Oxidants are generated under various physiological conditions that include mitochondrial electron transport, peroxisomal fatty acid metabolism, phagocytosis by macrophages, and bone resorption by osteoclasts. However, increased oxidative stress has been correlated to a varying extents with common age-related diseases, such as adult-onset diabetes mellitus, atherosclerosis, some types of cancer, and some forms of neurodegeneration including cerebellar ischemia.
The increasing prevalence of obesity and other nutrition-related chronic diseases, which usually accompany aging, has prompted considerable efforts to understand their pathogenesis and treatment. One experimental approach is to overexpress, inactivate, or manipulate specific genes that regulate energy metabolism and fat storage. Many such techniques are fully amenable and have been established as routine tools in zebrafish, as well as in Drosophila and C. elegans. In the future, these elegant models will be complementarily helpful in dissecting endocrine problems and metabolic pathways, associated with aging and senescence. Particularly, once zebrafish counterparts of essential signaling molecules, such as Sir2 and FoxOs, involved in regulation of energy metabolism are available, development of model systems appear to be within of our current technologies and fat storage, are obtained, development of new vertebrate aging models appears to be within the scope of our current technologies.
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