Diabetic peripheral neuropathy (DPN) is a leading risk factor for diabetes-related mortality and morbidity. However, only a few have been utilized in systematic studies designed to answer unsolved problems associated with the disorder in man such as molecular basis, pathogenesis of the vascular and neural lesions, and the roles of diet, exercise and obesity. Typical apoptotic nuclear and cytoplasmic changes are observed. Thirteen days of treatment with fenofibrate, a peroxisome proliferator-activated receptor alpha (PPARα) selective agonist, produced a dose-dependent decrease in serum lipid levels. Unfortunately, this strain is relatively resistant to the development of DN [18•]; therefore, a lengthy and expensive breeding program may be required to backcross genetic mutations onto a more susceptible strain such FVB and DBA/2J mice. Increased vanin activity was observed in plasma and liver of high fat diet (HFD)-induced obese mice, as well as ZDF-diabetic rats. A neuropathy phenotype in rodents was defined as the presence of statistically different values between diabetic and control animals in 2 of 3 assessments (nocifensive behavior, nerve conduction velocities, or nerve structure).
Mice were killed according to the established Institutional Animal Care and Use Committee guidelines. O. In patients with diabetes, atherosclerosis represents a complex multifactorial disease with increased lesion progression and severity compared to the nondiabetic population. Lai and A.