showed that AMPK and CPT1 were significantly positively correlated with nonanal (P < 0.001), while ACC was significantly negatively correlated with nonanal and decanal (P < 0.001). In conclusion, the addition of C. butyricum to the diet can affect the volatile flavor substances in the meat of small-tailed Han sheep during postmortem aging by regulating the AMPK-ACC-CPT1 signaling pathway.

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