Streptozotocin dose-response curve in tilapia, a glucose-responsive teleost fish

James R. Wright, Cherrie Abraham, Brendan C. Dickson, Hua Yang, Carol M. Morrison

Research output: Contribution to journalArticle

31 Scopus citations

Abstract

Streptozotocin (STZ) causes β cell necrosis and insulin-dependent diabetes in many species. The specificity of this β cell toxin relates to its structure as an alkylating agent with an attached glucose moiety. STZ uptake by rodent β cells appears to be via the GLUT-2 glucose transporter. Teleost fish, in general, are severely glucose intolerant. The effects of STZ were examined in tilapia, a teleost fish with highly glucose-responsive islets. Fasted tilapia were given 0, 100, 150, 200, 250, 300, or 350 mg/kg STZ iv. Plasma glucose levels were followed for 72 h and the fish autopsied. Histological sections of islets were stained by immunoperoxidase for tilapia insulin. Severe hyperglycemia was seen in 20, 80, and 100% of fish receiving 250, 300, and 350 mg/kg doses; however, sections of islets showed only partial degranulation with no evidence of β cell necrosis. Another group of fish receiving the highest dose were followed longer to determine whether β cell necrosis and permanent hyperglycemia ensued. All fish died or were killed within 9 days because of severe hepatic failure characterized by hepatic necrosis, jaundice, and ascites; islet morphology was relatively normal suggesting, even in a glucose-sensitive species, that fish islets either do not take up STZ or are highly resistant to its 'diabetogenic' effects. Tilapia may thus be a useful model to elucidate mechanisms of action of STZ. Furthermore, STZ may provide important insights into differences in glucose uptake and metabolism by mammalian and piscine β cells.

Original languageEnglish (US)
Pages (from-to)431-440
Number of pages10
JournalGeneral and Comparative Endocrinology
Volume114
Issue number3
DOIs
StatePublished - Jun 1999

ASJC Scopus subject areas

  • Animal Science and Zoology
  • Endocrinology

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