Islet amyloid, increased A-cells, reduced B-cells and exocrine fibrosis: quantitative changes in the pancreas in type 2 diabetes.
Islet amyloid, increased A-cells, reduced B-cells and exocrine fibrosis: quantitative changes in the pancreas in type 2 diabetes.
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发表时间：
1988-12
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通讯作者：
Anne Clark;C. Wells;I. Buley;J. Cruickshank;R. Vanhegan;David R. Matthews;Garth J. S. Cooper;Rury R. Holman;Robert C. Turner
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作者：
Anne Clark;C. Wells;I. Buley;J. Cruickshank;R. Vanhegan;David R. Matthews;Garth J. S. Cooper;Rury R. Holman;Robert C. Turner
对 15 名 2 型糖尿病患者和 10 名年龄匹配的对照受试者的免疫过氧化物酶染色的死后组织进行了内分泌和外分泌胰腺的形态计量分析。 15 名 2 型糖尿病患者中有 13 名在体部（身体、尾部和头部前部）有胰岛淀粉样蛋白沉积（平均 6.5% 胰岛面积），但在头部（头部“富含胰多肽”的部分）没有，而在对照受试者中则没有发现。在糖尿病受试者体内，与对照组相比，B 细胞的胰腺面积密度降低了 24%（p = 0.005），A 细胞增加了 58%（p 小于 0.001）。语料库中的平均 A/B 细胞比率从对照受试者的 0.27 增加到 2 型糖尿病患者的 0.57。在糖尿病受试者的胰岛淀粉样蛋白以及对照和糖尿病受试者的 B 细胞中证明了淀粉样蛋白成分肽（糖尿病相关肽）的阳性免疫反应性。 A 细胞的增加可能导致 2 型糖尿病的高胰高血糖素血症和高血糖。 2 型糖尿病中胰岛素分泌受损可能是由于 B 细胞减少和淀粉样蛋白破坏胰岛结构所致。对照组和糖尿病受试者的外分泌脂肪相似，两组体内的外分泌脂肪都多于头部。糖尿病受试者的体部区域外分泌纤维化增加（p 小于 0.001），但头部区域则没有。外分泌纤维化可能继发于胰岛细胞功能紊乱。
Morphometric analysis of the endocrine and exocrine pancreas was done on immunoperoxidase stained post-mortem tissue from 15 Type 2 diabetic and 10 age-matched control subjects. Thirteen of the 15 Type 2 diabetic patients had islet amyloid deposits (mean, 6.5% islet area) in the corpus (body, tail and anterior part of the head) but not in the caput (the "pancreatic polypeptide rich" part of the head) whereas none was seen in control subjects. In the corpus in diabetic subjects, the pancreatic area density of B-cells was decreased by 24% (p = 0.005) and A-cells increased by 58% (p less than 0.001) compared with control subjects. The mean A/B-cell ratio increased in the corpus from 0.27 in control subjects to 0.57 in Type 2 diabetic patients. Positive immunoreactivity for the amyloid constituent peptide, Diabetes Associated Peptide, was demonstrated in islet amyloid of diabetic subjects and in B-cells of control and diabetic subjects. The increase in A-cells may contribute to the hyperglucagonaemia and hyperglycaemia of Type 2 diabetes. The impaired insulin secretion in Type 2 diabetes may be due to a decrease in B-cells and to disruption of the islet structure by amyloid. Exocrine fat was similar in the control and diabetic subjects with both groups having more in the corpus than the caput. Diabetic subjects had increased exocrine fibrosis in the corpus region (p less than 0.001), but not in the caput. Exocrine fibrosis may be secondary to disordered islet cell function.