Premium
Interleukin‐1β inhibits glucokinase activity in clonal HIT‐T15 β‐cells
Author(s) -
Beggs Mark,
Beresford Guy,
Clarke Jennifer,
Mertz Robert,
Espinal Joseph,
Hammonds Peter
Publication year - 1990
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(90)80928-c
Subject(s) - glucokinase , hexokinase , glycolysis , carbohydrate metabolism , medicine , insulin , endocrinology , chemistry , glucose 6 phosphatase , enzyme , biology , biochemistry
Interleukin‐1β (IL‐1β) has been implicated in the pathogenesis of insulin‐dependent diabetes mellitus. In the present study we have investigated the effects of IL‐1β on glucose metabolism in clonal HIT‐T15 β cells. In the short‐term (1 h), 25IL‐1β significantly increased the rates of insulin release and glucose utilisation, but not glucose oxidation. In contrast, after 48 h, IL‐1β inhibited insulin release and glucose utilisation and oxidation. By assaying enzymes (hexokinase, glucokinase, pyruvate dehydrogenase, glucose 6‐phosphatase) and nucleotides (ATP, ADP) associated with the regulation of glycolysis and glucose oxidation, we conclude that the inhibitory effects of IL‐1β may be due to impaired glucokinase activity.