Effect of Endotoxin on Insulin-like Growth Factor-1 Expression in Small Intestine and Intrauterine Growth of Rabbit Fetus.
- Author:
Seon Yong KO
1
;
Jeong Jae LEE
;
Hae Hyeog LEE
;
Kwon Hae LEE
Author Information
1. Department of Obstetrics and Gynecology, College of Medicine, Soonchunhyang University, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Endotoxin;
Insulin like growth factor-1;
Intrauterine growth retardation
- MeSH:
Bacterial Infections;
Fetal Growth Retardation;
Fetal Weight;
Fetus*;
Insulin-Like Growth Factor I;
Intestine, Small*;
Placenta;
Polymerase Chain Reaction;
Rabbits;
Reverse Transcription;
RNA, Messenger;
Uterus
- From:Korean Journal of Obstetrics and Gynecology
2002;45(4):610-616
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVE: New Zealand White Rabbits were utilized to determine whether fetal insulin-like growth factor-1 (IGF-1) expression in small intestine is altered in response to maternal enodotoxin administration. STUDY DESIGN: Six pregnant rabbits were intramuscularly injected with lipopolysaccharide of E. coli (serotype 055:B5) 30 microgram/kg, whereas normal saline 0.3 mL/kg were injected to the other six pregnant rabbits on gestational day 25 and 26. Fetuses were harvested on gestational day 27 and were identified as favored (Fav) or runt (Runt) depending on the location in the uterus. Fetal weight and small intestinal length were recorded. Three parts of small intestine (proximal, middle and distal) were collected. Reverse transcription polymerase chain reaction (RT-PCR) was used to measure IGF-1/beta-actin mRNA densitometric band ratios. Statistical analysis was performed using paired Student's t-test and Pearson correlation test. RESULTS: The ratio of mRNA IGF-1/beta-actin was lower in endotoxin group (0.80+/-0.24, n=24) than control group (1.13+/-0.31, n=24, P<0.05). Fetal weights were decreased with endotoxin group (24.7+/-8.59 gm) compared to control group (28.5+/-4.35 gm, p<0.05). Fav fetuses (1.09+/-0.42, n=12) showed increased expression of IGF-1 mRNA in the small intestine than Runt fetuses (0.84+/-0.35, n=12) in control group. In endotoxin group, there was no statistically significant difference in expression of IGF-1 mRNA between Fav (0.82+/-0.31, n=12) and Runt (0.79+/-0.43, n=12) group. Lengths of small intestine showed no statistically significant difference between control and endotoxin group, and Fav and Runt (p>0.05). CONCLUSION: In our study, maternal endotoxin administration suppressed IGF-1 production in small intestine of fetal rabbit. Endotoxin in maternal serum might be transferred to fetus through placenta and decreased production of mRNA of IGF-1 in small intestine. Further studies are warranted to investigate the correlation between intrauterine growth retardation and maternal gram negative bacterial infection.
