Fig. 6: Insulin-mediated protection against palmitoleic acid-induced inhibition of the PMCA is abolished in pancreatic acinar cells from PACIRKO mice.

Representative traces showing time-matched control in situ [Ca²⁺]_i clearance experiments (a, d) and the effect of POA (b, e) on [Ca²⁺]_i clearance in untreated cells (b, e) and cells pre-treated with 10 nM insulin (c, f) in pancreatic acinar cells from IR^lox/lox (a–c) and PACIRKO mice (d–f). Cells were treated with 30 μM CPA (arrow) in the absence of external Ca²⁺ (1 mM EGTA; white bar) or 20 mM Ca²⁺ (grey bar) to induce store-operated Ca²⁺ influx phases. POA was added prior to the re-addition of 20 mM external Ca²⁺.during the second influx-clearance phase (black bar). Inset dashed box (a–f) shows superimposed expanded time-courses of first (black trace) and second clearance phase (grey trace). Traces are representative of 5 (IR^lox/lox time-matched control, a), 4 (IR^lox/lox POA, b), 3 (IR^lox/lox POA with insulin, c), 5 (PACIRKO time-matched control, d). 4 (PACIRKO POA, e) and 5 (PACIRKO POA with insulin, f) separate experiments. Linear clearance rate (in the presence of POA) was normalized to the initial clearance rate in each cell (% relative clearance rate). g Mean % relative clearance (±SEM) of corresponding time-matched control (white bar), POA treatment (30 μM; dark grey bar), and POA with insulin (light grey bar). Significance (specifc p values as indicated) was determined by one-way ANOVA with Sidak’s multiple comparisons. Data were derived from individual values from multiple cells (3-19 cells per experiment) in the field of view for each experiment. These values were averaged giving the experimental mean, that were in turn averaged across multiple experiments giving the true mean ± SEM as indicated in (g).