Leung M K, Folkes G A, Ramamurthy N S, Schneir M, Golub L M
Biochim Biophys Acta. 1986 Feb 19;880(2-3):147-52. doi: 10.1016/0304-4165(86)90074-7.
To identify the mechanisms responsible for the paucity of recently synthesized collagen in connective tissues during diabetes, in vitro procollagen metabolism was studied in non-diabetic (control) and diabetic rats. Achilles tendons from the two groups were incubated for 1-8 h (35 degrees C) in medium containing [14C]proline and the radiolabeled collagen in the tissue, and that released into the media, were examined by SDS-polyacrylamide gel electrophoresis and fluorography. The bulk of the radiolabeled collagen in tendon from the diabetics was recovered as degradation products; these, but also procollagen and collagen components, were prominent in the control tissues. Moreover, the collagenous components synthesized by the diabetic rat tendons were more readily digested in vitro by trypsin than those produced by control tissues. We conclude that diabetes reduces collagen accretion in connective tissues in part due to increased intracellular degradation of procollagen.
为了确定糖尿病期间结缔组织中近期合成的胶原蛋白缺乏的机制，我们对非糖尿病（对照）大鼠和糖尿病大鼠的体外前胶原代谢进行了研究。将两组大鼠的跟腱在含有[14C]脯氨酸的培养基中于35℃孵育1 - 8小时，通过SDS - 聚丙烯酰胺凝胶电泳和荧光自显影检查组织中以及释放到培养基中的放射性标记胶原蛋白。糖尿病大鼠肌腱中大部分放射性标记的胶原蛋白以降解产物形式回收；这些降解产物以及前胶原和胶原成分在对照组织中很突出。此外，糖尿病大鼠肌腱合成的胶原成分在体外比对照组织产生的胶原成分更容易被胰蛋白酶消化。我们得出结论，糖尿病导致结缔组织中胶原蛋白积累减少，部分原因是前胶原的细胞内降解增加。
