[Effect of intestinal ischemia/reperfusion injury on leptin and orexin-A levels].
OBJECTIVE
To explore the effect of intestinal ischemia/reperfusion (I/R) injury on leptin and orexin-A levels in peripheral blood and central secretory tissues, and investigate the roles of leptin and orexin-A in acute inflammatory responses.


METHODS
An intestinal I/R injury rat model was established, and the rats were grouped according to duration of the reperfusion time following a 60-min ischemia. Radioimmunoassay was used to examine the protein levels of leptin in the serum and adipose tissue, and the protein levels of orexin-A in the plasma and hypothalamus. Reverse transcriptase-polymerase chain reaction was also performed to detect the mRNA expressions of adipose leptin and hypothalamus orexin-A.


RESULTS
Compared with that before injury, serum leptin level of 60-min ischemia with 30-min reperfusion (I60'R30') group decreased significantly and that of I60'R360' increased significantly. Compared with the sham-operation group (sham) after injury, serum leptin level of I60'R360' group increased significantly, and adipose leptin protein levels of I60'R30' and I60'R90' groups decreased significantly, whereas that of I60'R360' group increased obviously. Compared with sham group after injury, adipose leptin mRNA expressions of I60'R30', I60'R240' and I60'R360' groups all increased significantly, while that of I60'R150' showed significant decrease. No significant changes were noted in the protein levels of orexin-A either in the plasma or hypothalamus after I/R injury. In comparison with sham group after injury, hypothalamus orexin-A mRNA expressions of I60'R30' and I60'R90' groups showed gradual but significant decrease, and till 150 min of reperfusion, the expression reached its lowest, followed then by slow recovery at 240 and 360 min, though still remaining significantly lower than that of sham group.


CONCLUSIONS
Leptin and orexin-A have a time-dependent response to intestinal I/R injury, but the former appears to exhibit a faster response, and they may play a certain role in the metabolic disorders of acute inflammation.
Lin
Ji
J
Research Laboratory of Biochemistry, General Hospital of PLA, Beijing 100853, China. panny@263.net
Yan
Guang-tao
GT
Gao
Xiao-ning
XN
Liao
Jie
J
Hao
Xiu-hua
XH
Zhang
Kai
K
D000818:Animals; D005260:Female; D007249:Inflammation / Q000097:blood / Q000235:genetics / Q000503:physiopathology; D007421:Intestine, Small / Q000098:blood supply* / Q000378:metabolism; D047908:Intracellular Signaling Peptides and Proteins / Q000097:blood* / Q000235:genetics; D020738:Leptin / Q000097:blood* / Q000235:genetics; D008297:Male; D009479:Neuropeptides / Q000097:blood* / Q000235:genetics; D000068797:Orexins; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D011817:Rabbits; D011863:Radioimmunoassay; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000097:blood / Q000235:genetics / Q000503:physiopathology*; D020133:Reverse Transcriptase Polymerase Chain Reaction
D047908:Intracellular Signaling Peptides and Proteins; D020738:Leptin; D009479:Neuropeptides; D000068797:Orexins; D012333:RNA, Messenger