Alternatives to the Streptozotocin-Diabetic Rodent

Abstract

The study of diabetic neuropathy has relied primarily on the use of streptozotocin-treated rat and mouse models of type 1 diabetes. This chapter will review the creation and use of other rodent models that have been developed in order to investigate the contribution of factors besides insulin deficiency to the development and progression of diabetic neuropathy as it occurs in obesity, type 1 or type 2 diabetes. Diabetic peripheral neuropathy is a complex disorder with multiple mechanisms contributing to its development and progression. Even though many animal models have been developed and investigated, no single model can mimic diabetic peripheral neuropathy as it occurs in humans. Nonetheless, animal models can play an important role in improving our understanding of the etiology of diabetic peripheral neuropathy and in performing preclinical screening of potential new treatments. To date treatments found to be effective for diabetic peripheral neuropathy in rodent models have failed in clinical trials. However, with the identification of new endpoints for the early detection of diabetic peripheral neuropathy and the understanding that a successful treatment may require a combination therapeutic approach there is hope that an effective treatment will be found.

New Horizons in Diabetic Neuropathy: Mechanisms, Bioenergetics, and Pain

“…With the recent advent of over 20 murine models of DN, there is a rich variety of experimental models from which to choose from for DN research beyond the STZ rat. These experimental models provide the tools for future research to more fully understand the differences between DN in T1D and T2D (Islam, 2013; O’Brien et al, 2014b; Yorek, 2016). …”

C-Peptide replacement therapy in type 1 diabetes: are we in the trough of disillusionment?

“…Consequently, the authors question the validity of the diabetic rodent to be an accurate representation of diabetes in humans due to this difference in hyperglycemic time-scale, and this may be the cause of contradictory results observed between human and diabetic-animal model studies of C-peptide replacement and other diabetes drugs. 44 …”

Wound healing mechanisms in rats with streptozotocin-induced diabetes mellitus

“…Результаты теста болевой чувствительности показали, что у крыс группы СД на исследуемых сроках ранозаживления развивается периферическая нейропатия, затрагивающая чувствительные нервные окончания [11,12]. Морфологические изменения кожи животных и иммуногистохимические данные согласуются с развитием нейропатии, что позволяет говорить о взаимосвязи этих изменений.…”

“…Такие клетки формируют неполноценные щелевые контакты, в них усиливается окислительный стресс, повышается уровень апоптоза. В окружающих кератиноциты тканях при сахарном диабете нарушен ангиогенез, избыточно продуцируются матриксные металлопротеиназы, высоки риски инфицирования [10][11][12]. Все это способствует формированию хронической незаживающей раны.…”