Webbläsaren som du använder stöds inte av denna webbplats. Alla versioner av Internet Explorer stöds inte längre, av oss eller Microsoft (läs mer här: * https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Var god och använd en modern webbläsare för att ta del av denna webbplats, som t.ex. nyaste versioner av Edge, Chrome, Firefox eller Safari osv.

Obstructive jaundice results in increased liver expression of uncoupling protein 2 and intact skeletal muscle glucose metabolism in the rat

Författare

  • B Isaksson
  • Catarina Rippe
  • R Simonoska
  • JE Holm
  • H Glaumann
  • R Segersvard
  • J Larsson
  • Charlotte Erlanson-Albertsson
  • J Permert

Summary, in English

Background: A majority of patients with pancreatic cancer have obstructive jaundice and diabetes with skeletal muscle insulin resistance. Surgery for these patients is associated with significant morbidity. Uncoupling protein 2 (UCP2) has been proposed to regulate energy expenditure and promote liver vulnerability. The effects of obstructive jaundice on muscle glucose metabolism and expression of UCP2 in liver and muscle are unknown. Methods: Rats were operated with bile duct ligation (BDL). After 7 days, UCP2 mRNA levels were determined in liver and muscle. Simultaneously, insulin-stimulated glucose transport and glycogen synthesis in skeletal muscle were analyzed in vitro. Results: The jaundiced rats lost more weight than pair-fed controls. UCP2 mRNA levels were increased 5-fold in liver but not in muscle in jaundiced rats compared to pair-fed controls. The jaundiced rats were hypoglycemic and hypoinsulinemic but demonstrated intact or enhanced insulin action on skeletal muscle glucose transport and glycogen synthesis in vitro. Muscle glycogen content was increased in the jaundiced rats. Conclusions: Experimental obstructive jaundice in the rat is associated with increased liver expression of UCP2. rapid weight loss, and intact insulin action on skeletal Muscle glucose metabolism. Obstructive jaundice. by upregulated liver UCP2. may contribute to the cachexia and high surgical morbidity observed in these patients, but not to skeletal muscle insulin resistance in pancreatic cancer patients.

Avdelning/ar

Publiceringsår

2002

Språk

Engelska

Sidor

104-111

Publikation/Tidskrift/Serie

Scandinavian Journal of Gastroenterology

Volym

37

Issue

1

Dokumenttyp

Artikel i tidskrift

Förlag

Taylor & Francis

Ämne

  • Gastroenterology and Hepatology

Nyckelord

  • obstructive jaundice
  • glycogen
  • glucose metabolism
  • glucose transport
  • uncoupling protein

Status

Published

ISBN/ISSN/Övrigt

  • ISSN: 1502-7708