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非胰岛素依赖型糖尿病——节俭基因与富足社会之间的冲突。

Non-insulin-dependent diabetes mellitus--a collision between thrifty genes and an affluent society.

作者信息

Groop L C, Tuomi T

机构信息

Department of Endocrinology, Lund University, Malmö, Sweden.

出版信息

Ann Med. 1997 Feb;29(1):37-53. doi: 10.3109/07853899708998742.

DOI:10.3109/07853899708998742
PMID:9073323
Abstract

Non-insulin-dependent diabetes mellitus (NIDDM) is one of the most common non-communicable diseases in the world. It has become obvious that NIDDM is the result of a collision between thrifty genes and an affluent society. Genes predisposing to NIDDM might have been survival genes for our ancestors, helping them to store energy during long periods of starvation. When these genes are exposed to a sedentary lifestyle and high caloric intake typical to the Western world, they predispose to obesity and insulin resistance. NIDDM results when beta cells cannot compensate for insulin resistance by increasing insulin secretion. Therefore, at least two inherited defects can be expected in NIDDM, one causing obesity and insulin resistance and the other inability to increase insulin secretion. In reality there may be more inherited defects. It has become quite clear that diabetes cannot simply be divided into NIDDM and insulin-dependent diabetes mellitus (IDDM). The disease is more heterogeneous; unmasking this heterogeneity and identifying new subgroups of diabetes presents a challenge to modern molecular biology.

摘要

非胰岛素依赖型糖尿病(NIDDM)是世界上最常见的非传染性疾病之一。很明显,NIDDM是节俭基因与富裕社会碰撞的结果。易患NIDDM的基因可能曾是我们祖先的生存基因,帮助他们在长期饥饿期间储存能量。当这些基因暴露于西方世界典型的久坐不动的生活方式和高热量摄入时,它们会导致肥胖和胰岛素抵抗。当β细胞无法通过增加胰岛素分泌来补偿胰岛素抵抗时,就会发生NIDDM。因此,预计NIDDM中至少会有两种遗传缺陷,一种导致肥胖和胰岛素抵抗,另一种导致无法增加胰岛素分泌。实际上可能存在更多的遗传缺陷。很明显,糖尿病不能简单地分为NIDDM和胰岛素依赖型糖尿病(IDDM)。这种疾病更加异质性;揭示这种异质性并识别糖尿病的新亚组对现代分子生物学提出了挑战。

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