AICAR Protects against High Palmitate/High Insulin-Induced Intramyocellular Lipid Accumulation and Insulin Resistance in HL-1 Cardiac Cells by Inducing PPAR-Target Gene Expression

Figure 5

AICAR stimulation attenuates HP/HI-induced glucose uptake impairment in HL-1. HL-1 cells were stimulated with HP/HI for 16 h in the presence or absence of AICAR (24 h), and [³H]-deoxyglucose uptake (up) and AKT phosphorylation (down) were assessed in the presence (a) and absence (b) of insulin (200 nmol/L, 10 min). [³H]-deoxyglucose uptake (up) and AKT phosphorylation (down) determination in HL-1 cells stimulated with AICAR (24 h) in the presence and absence of insulin (200 nmol/L, 10 min) (c). Data are expressed as mean ± SD of 4 different experiments performed in duplicate. (, versus control cells without insulin stimulation; versus control cells stimulated with insulin; versus HP/HI-challenged cells stimulated with insulin (a) or without insulin (b); versus AICAR-treated cells stimulated with insulin).

(a)

(b)

(c)