Goodson W H, Hunt T K
Diabetes. 1986 Apr;35(4):491-5. doi: 10.2337/diab.35.4.491.
We used C57-BL ob/ob mice as a model to study wound healing in type II (adult-onset) diabetes. Planimetry was used to assess rate of closure in standard open skin wounds. In agreement with previous subcutaneous wound collagen-accumulation studies, closure was slower in the ob/ob mice. Subcutaneous implants were used to evaluate wound collagen accumulation. Weanling mice have collagen accumulation similar to lean littermates (mean 3.43 micrograms/cm vs. 3.46 micrograms/cm), but the same ob/ob animals had decreased wound collagen (mean 2.39 micrograms/cm vs. 3.02 micrograms/cm, P less than 0.04) when mature. Other ob/ob animals fed a restricted diet (and thus not obese) had normal collagen accumulation at the same age. Neither insulin nor diet restriction restored wound collagen accumulation in phenotypically obese mice. Because collagen accumulation is not improved by measures that control hyperglycemia (insulin and diet restriction) and the defect was seen only in phenotypically obese ob/ob mice, the decreased wound collagen accumulation may be due in part to structural changes in adipose tissue.
我们使用C57-BL ob/ob小鼠作为模型来研究II型（成年发病型）糖尿病的伤口愈合情况。采用面积测量法评估标准开放性皮肤伤口的闭合速率。与之前皮下伤口胶原积累的研究一致，ob/ob小鼠的伤口闭合较慢。采用皮下植入物评估伤口胶原积累。断奶小鼠的胶原积累与瘦的同窝小鼠相似（平均3.43微克/厘米对3.46微克/厘米），但相同的ob/ob动物成熟时伤口胶原减少（平均2.39微克/厘米对3.02微克/厘米，P<0.04）。其他喂食限食（因此不肥胖）的ob/ob动物在相同年龄时胶原积累正常。胰岛素和饮食限制均未恢复表型肥胖小鼠的伤口胶原积累。由于控制高血糖的措施（胰岛素和饮食限制）并未改善胶原积累，且仅在表型肥胖的ob/ob小鼠中出现这种缺陷，伤口胶原积累减少可能部分归因于脂肪组织的结构变化。
