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通过新生期刺激β细胞预防BB大鼠患糖尿病

Prevention of diabetes mellitus in BB rats by neonatal stimulation of beta cells.

作者信息

Buschard K, Jørgensen M, Aaen K, Bock T, Josefsen K

机构信息

Bartholin Institute, Kommunehospitalet, Copenhagen, Denmark.

出版信息

Lancet. 1990 Jan 20;335(8682):134-5. doi: 10.1016/0140-6736(90)90004-o.

DOI:10.1016/0140-6736(90)90004-o
PMID:1967433
Abstract

Antigen expression in type 1 (insulin-dependent) diabetes may depend on the functional state of beta cells. At birth, beta cells are immature, produce only a basal amount of insulin, and are unresponsive to glucose--but are sensitive to glucagon and arginine. beta cells of spontaneously diabetic BB rats were stimulated for the first 6 days after birth by glucose with glucagon or arginine to accelerate beta cell maturation, and possibly to induce antigen expression and tolerance. Over the first 200 days of life, only 23% of glucose and glucagon-treated BB rats, and 20% of glucose and arginine-treated BB rats developed diabetes, compared with 65% of untreated controls. This finding may explain the observation that children of mothers who have type 1 diabetes are three times less likely to develop the disease than children of fathers with type 1 diabetes. Earlier maturation of beta cells during the diabetic pregnancy may protect against diabetes in later life.

摘要

1型(胰岛素依赖型)糖尿病中的抗原表达可能取决于β细胞的功能状态。出生时,β细胞不成熟,仅产生基础量的胰岛素,并且对葡萄糖无反应,但对胰高血糖素和精氨酸敏感。对自发性糖尿病BB大鼠的β细胞在出生后的头6天用葡萄糖联合胰高血糖素或精氨酸进行刺激,以加速β细胞成熟,并可能诱导抗原表达和耐受性。在生命的前200天里,接受葡萄糖和胰高血糖素治疗的BB大鼠中只有23%患糖尿病,接受葡萄糖和精氨酸治疗的BB大鼠中这一比例为20%,而未治疗的对照组中这一比例为65%。这一发现可能解释了以下观察结果:患有1型糖尿病的母亲的孩子患该病的可能性比患有1型糖尿病的父亲的孩子低三倍。糖尿病妊娠期间β细胞的提前成熟可能预防日后患糖尿病。

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