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Epidemiological studies have shown that obesity and diabetes mellitus may be risk factors for colon cancer. However, the underlying mechanisms of how these chronic diseases promote colon carcinogenesis remain unknown. C57BL/KsJ-db/dbmice have obese and diabetic phenotypes because of disruption of the leptin receptor. The present study was designed to investigate whether development of azoxymethane (AOM)-induced dysplastic and early neoplastic (premalignant) lesions of the colon is modulated indb/dbmice. Homozygousdb/dbmice, heterozygousdb/+ mice and littermate controls (+/+) were injected with AOM under food restriction (∼10.8 kcal/mouse/day) and killed 5 weeks after the carcinogen treatment. Their colons were assessed for premalignant lesions induced by AOM. We found a significant increase in the multiplicity of the total premalignant lesions indb/dbmice when compared withdb/+ or +/+ mice. Phenotypically, serum leptin and insulin levels indb/dbmice were significantly higher than those indb/+ or +/+ mice, whereas the body weights and glucose levels in blood ofdb/db,db/+ and +/+ mice were comparable. In addition, immunostaining of the leptin receptor and insulin-like growth factor-I receptor showed up-regulation of these protein levels specifically in the lesions. Our data indicate that development of AOM-induced premalignant lesions is enhanced indb/dbmice with hyperleptinemia and hyperinsulinemia. The results have important implications for further exploration of the possible underlying events that affect the positive association between colon cancer and chronic diseases (obesity and diabetes).

carcinogenesis

Enhancement of development of azoxymethane-induced colonic premalignant lesions in C57BL/KsJ-              db              /              db               mice