ABSTRACT
Objective To examine the effect and mechanism of different targets of glucose control on liver damage in rats with sepsis .Methods The rat sepsis model was established by cecal ligation and puncture (CLP) .Forty Sprague‐Dawley rats were randomly divided into five groups (eight rats to each group):sham operation (sham group) ,sepsis (CLP group) ,glycemic control A group (glucose target 4 .6‐6 .1 mmol/L ) ,glycemic control B group (glucose target 6 .2‐8 .3 mmol/L ) and glycemic control C group (glucose target 8 .4‐10 .0 mmol/L) .The animals were sacrificed 12 hours after CLP .Venous blood was sampled for testing alanine transaminase (ALT ) , aspartate transaminase (AST ) and free fatty acid (FFA ) . Peroxisome proliferator activated receptor‐α (PPAR‐α) and liver carnitine palmitoyltransferase 1 (CPT‐1 ) protein were determined by immunohistochemistry .The pathological changes of liver tissue was observed under an optical microscope .Results The levels of ALT ,AST and FFA in venous blood and the pathological tissue injury score in sepsis groups were higher than those in sham group and all glycemic control groups (P0 .05) .The levels of PPARαand liver CPT‐1 were significantly higher in group A than in group B or group C (P<0 .05) ,and lower in group C than in group B(P<0 .05) .Conclusions The lowest target of glucose control(4 .6‐6 .1 mmol/L)shows better protective effects on liver damage in rats with sepsis ,the mechanism of which may be related to upregulation of PPARα and liver CPT‐1 expression .