open access

https://hdl.handle.net/2115/84549

Multiple Fatty Acid Sensing Mechanisms Operate in Enteroendocrine Cells

英語

2004

Journal of Biological Chemistry

279(25)

26082-26089

Fatty acids (FA) with at least 12 carbon atoms increase intracellular Ca2+ ([Ca2+]i) to stimulate cholecystokinin release from enteroendocrine cells. Using the murine enteroendocrine cell line STC-1, we investigated whether candidate intracellular pathways transduce the FA signal, or whether FA themselves act within the cell to release Ca2+ directly from the intracellular store. STC-1 cells loaded with fura-2 were briefly (3 min) exposed to saturated FA above and below the threshold length (C8, C10, and C12). C12, but not C8 or C10, induced a dose-dependent increase in [Ca2+]i, in the presence or absence of extracellular Ca2+. Various signaling inhibitors, including d-myo-inositol 1,4,5-triphosphate receptor antagonists, all failed to block FA-induced Ca2+ responses. To identify direct effects of cytosolic FA on the intracellular Ca2+ store, [Ca2+]i was measured in STC-1 cells loaded with the lower affinity Ca2+ dye magfura-2, permeabilized by streptolysin O. In permeabilized cells, again C12 but not C8 or C10, induced release of stored Ca2+. Although C12 released Ca2+ in other permeabilized cell lines, only intact STC-1 cells responded to C12 in the presence of extracellular Ca2+. In addition, 30 min exposure to C12 induced a sustained elevation of [Ca2+]i in the presence of extracellular Ca2+, but only a transient response in the absence of extracellular Ca2+. These results suggest that at least two FA sensing mechanisms operate in enteroendocrine cells: intracellularly, FA (≥C12) transiently induce Ca2+ release from intracellular Ca2+ stores. However, they also induce sustained Ca2+ entry from the extracellular medium to maintain an elevated [Ca2+]i.

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This research was originally published in the Journal of Biological Chemistry. Author(s). Multiple Fatty Acid Sensing Mechanisms Operate in Enteroendocrine Cells. J. Biol. Chem. 2004; Vol.279: 26082–26089. © the American Society for Biochemistry and Molecular Biology or © the Author(s).

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