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2．糖尿病的治疗措施有哪些？
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参考文献
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[1] 沈洁，谷卫．新发现的1型糖尿病相关基因．国际内分泌代谢杂志，2006，1
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[2] 胡承，贾伟平．2型糖尿病易感基因定位研究．中华内分泌代谢杂志，2008，2
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[3] 第17届国际糖尿病大会简介．中国糖尿病杂志，2001，2
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[4] Aiston S, Agius L. Leptin enhances glycogen storage in hepatocytes by inhibition of phosphorylase and exerts an additive effect with insulin. Diabetes, 1999 48
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[5] Barzilay J, Abraham L, Heckbert SR, et al. The Relation of markers of inflammation to the development of glucose disorders in the elderly: The cardiovascular health study. Diabetes, 2001, 50
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[10] Yki-Jarvinen H, Kauppinen-Makelin R, Tiikkainen M, et al. Insulin glargine or NPH combined with metformin in type 2 diabetes: the LANMET study. Diabetologia, 2006, 49
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[11] Green, BD, Flatt, PR & Bailey, CJ. Dipeptidyl peptidase IV inhibitors: a newly emerging drug class for the treatment of type 2 diabetes. Diab Vasc Dis Res, 159-165.
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（童钟杭）
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内科学新进展 第六章 肾脏疾病
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第一节 肾脏疾病慢性进展理论与实践
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摘 要 慢性肾功能衰竭（CRF）发病机理甚为复杂，迄今尚未完全明了。历年来先后提出“尿毒症毒素学说”、“完整肾单位学说”、“矫枉失衡学说”、“肾小球高滤过学说”、“脂质代谢紊乱学说”等等，但没有一种学说能完整解释其全部的发病过程。近年来，随着分子生物学的飞速发展及其在肾脏病领域的应用，加深了人们对慢性肾功能衰竭发病机理的认识，已有的学说不断得到补充和纠正，新的学说不断涌现，特别是逐渐认识了各种生长因子和血管活性物质在慢性肾功能衰竭进展中的作用，使慢性肾功能不全发展过程中的多种变化有了更深入细致的认识。随着慢性肾功能衰竭发病机理的逐渐阐明，延缓慢性肾功能衰竭进展的治疗方法不断完善。
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Abstract The pathogenesis of Chronic renal failure（CRF）is very complicated, and has not yet been fully understood. Over the years the “uremic toxics hypothesis,” “integrity nephron hypothesis”, “trade-off hypothesis”, “glomerular homo-filtration hypothesis”, “lipid metabolism disorder hypothesis”, and so on have been put forward, but none of them can completely explain the whole pathogenesis. In recent years, with the rapid development of molecular biology and its applications in the field of kidney disease, we have understood the pathogenesis of chronic renal failure more deeply, the existent hypothesis has been constantly added and corrected and new theories are emerging. Particularly, with the growing recognition of the various growth factors and vasoactive substances which affect in the progress of chronic renal failure, people have got a more in-depth and detailed understanding of the various changes in the development of chronic renal insufficiency. With the pathogenesis of chronic renal failure being gradually clarified, the treatment that delay the progress of chronic renal failure has been continuously improved.
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一、慢性肾功能衰竭发病机理进展
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（一）肾小球高滤过学说
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20世纪80年代初，Brenner等在5/6肾切除大鼠，应用微穿刺研究证实残余肾单位肾小球滤过率增高（高滤过）、血浆流量增高（高灌注）和毛细血管跨膜压增高（高压力），即著名的“三高学说”或“肾小球高滤过学说”。
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近年来的研究认为，其产生机制主要是残余肾单位入球小动脉较出球小动脉扩张更加显著所致。一般认为，入球小动脉扩张与该动脉处扩血管物质前列腺素分泌过多，局部内皮细胞来源血管舒张因子（现认为主要是NO）分泌增多，以及该动脉对血管紧张素Ⅱ不敏感有关；而出球小动脉扩张相对较少则与该动脉对血管紧张素Ⅱ敏感性增加有关。
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在高滤过、高灌注、高压力的血流动力学状态下，肾小球可显著扩展，进而牵拉系膜细胞。周期性机械性牵拉系膜细胞，可以使胶原Ⅳ、V、Ⅰ、Ⅱ、纤维连接蛋白和层黏连蛋白的合成增多，细胞外基质增加，肾小球肥大在某种程度内得到缓冲并减轻了肾小球压力。然而，大量细胞外基质积聚，加以高血流动力学引起肾小球细胞形态和功能异常，又会使肾小球进行性损伤，最终发展为不可逆的病理改变即肾小球硬化。
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