Zinc, copper, and metallothionein metabolism after jejunoileal bypass surgery ou small bowel resection in rats

Citation
Ja. Rodriguez et al., Zinc, copper, and metallothionein metabolism after jejunoileal bypass surgery ou small bowel resection in rats, AM SURG, 66(11), 2000, pp. 1004-1010
Citations number
37
Categorie Soggetti
Surgery
Journal title
AMERICAN SURGEON
ISSN journal
00031348 → ACNP
Volume
66
Issue
11
Year of publication
2000
Pages
1004 - 1010
Database
ISI
SICI code
0003-1348(200011)66:11<1004:ZCAMMA>2.0.ZU;2-A
Abstract
Liver dysfunction is a frequent complication of jejunoileal bypass (JIB) su rgery, a procedure commonly used until recently to treat morbid obesity. It has been suggested that liver failure in TIE patients is due to bacterial overgrowth and translocation from the bypassed intestine. Because invading microorganisms cause hepatic inflammation these experiments evaluated zinc, copper, and metallothionein (MT) in two experimental rat models of intesti nal surgery to determine whether their distribution in plasma and tissues w as similar to the highly characteristic pattern observed during an inflamma tory response. In the JIB rat model 90 per cent of the small intestine was isolated from the flow of digesta but remained viable in the abdominal cavi ty. In the small bowel resection (SBR) model 90 per cent of the small intes tine was removed and the remaining intestine was resected. Data collected 2 1 days after surgery showed decreased growth rate and plasma zinc in the SB R and TIE rats that was significantly improved by supplemental zinc. All ot her measures of zinc, copper, and MT metabolism in the SBR rats were simila r to those of controls. In JIB rats, however, liver copper, MT protein, and MT mRNA were significantly elevated, and a high proportion of the intracel lular zinc and copper was associated with MT. The pattern of zinc, copper, and MT distribution in systemic circulation and liver of JIB rats suggests hepatic inflammation superimposed on low zinc and copper status. Lack of a similar response in the SBR rats confirms the involvement of the bypassed i ntestinal segment and supports the hypothesis that bacterial overgrowth and translocation are responsible for liver inflammation and dysfunction in JI B patients.