ARS | Publication request: Letters to the Editor: Reply to J Gomez-Ambrosi Et Al

Submitted to: American Journal of Clinical Nutrition
Publication Type: Other
Publication Acceptance Date: January 1, 2004
Publication Date: May 1, 2004
Citation: Taylor, A. 2004. Letters to the Editor: Reply to J Gomez-Ambrosi et al. American Journal of Clinical Nutrition. 79(5):889.

Technical Abstract: Drs Gomez-Ambrosi, Salvador, and Fuhbeck posit an attractive hypothesis: that the relation we reported between overweight and elevated odds for posterior subcapsular opacities (1) may have etiologic factors which include responses to elevated leptin. Their hypothesis is based upon observations that 1) overweight is associated with elevated leptin levels, 2) elevated leptin levels appear to cause at least (2) transient elevations of reactive oxygen species, and 3) elevated reactive oxygen species have been related to cataractogenesis. To date there is a paucity of information to allow direct pursuit of this hypothesis. What is known is that ROS are second messengers resulting from leptin-induced, leptin receptor mediated signaling in endothelial cells; and it is suggested that chronic oxidative stress in endothelial cells under hyperleptinemia may activate atherogenic processes and contribute to the development of vascular pathology (3). Consistent with these data, leptin was found to be an angiogenic factor, and its vitreous levels are associated with angiogenic eye diseases such as proliferative diabetic retinopathy. In addition to oxidants, the biological effects of leptin appear to involve antioxidants, and several growth factors, including vascular endothelial growth factor and pigment epithelium-derived factor, which are also present in the vitreous of eyes with angiogenic diseases (4). However, while leptin receptor was found in the choroids, sclera and connective tissues of the limbus, there is no evidence as yet for a leptin receptor in lens (5). If supported by further research, this would imply that roles for leptin in the etiology of cataract are probably indirect ' perhaps reflecting a generalized oxidative stress originating in non-lens tissues ' comparable to that induced by smoking (6). While not trivial this will make elucidation of roles for leptin more difficult that if a direct role for leptin in lens cell function could be posited.