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Influence of Dietary Carbohydrate on the Induction of Diabetes in C57BL/KsJ-db/db Diabetes Mice¹

Edward H. Leiter^*, Douglas L. Coleman^*, Donald K. Ingram and Mark A. Reynolds

^* The Jackson Laboratory, Bar Harbor ME 04609 Gerontology Research Center, National Institute of Aging, Baltimore City Hospital, Baltimore, MD 21224

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.

KEY WORDS: • diabetes • mice • longevity • carbohydrate sensitivity • endocrine pancreas

¹ This research was supported by grants AM 17631 and AM 27722 from the National Institute of Arthritis, Diabetes, and Digestive and Kidney Diseases and by a grant from the Juvenile Diabetes Foundation.

Manuscript received 26 July 1982.