BACKGROUND: In morbid obesity and type 2 diabetes saturated fatty acid (SFA) levels are markedly increased. Palmitate, a SFA, crosses the placenta easily and may affect embryos of diabetic mothers. Palmitate induces inflammation and apoptosis in many cell types including cardiomyocytes. Transient cardiomyopathy can develop in offspring of diabetic mothers. We are testing the hypothesis that palmitate will increase apoptosis in chick embryo cardiomyocytes, making it vulnerable for later disease. METHODS: Hearts from chick embryos at Hamburger Hamilton stage 31 were harvested and digested into single cells using trypsin then plated. After 48 h of growth, cells were exposed to free palmitate (at ∼2.3:1, FFA:albumin ratio) at high physiological concentrations for 24 h. Apoptosis was measured with Annexin V and cell necrosis with propodium iodide using flow cytometry. RESULTS: Apoptosis was markedly elevated in chick embryo cardiomyocytes exposed to palmitate in a dose dependent manner (see Figure). Percentage of apoptotic cells increased from 11.9% in 0 μM palmitate to 32.0% and 44.1% in 150 μM and 300 μM respectively. The percentage of cells demonstrating non-apoptotic necrosis was low and did not change with increasing palmitate concentration. CONCLUSIONS: In chick embryo cardiomyocytes apoptosis is increased in a dose-dependent manner by brief exposure to palmitate. This may have important implications for intrauterine cardiac development in pregnant diabetic mothers and needs to be further explored.