School of Veterinary Science, The University of Queensland, Brisbane, Queensland, Australia.
Equine Vet J. 2009 Sep;41(7):671-7. doi: 10.2746/042516409x407648.
Anatomical changes in the hoof lamellar tissue induced by prolonged hyperinsulinaemia have not been described previously. Analysis of the induced lesions may promote understanding of hyperinsulinaemic laminitis pathogenesis and produce clinical benefit.
To use light and transmission electron microscopy (TEM) to document hoof lamellar lesions in ponies clinically lame after prolonged hyperinsulinaemia.
Nine clinically normal, mature ponies were allocated randomly to either a treatment group (n = 5) or control group (n = 4). The treatment group received insulin via a modified, prolonged euglycaemic hyperinsulinaemic clamp technique (EHCT) and were subjected to euthanasia when clinical signs of Obel grade II laminitis occurred. The control group was sham treated with an equivalent volume of 0.9% saline and killed at 72 h. Lamellar tissues of the right front feet were harvested and processed for TEM.
Lamellae from insulin treated ponies were attenuated and elongated with many epidermal basal cells (EBC) in mitosis. Unlike carbohydrate induced laminitis in horses there was no global separation at the lamellar dermal/epidermal interface among ponies. Sporadic EBC basement membrane (BM) separation was associated with the proximity of infiltrating leucocytes. In 2 ponies, the lamellar BM was thickened. The number of hemidesmosomes/microm of BM was decreased in all insulin treated ponies.
Prolonged hyperinsulinaemia causes unique lamellar lesions normally characteristic of acute and chronic laminitis. Lamellar proliferation may be an insulin effect through its mitogenic pathway. Aberrant lamellar mitosis may lengthen and weaken the lamellar, distal phalanx attachment apparatus and contribute to the clinical signs that developed.
The study shows that insulin alone, in higher than normal circulating concentrations, induces profound, changes in lamellar anatomy. Medical control of insulin resistance and hyperinsulinaemia may ameliorate lesions and produce clinical benefit.
先前尚未描述过长时间高胰岛素血症引起的蹄角质层组织的解剖学变化。分析诱导的病变可能有助于了解高胰岛素性蹄叶炎的发病机制并产生临床益处。
使用光镜和透射电子显微镜（TEM）记录经过长时间高胰岛素血症后临床跛行的小马的蹄角质层病变。
将 9 匹临床正常、成熟的小马随机分为治疗组（n = 5）或对照组（n = 4）。治疗组通过改良的、延长的血糖正常高胰岛素血症夹闭技术（EHCT）给予胰岛素，并在出现 Obel Ⅱ级蹄叶炎的临床症状时安乐死。对照组用等量 0.9%生理盐水假处理，并在 72 小时时处死。采集右前蹄的角质层组织并进行 TEM 处理。
与马的碳水化合物诱导的蹄叶炎不同，胰岛素处理的小马的角质层变薄和伸长，许多表皮基底层细胞（EBC）处于有丝分裂中。在小马中，角质层真皮/表皮界面没有出现全球性分离。散在的 EBC 基底膜（BM）分离与浸润白细胞的接近有关。在 2 匹小马中，角质层 BM 增厚。所有胰岛素处理的小马的 BM 中半桥粒/μm BM 的数量减少。
长时间高胰岛素血症可引起独特的角质层病变，这些病变通常是急性和慢性蹄叶炎的特征。角质层增生可能是胰岛素通过有丝分裂途径的作用。异常的角质层有丝分裂可能会延长和削弱角质层、远侧趾骨附着装置，并导致出现临床症状。
该研究表明，胰岛素本身在高于正常循环浓度下会引起角质层解剖结构的深刻变化。对胰岛素抵抗和高胰岛素血症的医学控制可能会减轻病变并产生临床益处。
