Aim: 

Bile acids increase the levels of cytosolic Ca²⁺ concentration ([Ca²⁺]c) in pancreatic acinar cells, which has been proposed as one of the triggering events in bile acid-induced acute pancreatitis. We sought to determine whether modification of membrane fatty acid profile of AR42J cells influences bile acid-induced [Ca²⁺]c responses.

Methods: 

Membrane fatty acid changes were evoked by culturing AR42J cells for 72 h in medium enriched with oleic (AR42J-O) or linoleic acid (AR42J-L) as described previously (Audi et al. 2007). For measurement of [Ca²⁺]c, cells were loaded with fura-2 and changes in fluorescence monitorized using a spectrofluorimeter. LDH leakage was determined photometrically using a commercial kit.

Results: 

The [Ca²⁺]c response elicited by 1 mM sodium taurochenodeoxycholate (TCDC) was significantly higher in AR42J-L cells compared with AR42J-O cells. The same pattern was evidenced when cells were treated simultaneously with TCDC and 1 nM cholecystokinin-octapeptide. Greater [Ca²⁺]c in AR42J-L cells was not paralleled by higher release of LDH after a 50-min incubation with the above agents, indicating that the effect was not due to increased membrane permeability.

Conclusions: 

Our results suggest a modulatory role for membrane lipid composition in Ca²⁺ signaling in pancreatic acinar cells exposed to bile acids. This may have pathophysiologic relevance considering that habitual intake of specific dietary fats influences the fatty acid profile of pancreatic membranes in vivo (Yago et al. 2004).

Audi et al. (2007). Exp Biol Med 232, 532-541.

Yago et al. (2004). Br J Nutr 91, 227–234.

Supported by the University of Granada (PP 008100)