Exp Clin Endocrinol Diabetes 2014; 122(2): 100-106
DOI: 10.1055/s-0033-1363234
Review
© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Animal Models of Diabetic Neuropathic Pain

F. Gao
1   Department of Endocrinology, First Hospital of Shijiazhuang City, Shijiazhuang, China
,
Z. M. Zheng
1   Department of Endocrinology, First Hospital of Shijiazhuang City, Shijiazhuang, China
› Author Affiliations
Further Information

Publication History

received 15 September 2013
first decision 21 November 2013

accepted 27 November 2013

Publication Date:
19 February 2014 (online)

Abstract

Diabetic neuropathy is a common complication of diabetes. It occurs in approximately 10–20% of patients with diabetes, or roughly 40–50% patients with diabetic neuropathy. However, the pathogenesis of diabetic neuropathic pain is still largely unknown. Several animal models have been used to study the underlying mechanisms for this complication. Some commonly used animal models include streptozotocin-induced rat and mouse models, diet/nutrition-induced models, combination of chemically- and nutrition-induced model, Zucker diabetic fatty rat model, type 1 insulinopenic BB/Wor and type 2 hyperinsulinemic diabetic BBZDR/Wor rat models, and transgenic/knock-out models. Even though the manifestations of diabetic neuropathic pain vary from thermal or chemical hyperalgesia, thermal or chemical hypoalgeia, allodynia, to spontaneous pain, some pathogenesis factors are shared among these symptoms. Increased AR activity, oxidative-nitrosative stress, protein kinase C, PARP and ACE activations, C-peptide deficiency, impaired neurotrophism, and proinflammatory responses have been identified in the development of diabetic neuropathic pain. This review discusses selected animal models for diabetic neuropathic pain, as well as some commonly shared pathways in these models.

 
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