Calcium signalling in streptozotocin-induced type 1 diabetic rat heart

Research output: Contribution to journalReview articlepeer-review


Administration of streptozotocin (STZ) to rats causes selective necrosis of pancreatic insulin producing beta-cells. In addition to hypoinsulinaemia, other characteristics of STZ-induced diabetic rat include hyperglycaemia, glucosuria, polydipsia, polyphagia, loss of body weight, hypercholesterolaemia and hypertriglyceridaemia. A variety of contractile defects have been frequently reported in various cardiac muscle preparations from STZ-treated rat. In ventricular myocytes defects include alterations to the time course and amplitude of contraction. During the process of excitation-contraction (E-C), coupling depolarisation of the ventricular myocyte membrane by an action potential opens voltage-gated L-type Ca2+ channels permitting a small influx of Ca2+ which triggers a large release of Ca2+ from the sarcoplasmic reticulum (SR) and a transient rise of intracellular Ca2+ concentration ([Ca2+]i). Binding of Ca2+ to troponin C initiates the process of contraction. During relaxation of heart contraction cytosolic Ca2+ is transported back into the SR and effluxed from the cell primarily via the Na+/Ca2+ exchange. This review is concerned with the defects in Ca2+ signalling that underlie contractile dysfunction in STZ-induced diabetic rat heart.

Original languageEnglish
Pages (from-to)98-104
Number of pages7
JournalInternational Journal of Diabetes and Metabolism
Issue number3
Publication statusPublished - Dec 2002


  • Ca transport
  • Contractile dysfunction
  • Diabetes
  • Heart
  • Streptozotocin
  • Ventricular myocytes

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism


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