Objective       To determine the effect of AMP activated protein kinase (AMPK)/acetyl CoA carboxylase (ACC) signal pathway on the deposition of intramyocellular lipids (IMCLs) and investigate its underlying mechanisms.       Methods       Fifty-four BALB/c mice were inflicted with 30% total body surface area full-thickness burns

and then randomly divided into 4 groups

that is

control

acadesine treatment (AICAR

AMPK activator)

burn control

and burn-AICAR treatment groups. First

mitochondria were isolated to test the activity of carnitine palmitoyl transferase-1 (CPT1) in gastrocnemius by isotope labeling. Second

Western blotting was used to detect the expression of ACC

AMPK-α and theirs phosphorylation in the gastrocnemius. Then IMCLs were evaluated by oil red O dye and triglyceride (TG) contents measurement.       Results       Burn injury resulted in a markedly increase in ACC content (P0.05)

and significant decrease in CPTI activity and expression of AMPK-α

p-AMPK-α and p-ACC in the gastrocnemius (P0.05). After AICAR treatment

the expression of p-AMPK-alpha (1.16±0.08 vs 2.38±0.22

P0.05) and p-ACC (1.74±0.10 vs 3.72±0.18

P0.05) were significantly increased in the gastrocnemius than in sham burn group

the activity of CPT1 was significantly increased [2.95±0.39 vs 6.35±0.68 nmol/(min·mg)

P0.05]

and the content of TG was markedly decreased (3.88±0.40 vs 2.89±0.54 mmol/g

P0.05). In contrast

the 2 burned groups did not show any marked difference with AICAR treatment (P0.05). Besides

burn injury induced more lipid deposition in the gastrocnemius. This deposition of IMCLs was not be attenuated by AICAR (P0.05).       Conclusion       AMPK phosphorylation disorder is one of important molecular mechanism for burn-induced IMCLs deposition.