Increased fatty acid oxidation was observed in UCP3 over-expression mouse studies or other over-expression systems. The exact role of UCP3 in fatty acid oxidation is still unclear, but one proposed role for UCP3 is in the export of fatty acid anions thus permitting continuous rapid fatty acid oxidation during an oversupply. It is also unclear how the increased lipolysis occurred in the synaptotagmin-7 KO mice. Sympathetic nerve activity and catecholamines are known triggers of increased lipolysis and UCP3 expression. Although deletion of synaptotagmin-7 impairs secretory granule exocytosis in chromaffin cells, we did not observe significant differences in epinephrine, norepinephrine or Pempidine dopamine levels between synaptotagmin-7 KO and control mice. In summary, the present study reveals altered metabolic responses in synaptotagmin-7 KO mice, including increased lipolysis, fatty acid transport and oxidation, and the increased use of fat as fuel. The increased fatty acid oxidation or utilization observed in the present study provides a plausible explanation for the lean phenotype in the synaptotagmin-7 KO mice. This study, however, does not indicate that changes to metabolism are a direct effect of synaptotagmin-7 deletion but possibly the result of systemic effect of glucagon deficiency on the overall animal metabolism. Our study corroborates certain beneficial effects of reduced glucagon signalling, and supports its therapeutic potential in the prevention and treatment of diabetes and other metabolicrelated diseases. The establishment of cell lines from human tissues involves genetic manipulation of telomerase, tumor suppressors and oncogenes. Telomerase is required to circumvent the finite number of divisions most somatic cells experience due to telomere shortening. In human cells, telomerase expression together with mutations in tumor suppressors leads to immortality. Rodent cells, in contrast to human cells become immortal spontaneously at high frequency. Expression of oncogenes such as Ras allows cells to be independent of growth factors. Expression of oncogenic Ras in human primary cells that lack telomerase activity causes senescence, but we discovered expressing a Ras oncogene inDrosophila primary embryonic cells promotes cell proliferation to rapidly give rise to immortal cell lines. This different response may be because Drosophila maintains telomere length without telomerase. Expression of RasV12 has Pentyl Chloroformate proved to be a useful genetic tool to create Drosophila mutant cell lines. By analogy with mammalian cells, inactivation of tumor suppressors could provide another genetic means to immortalize Drosophila cells.