Moderate caloric restriction delays cataract formation in the Emory mouse

• Published in: The FASEB journal Vol. 3; no. 6; p. 1741
• Main Authors: Taylor, A, Zuliani, A M, Hopkins, R E, Dallal, G E, Treglia, P, Kuck, J F, Kuck, K
• Format: Journal Article
• Language: English
• Published: United States 01-04-1989
• Subjects: Aging - metabolism; Animals; Cataract - metabolism; Cataract - prevention & control; Crystallins - metabolism; Disease Models, Animal; Electrophoresis, Polyacrylamide Gel; Energy Intake; Lens, Crystalline - metabolism; Macromolecular Substances; Mice; Mice, Inbred Strains; Solubility; Weight Gain
• ISSN: 0892-6638
• DOI: 10.1096/fasebj.3.6.2703107

Eye lens senile cataract is a major cause of blindness, affecting the elderly in particular. The etiology of the disorder has been elusive, and attempts to delay the onset of senile cataracts have been unsuccessful. The need for more information is underscored by epidemiologists who estimate that the ability to delay cataract formation in humans by only 10 years would eliminate the need for 50% of the cataract extractions performed annually in the United States. The Emory mouse provides the best model for human senile cataracts. Feeding Emory mice a diet that was restricted in calories by approximately 21% delayed the onset of cataracts. This is the first study that demonstrates in vivo the delay of senile-type cataracts. In these animals, aging and cataracts are associated with diverse changes in the proportion of various proteins (particularly 21, 22, 31-34 kDa) and with transformation of proteins from a soluble to an insoluble state. In advanced cataracts, there is a loss of total protein. Within a cataract grade, there is no difference between restricted and nonrestricted animals in relative proportion of specific lens proteins or in amounts of total or soluble proteins. The transition from a clear to cataractous lens appears when the soluble-to-total protein ratio falls below about 0.58. The exclusive use of gamma-crystallin as an indicator of lens viability is questioned. To the extent that cataract formation is due to lens protein oxidation and/or an inability to proteolytically remove damaged protein, it would appear that caloric restriction results in enhanced protection against lens oxidative stress or in prolonged proteolytic function.