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The cytoplasmic Ca 2+ response to glucose as an indicator of impairment of the pancreatic β‐cell function
Author(s) -
HELLMAN B.,
BERNE C.,
GRAPENGIESSER E.,
GRILL V.,
GYLFE E.,
LUND P.E.
Publication year - 1990
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1990.tb01771.x
Subject(s) - tolbutamide , medicine , endocrinology , insulin , diabetes mellitus , alloxan , beta cell , streptozotocin , cytoplasm , beta (programming language) , depolarization , chemistry , islet , biochemistry , computer science , programming language
. The effects of glucose on the cytoplasmic Ca 2+ concentration (Ca 2+ i ) regulating insulin release were investigated using pancreatic β‐cells representative for the normal and diabetic situations. Increase of the glucose concentration resulted in a slight lowering of Ca 2+ i followed by a rise, often manifested as high amplitude oscillations. The Ca 2+ i ‐lowering component in the glucose action associated with suppression of insulin release became particularly prominent when the β‐cells were already depolarized by tolbutamide. Glucose‐induced inhibition of insulin release was observed also in experiments with rats made diabetic with streptozotocin or alloxan. Other studies indicated lowering of plasma insulin after intravenous glucose administration in patients with insulin‐ and noninsu‐lin‐dependent diabetes mellitus. Brief exposure of β‐cells to 2–2 mmol 1 ‐1 streptozotocin resulted in impairment of the response to glucose, manifested as disappearance of the cyclic variation of Ca 2+ i . The results indicate that glucose‐induced depolarisation is a vulnerable process, the disturbance of which may contribute to insulin secretory defects in diabetes mellitus.