Abstract
Diabetic cataractogenesis, a multifactorial process, was examined with nuclear magnetic resonance (NMR). P-31 NMR spectroscopic studies showed substantial alteration of both energy and membrane metabolism in the diabetic lens. Findings from a C-13 NMR spectroscopic determination of the sorbitol pathway flux in lenses incubated in 35.5 mmol/L glucose revealed that (1) one-third of total glucose consumed was channeled through this pathway, and (2) the turnover rate of NADPH to NADP was 3,000%/hr. Furthermore, a competition for NADPH between aldose reductase and glutathione reductase was demonstrated. It is important to note that all metabolic changes in hyperglycemic/diabetic lenses can be prevented by aldose reductase inhibitors, eg, sorbinil.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adenosine Triphosphate / analysis
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Adenosine Triphosphate / metabolism
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Aldehyde Reductase / antagonists & inhibitors
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Aldehyde Reductase / metabolism*
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Animals
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Cataract / etiology
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Cataract / metabolism*
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Cell Membrane / metabolism
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Diabetes Complications
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Glucose / metabolism
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Glucose / pharmacology*
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Glycerophosphates / analysis
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Humans
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Imidazoles / pharmacology
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Imidazolidines*
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Lens, Crystalline / analysis
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Lens, Crystalline / drug effects
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Lens, Crystalline / enzymology
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Lens, Crystalline / metabolism*
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Magnetic Resonance Spectroscopy
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NADP / metabolism
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Oxidation-Reduction*
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Rats
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Sorbitol / metabolism
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Sugar Alcohol Dehydrogenases / metabolism*
Substances
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Glycerophosphates
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Imidazoles
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Imidazolidines
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Sorbitol
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NADP
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Adenosine Triphosphate
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alpha-glycerophosphoric acid
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Sugar Alcohol Dehydrogenases
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Aldehyde Reductase
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sorbinil
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Glucose