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Editor,—The non-obese diabetic (NOD) mouse is a spontaneous model of type 1 (insulin dependent) diabetes mellitus, frequently used in diabetes research.1 The colony at the medical college of St Bartholomew’s Hospital (NOD/Ba) was established in 1987 and some 55% of females and 15% of male mice spontaneously develop diabetes by 30 weeks of age.2 Cataracts are not a characteristic normally found in NOD mice but were observed during routine inspection in 1988. All animals in the substrain NOD/Ba/Lop19 now spontaneously develop cataracts in both eyes (typically at 104–199 days of age). There are differences between NOD/Ba/Lop19 and the other mice of the colony with puberty, gestation period, teeth eruption, and eye opening all taking place later. Cataracts of the type seen are often the result of metabolic disturbances; however, although blood glucose levels greater than 12 mmol/l are known to cause cataracts in experimental models,3 their development in NOD/Ba/Lop19 is not related to the development of diabetes (normally at 112–133 days) as they occur before blood glucose levels exceed 11.5 mmol/l. This is unusual in that cataract formation in other susceptible laboratory rodents usually precedes the development of a general disease state.4
The cataracts initially take the form of a visible dense white sclerotic central area (see Fig 1), accompanied by clouding of the lens itself, which becomes denser over a few days. Both eyes are usually affected within 5 days of each other. Back cross breeding experiments show the Mendelian inheritance patterns typical of a single recessive gene. It has been suggested that there may be a subset of young diabetic patients with unusual susceptibility to cataracts and other complications of diabetes affecting the eye5 and NOD/Ba/Lop19 could act as a specific model for this group. If the mechanism by which cataract formation occurs in NOD/Ba/Lop19 mice could be established then it could prove useful to determine if any diabetic patients who develop cataracts have the same genotypic and/or metabolic characteristics. This then raises the possibility of preventative treatment.
The support of the Joint Research Board of St Bartholomew’s Hospital is gratefully acknowledged.
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