Sima A A, Chakrabarti S, Garcia-Salinas R, Basu P K
Curr Eye Res. 1985 Oct;4(10):1087-92. doi: 10.3109/02713688509003353.
The pathogenesis of diabetic retinopathy has not been fully explained. The earliest histological lesion is the loss of intramural pericytes and thickening of the basement membrane. Increased activity of the polyol pathway is a probable mechanism for these two abnormalities. Investigations have suffered from the lack of an exact animal model simulating the human condition. Examination of the retina in the spontaneously diabetic BB-rat demonstrated degeneration and loss of intramural pericytes, a progressive increase in basement membrane thickness, and microinfarctions with areas of non-perfusion. Therefore, this model may be used to clarify the biochemical mechanism(s) linking the metabolic abnormalities of diabetes and the retinopathy.
糖尿病视网膜病变的发病机制尚未完全阐明。最早的组织学病变是壁内周细胞丢失和基底膜增厚。多元醇途径活性增加可能是这两种异常的机制。以往的研究因缺乏模拟人类情况的精确动物模型而受到影响。对自发性糖尿病BB大鼠视网膜的检查显示壁内周细胞变性和丢失、基底膜厚度逐渐增加以及出现无灌注区域的微梗死。因此,该模型可用于阐明将糖尿病代谢异常与视网膜病变联系起来的生化机制。