The prevalence of Obesity during pregnancy or maternal obesity is increasing in the US and is associated with increased white adipose tissue and enhanced saturated free fatty acids in the circulation. Fatty acids are essential for optimal cell functions, but excess fatty acid can perturb cellular functions leading to pathological conditions. We have shown that saturated free fatty acids (FFAs) can induce trophoblast lipoapoptosis and palmitoleate prevents trophoblast lipoapoptosis. However, signaling mechanisms underlying the activation of lipoapoptosis in response to FFA and the protective role of palmitoleate in trophoblasts is unclear. We now identified that FFAs induce a caspase dependent trophoblast lipoapoptosis. Next, we observed that treatment of palmitate (PA) resulted in the activation of mitogen activated protein kinases (MAPKs) and Endoplasmic Reticulum (ER) stress responses. Further analysis also revealed that PA-induced formation of stress granules in trophoblasts. We have also explored the protective role of an omega-7 monounsaturated fatty acid, palmitoleate (PO), as a potential anti-inflammatory molecule in macrophages and trophoblasts. Our data showed that palmitoleate was able to protect against lipopolysaccharide-induced inflammatory signal in macrophages and trophoblasts. Further, palmitoleate was shown to be protective against LPS and FFA-induced inflammatory cell death in macrophages.