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THE CONTRIBUTION OF INOSITOL EXCHANGE TO AGONIST‐STIMULATED BREAKDOWN OF MYO ‐ [2‐ 3 H] INOSITOL‐LABELLED PHOSPHATIDYLINOSITOL IN MOUSE EXOCRINE PANCREAS
Author(s) -
Tennes KA,
Roberts ML
Publication year - 1984
Publication title -
australian journal of experimental biology and medical science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0004-945X
DOI - 10.1038/icb.1984.30
Subject(s) - inositol , phosphatidylinositol , chemistry , agonist , exocrine pancreas , endocrinology , biochemistry , medicine , receptor , pancreas , signal transduction , biology
Summary Agonists stimulate the release of myo ‐inositol from phosphatidylinositol (PtdIns) labelled in vivo with myo ‐[2‐ 3 H] inositol. In the presence of lithium, which inhibits myo ‐inositol‐1‐phosphatase, the compound which accumulates following the breakdown of pre‐labelled PtdIns is inositol‐1‐phosphate. This indicates that the agonist‐stimulated release of the head group from this lipid is not the result of inositol exchange and is due to phosphodiesterase activity. The total amount of 3 H‐labelled compounds released from PtdIns in the presence and absence of lithium is the same, which indicates the labelled compounds which are released are not re‐incorporated. Agonist‐induced release of myo ‐[2‐ 3 H] inositol can be used as a reliable indication of PtdIns breakdown in the exocrine pancreas.