Our findings provide evidence for an inhibitory effect of leptin on the cell apoptosis program. In addition, we have provided some evidence for the possible anti-apoptotic mechanisms of the leptin produced by trophoblastic cells. However, further additional studies are needed to fully explain the effect of leptin on the regulation of BCL-2, BAX and p53 expression. More precisely, we have demonstrated the autocrine anti-apoptotic effect of leptin in trophoblastic cells, providing new insights into the functions of leptin in placental apoptosis. Since apoptosis plays a central role in placental physiology, our work further support the importance of leptin in human placenta. GLP-1 and GIP are incretin hormones released from intestinal enteroendocrine cells in response to feeding. In addition to glucose-dependent stimulation of insulin secretion, they exert a variety of other actions on beta cells including stimulation of insulin biosynthesis and beta cell replication together with protection against chemical attack and inhibition of apoptosis. Other actions of GLP-1 include inhibition of glucagon secretion, gastric emptying and feeding, with additional positive effects on cardiac muscle and, in common with GIP, improvement of cognition and bone formation. These attributes of GLP-1 have been captured for treatment of type 2 diabetes by development of stable GLP-1 mimetics and DPPIV inhibitors which inhibit the normal rapid degradation of both incretin hormones. Much has been elucidated concerning the pancreatic and extrapancreatic actions of GLP-1 and GIP together with mechanisms regulating the secretion of the two incretin hormones from intestinal L and K-cells, respectively. However, recent studies have opened a whole new aspect of research by demonstrating that GLP-1 and GIP are not generated exclusively in the gut but may also be present in islet cells. Thus, recent studies have shown that the normal proglucagon processing to glucagon in islet alpha cells by PC2 can be modified by expression of PC1/3 yielding GLP-1 and related peptides normally produced by intestinal L-cells. Accordingly GLP-1 has been demonstrated by immunochemical staining, immunoassay, bioassay and mass spectroscopy techniques in both animal and human alpha cells, giving rise to speculation that islet-derived GLP-1 may play a key role in beta cell function. Use of antibodies or chemical antagonists of GLP-1 indicate that GLP-1 released from islet alpha cells in vitro may stimulate insulin release from adjacent beta cells via paracrine or local islet cell interactions. Further studies also indicate that GIP, or more likely the equally biologically active fragment GIP generated by the action of PC2, is also produced by islet alpha cells. More recently still, transgenic mice with global deficiency in proglucagon-derived peptides have been shown to exhibit ectopic expression of biologically active GIP in islet beta cells.