Thickness and Collagen Metabolism of Lens Capsule from Genetically Prediabetic Mice

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Abstract
Genetically diabetic KK mice develop spontaneous chemical diabetes with thickened capillary basement membranes and human-like diabetic microangiopathy. These alterations are preceded by a stage of genetic prediabetes (up to 6 wk old) with normal glycemia and normal tolerance to glucose. The structural and biochemical abnormalities of the lens capsule were examined as a model of avascular basement membrane in the young prediabetic mice (5 wk old). A significant increase of anterior lens capsule thickness was observed in young prediabetic mice. After in vitro labeling of lenses from control and prediabetic mice with (3H)-proline the specific activity of hydroxy-(3H)-proline from lens capsules of prediabetic mice increased; the specific activity of (3H)-proline decreased. The chromatographic pattern of the pepsin-soluble collagen isolated from lens capsule was quite similar in control and prediabetic mice. In both strains a procollagenous material with an apparent MW of 180,000 was synthesized by lenses in the medium. The synthesis of this material was increased in the prediabetic lens capsule. After labeling of lenses with (3H)-glucosamine, (3H)-glucosamine incorporated in the collagenase-resistant glycoproteins of prediabetic lens capsules was significantly decreased. In hereditary prediabetic mice the abnormal thickening of lens capsule apparently is accompanied by a significant increase of (3H)-proline incorporated in the collagenous moiety of the lens capsule. These structural and biochemical alterations of a typical basement membrane occurring before the onset of carbohydrate intolerance seem genetically determined and not directly related to hyperglycemia.