Effects of insulin-like growth factor-1 on endotoxin translocation in burned rats receiving total parenteral nutrition.
The purpose of this study was to investigate the effect of insulin-like growth factor-1 (IGF-1) on the translocation of endotoxin from the gut of burned rats. Twenty-eight male Sprague-Dawley rats (7-wk-old) were subjected to 20% full-thickness scald burns and were divided into two groups. One group received 4 mg.kg-1.d-1 of IGF-1 (IGF-1 group, n = 14), and the other received saline (control group, n = 13). All rats were fed exclusively by total parenteral nutrition (TPN). On the second postburn day, rats were killed. The amount of endotoxin in the liver and spleen were measured. RNA from the terminal ileum was extracted, and Northern blot analyses of alpha-tubulin, beta-actin, cell division cycle-2 (cdc2), and immunoglobulin-A (IgA) were performed. Nitrogen balance was improved (p < 0.001), and the wet weight of intestine and its mucosa were increased significantly in the burned rats that received IGF-1. Gene expression of alpha-tubulin and beta-actin were not changed. Cdc2 was elevated (P < 0.05), but IgA was decreased (P < 0.05) in the IGF-1 group. Levels of endotoxin in the liver and spleen were significantly reduced (P<0.05) by the administration of IGF-1. A negative correlation between the levels of endotoxin in the liver and the weight of the intestinal mucosa was observed. In conclusion, IGF-1 improved nitrogen balance, promoted the proliferation of intestinal mucosa and reduced the translocation of endotoxin.
Sugiura
T
T
First Department of Surgery, Chiba University School of Medicine, Japan.
Tashiro
T
T
Yamamori
H
H
Morishima
Y
Y
Otsubo
Y
Y
Hayashi
N
N
Furukawa
K
K
Nitta
H
H
Nakajima
N
N
Ishizuka
T
T
Tatibana
M
M
Ino
H
H
Ito
I
I
D000199:Actins / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D000704:Analysis of Variance; D000818:Animals; D001284:Atrophy; D001483:Base Sequence; D015152:Blotting, Northern; D002056:Burns / Q000378:metabolism* / Q000628:therapy*; D016203:CDC2 Protein Kinase / Q000032:analysis / Q000378:metabolism; D018076:DNA, Complementary / Q000032:analysis / Q000737:chemistry / Q000235:genetics; D004731:Endotoxins / Q000032:analysis / Q000378:metabolism*; D005786:Gene Expression Regulation; D007082:Ileum / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism; D007070:Immunoglobulin A / Q000032:analysis / Q000378:metabolism; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology*; D007413:Intestinal Mucosa / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism; D008099:Liver / Q000737:chemistry / Q000378:metabolism / Q000382:microbiology; D008297:Male; D009584:Nitrogen / Q000032:analysis / Q000378:metabolism; D010289:Parenteral Nutrition, Total; D012333:RNA, Messenger / Q000032:analysis / Q000737:chemistry / Q000235:genetics; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013154:Spleen / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism; D014404:Tubulin / Q000032:analysis / Q000235:genetics / Q000378:metabolism
D000199:Actins; D018076:DNA, Complementary; D004731:Endotoxins; D007070:Immunoglobulin A; D012333:RNA, Messenger; D014404:Tubulin; D007334:Insulin-Like Growth Factor I; D016203:CDC2 Protein Kinase; D009584:Nitrogen