We appreciate Dr. Wagner's interest in our article and her comments regarding sex differences between the TallyHo/JnJ mice. In our recent article, “The TallyHo Polygenic Mouse Model of Diabetes: Implications in Wound Healing,”1 we used only male TallyHo mice. Sex dimorphism for the diabetic phenotype is commonly observed in murine models of type 2 diabetes, and the TallyHo strain is no exception. In 2006, Kim et al. published an extensive phenotypic analysis of the TallyHo strain, demonstrating that male mice developed diabetes whereas female mice did not.2 It has been postulated that the protection of diabetes in female mice is at least partially attributable to estrogen-dependent increases in insulin receptors in the hepatocyte membranes and low hepatic estrogen sulfotransferase activity, which prevent insulin resistance and virilization of liver metabolism, respectively.3,4 Although female TallyHo mice do not express an overt diabetic phenotype, they are more obese, with mild hyperinsulinemia, mild hypertriglyceridemia, and pancreatic islet cell hypertrophy when compared with nondiabetic control mice. As a result, they do represent an obese, nondiabetic murine model.
Although there is a paucity of literature specifically defining blood glucose levels required for the diagnosis of diabetes in mice, there is substantial evidence regarding the development of the cellular derangements characteristic of diabetes and the correlative blood glucose levels at which they occur.2 The progression of type 2 diabetes is characterized by impaired glucose tolerance, insulin resistance, and finally failure of insulin secretion. Simplistically, these events could be characterized by hyperglycemia, hyperinsulinemia, and pancreatic islet cell hypertrophy and/or atrophy. The male TallyHo mouse begins this progression at 4 weeks of age and, by the eighth week of life, exhibits significantly impaired glucose tolerance, insulin resistance, and islet cell hypertrophy, consistent with diabetes. The blood glucose levels at 8 weeks are above the 200-mg/dl range and continue to rise, peaking in the 300- to 400-mg/dl range by 14 weeks of life.1
Donald W. Buck, II, M.D.
Thomas A. Mustoe, M.D.
Division of Plastic and Reconstructive Surgery, Northwestern University, Feinberg School of Medicine, Chicago, Ill.
1. Buck DW II, Jin DP, Geringer M, Hong SJ, Galiano RD, Mustoe TA. The TallyHo polygenic mouse model of diabetes: Implications in wound healing. Plast Reconstr Surg. 2011;128:427e–437e. Epublished ahead of print July 5, 2011.
2. Kim JH, Stewart TP, Soltani-Bejnood M, et al.. Phenotypic characterization of polygenic type 2 diabetes in TALLYHO/JngJ mice. J Endocrinol. 2006;191:437–446.
3. Leiter EH, Chapman HD. Obesity-induced diabetes (diabesity) in C57BL/KsJ mice produces aberrant trans-regulation of sex steroid sulfotransferase genes. J Clin Invest. 1994;93:2007–2013.
4. Krakower GR, Meier DA, Kissebah AH. Female sex hormones, perinatal, and peripubertal androgenization on hepatocyte insulin dynamics in rats. Am J Physiol. 1993;264:E342–E347.
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