PREVENTION OF VASCULAR & NEURAL DYSFUNCTION IN DIABETIC RATS BY C-PEPTIDE

C-肽，胰岛素原加工过程中的裂解产物 胰岛素，一直被认为具有很少的生物学活性 除了参与胰岛素合成以外的其他活动。注射法 预防或减弱血管和神经的人C肽 (电生理)功能障碍与Na+和K+依赖受损 糖尿病大鼠组织中三磷酸腺苷的活性。 多肽中间部分需要非极性氨基酸。 这些生物效应。合成反向序列(追溯)和 全D-氨基酸(对映体)C-肽与天然的等效性 C-肽，提示C-肽在糖尿病中的作用 非手性介导的血管和神经功能障碍 相互作用，而不是立体特异的受体或结合部位。 组织山梨醇水平用GC/MS测定，不受 C-肽。

C-peptide, a cleavage product from the processing of proinsulin to insulin, has been considered to possess little if any biological activity other than its participation in insulin synthesis. Injection of human C-peptide prevented or attenuated vascular and neural (electro-physiological) dysfunction and impaired Na+- and K+-dependent adenosine triphosphate activity in tissues of diabetic rats. Non-polar amino acids in the mid-portion of the peptide were required for these biological effects. Synthetic reverse sequence (retro) and all-D-amino acid (enantio) C-peptides were equipotent to native C-peptide, which indicates that the effects of C-peptide on diabetic vascular and neural dysfunction were mediated by non-chiral interactions instead of stero-specific receptors or binding sites. Tissue sorbitol levels were measured by GC/MS and were not affected by C-peptide.