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膳食碳水化合物对C57BL/KsJ-db/db糖尿病小鼠糖尿病诱导的影响。

Influence of dietary carbohydrate on the induction of diabetes in C57BL/KsJ-db/db diabetes mice.

作者信息

Leiter E H, Coleman D L, Ingram D K, Reynolds M A

出版信息

J Nutr. 1983 Jan;113(1):184-95. doi: 10.1093/jn/113.1.184.

DOI:10.1093/jn/113.1.184
PMID:6337242
Abstract

Genetically diabetic C57BL/KsJ-db/db and normal littermate mice of both sexes were fed one of nine defined diets from weaning. The objective was to study dietary carbohydrate interaction with the diabetogenic genes through isocaloric substitution of protein for carbohydrate (either sucrose or dextrin starch) at concentrations of 0, 8, 24, and 60%. In addition, at 60% concentration, the effect of type of carbohydrate (e.g., glucose, fructose, sucrose or dextrin starch) on the deterioration of endocrine pancreatic structure and function was analyzed. The carbohydrate-free diet produced the greatest survival to 1 year of age and allowed the expression of an obesity syndrome uncomplicated by severe hyperglycemia or by extensive necrosis of pancreatic beta cells and islet atrophy. Those diets containing intermediate levels of carbohydrate (8 or 24% of sucrose or dextrin), or 60% dextrin starch, in comparison to diets containing 60% refined carbohydrates, extended life span and produced a more protracted pathogenesis, but were unable to circumvent eventual severe hyperglycemia and islet destruction. The diets containing 60% glucose, fructose, or sucrose all led to the rapid induction of diabetes. Thus, pathogenesis entails an interaction between dietary carbohydrate, the db gene, and other diabetes-predisposing genes in the genome.

摘要

将遗传性糖尿病的C57BL/KsJ-db/db小鼠及其正常同窝出生的雌雄小鼠从断奶起喂食九种规定饮食中的一种。目的是通过在0%、8%、24%和60%的浓度下用蛋白质等热量替代碳水化合物(蔗糖或糊精淀粉)来研究饮食碳水化合物与致糖尿病基因的相互作用。此外,在60%的浓度下,分析碳水化合物类型(如葡萄糖、果糖、蔗糖或糊精淀粉)对内分泌胰腺结构和功能恶化的影响。无碳水化合物饮食使活到1岁的存活率最高,并使肥胖综合征得以表现,且未并发严重高血糖或胰腺β细胞广泛坏死及胰岛萎缩。与含60%精制碳水化合物的饮食相比,含中等水平碳水化合物(8%或24%的蔗糖或糊精)或60%糊精淀粉的饮食可延长寿命并产生更持久的发病过程,但无法避免最终的严重高血糖和胰岛破坏。含60%葡萄糖、果糖或蔗糖的饮食均导致糖尿病的快速诱导。因此,发病机制涉及饮食碳水化合物、db基因和基因组中其他糖尿病易感基因之间的相互作用。

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