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Fatty acids stimulate cholecystokinin secretion via an acyl chain length‐specific, Ca 2+ ‐dependent mechanism in the enteroendocrine cell line STC‐1
Author(s) -
McLaughlin J. T.,
Lomax R. B.,
Hall L.,
Dockray G. J.,
Thompson D. G.,
Warhurst G.
Publication year - 1998
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1998.011by.x
Subject(s) - cholecystokinin , enteroendocrine cell , secretion , chemistry , mechanism (biology) , biochemistry , cell , biophysics , microbiology and biotechnology , stereochemistry , endocrine system , endocrinology , biology , hormone , receptor , philosophy , epistemology
1 The present study has investigated whether fatty acids directly influence peptide release from enteroendocrine cells using STC‐1, a mouse intestinal endocrine tumour cell line, previously shown to release cholecystokinin (CCK) in response to other physiological stimuli. 2 Fatty acids elicited a chain length‐ and dose‐dependent stimulation of CCK secretion. Dodecanoic acid (C12) was most effective, producing up to a 5‐fold increase in CCK secretion. Fatty acids with less than ten carbon atoms did not increase secretion. The chain length dependence of these effects mimics closely fatty acid‐induced CCK secretion previously observed in humans in vivo.3 Esterification of C12 abolished CCK secretion, indicating a critical role for a free carboxyl group in eliciting secretion. In contrast, modification of the methyl terminus had no effect on C12‐induced secretion. The non‐metabolizable C12 analogue 2‐bromododecanoic acid was equally effective. 4 C12 elicited a marked increase in intracellular calcium levels (200–300 n m ) in STC‐1 cells which was abolished by the L‐type Ca 2+ channel antagonist nicardipine. In contrast, C8 produced a smaller and more transient Ca 2+ response. C12‐induced CCK secretion was also blocked by nicardipine. 5 These data suggest that fatty acids can interact directly with enteroendocrine cells to stimulate CCK secretion via increases in intracellular calcium mediated primarily by L‐type Ca 2+ channels.