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胰岛素样生长因子I对糖尿病大鼠萎缩胸腺的再填充作用。

Repopulation of the atrophied thymus in diabetic rats by insulin-like growth factor I.

作者信息

Binz K, Joller P, Froesch P, Binz H, Zapf J, Froesch E R

机构信息

Department of Medicine, University Hospital, Zürich, Switzerland.

出版信息

Proc Natl Acad Sci U S A. 1990 May;87(10):3690-4. doi: 10.1073/pnas.87.10.3690.

DOI:10.1073/pnas.87.10.3690
PMID:2187189
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC53968/
Abstract

Atrophy of the thymus is one of the consequences of severe insulin deficiency. We describe here that the weight and the architecture of the thymus of diabetic rats is restored towards normal not only by insulin but also by insulin-like growth factor I (IGF-I) treatment. In contrast to insulin, this effect of IGF-I occurs despite persisting hyperglycemia and adrenal hyperplasia. We also investigated the in vivo effect of IGF-I on replication and differentiation of thymocytes from streptozotocin-induced diabetic rats. Thymocytes from diabetic rats incorporated less [3H]thymidine than did thymocytes from healthy rats. Insulin, as well as IGF-I treatment of diabetic rats increased [3H]thymidine incorporation by thymocytes. Flow cytometry of thymocytes labeled with monoclonal antibodies revealed a decreased expression of the Thy-1 antigen in diabetic rats compared with control rats. In addition, a major deficiency of thymocytes expressing simultaneously the W3/25 and the Ox8 antigens (corresponding to immature human CD4+/CD8+ thymocytes) was observed. These changes were restored towards normal by insulin as well as by IGF-I treatment. The antibody response to a T cell-dependent antigen (bovine serum albumin) was comparable in normal and diabetic rats. We conclude that IGF-I has important effects on the thymocyte number and the presence of CD4+/CD8+ immature cells in the thymus of diabetic rats despite persisting hyperglycemia. However, helper T-cell function for antibody production appears to be preserved even in the severely diabetic state.

摘要

胸腺萎缩是严重胰岛素缺乏的后果之一。我们在此描述，糖尿病大鼠的胸腺重量和结构不仅通过胰岛素，而且通过胰岛素样生长因子I（IGF-I）治疗可恢复正常。与胰岛素不同，尽管存在持续性高血糖和肾上腺增生，IGF-I仍有此作用。我们还研究了IGF-I对链脲佐菌素诱导的糖尿病大鼠胸腺细胞增殖和分化的体内作用。糖尿病大鼠的胸腺细胞比健康大鼠的胸腺细胞掺入的[3H]胸腺嘧啶核苷更少。胰岛素以及对糖尿病大鼠的IGF-I治疗增加了胸腺细胞对[3H]胸腺嘧啶核苷的掺入。用单克隆抗体标记胸腺细胞的流式细胞术显示，与对照大鼠相比，糖尿病大鼠中Thy-1抗原的表达降低。此外，观察到同时表达W3/25和Ox8抗原（对应于未成熟的人CD4+/CD8+胸腺细胞）的胸腺细胞存在严重缺陷。这些变化通过胰岛素以及IGF-I治疗恢复正常。对T细胞依赖性抗原（牛血清白蛋白）的抗体反应在正常和糖尿病大鼠中相当。我们得出结论，尽管存在持续性高血糖，IGF-I对糖尿病大鼠胸腺中的胸腺细胞数量和CD4+/CD8+未成熟细胞的存在仍有重要影响。然而，即使在严重糖尿病状态下，辅助性T细胞产生抗体的功能似乎仍得以保留。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f019/53968/6a0b5772d45a/pnas01035-0066-d.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f019/53968/1f7022d4a94a/pnas01035-0066-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f019/53968/c21af2c63df7/pnas01035-0066-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f019/53968/370d7e188ec6/pnas01035-0066-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f019/53968/6a0b5772d45a/pnas01035-0066-d.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f019/53968/1f7022d4a94a/pnas01035-0066-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f019/53968/c21af2c63df7/pnas01035-0066-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f019/53968/370d7e188ec6/pnas01035-0066-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f019/53968/6a0b5772d45a/pnas01035-0066-d.jpg

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本文引用的文献

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Reduced resistance to Pseudomonas septicaemia in diabetic mice.糖尿病小鼠对败血假单胞菌的抵抗力降低。
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