The goal of this research is understand if obesity is a major factor for neuropathy development in patients with and without Type 2 diabetes. This study will examine the relationship between weight, metabolism, and nerve function and regeneration.
Peripheral neuropathy causes progressive injury to the longest nerves of the body, starting in the toes, then progressing slowly up the leg. Neuropathy often causes pain, numbness, and weakness if the feet and can lead to reduced mobility, foot ulcers, and even amputation. The most common cause is diabetes, but work at the University of Utah finds that prediabetes and other consequences of obesity, including abnormal cholesterol levels, may be associated with neuropathy. Research has shown that these risk factors may damage nerves and interfere with the ability of nerves to grow back after an injury. This study aims to 1. characterize peripheral nerve function and cutaneous nerve structure in obese bariatric surgery candidates; 2. evaluate peripheral nerve regeneration capacity (and other nerve function measures) before and after bariatric surgery in obese subjects with no or mild neuropathy; 3. examine the relationship between ectopic lipid accumulation, lipotoxic mediators, neuropathy and regeneration capacity in surgical candidates before and one year after surgery.
Study Type
OBSERVATIONAL
Enrollment
205
University of Utah
Salt Lake City, Utah, United States
Change in reinnervation capacity
Time frame: 4 - 1 months prior to bariatric surgery, compared to 9 - 12 months after surgery
Change in Utah Early Neuropathy Scale (UENS)
Time frame: Baseline to 12 months after bariatric surgery
Change in Nerve Conduction Study measures
Nerve Conduction Study is a procedure routinely used in the diagnosis of neuropathy. Measures will include Sural sensory and Peroneal motor amplitudes and conduction velocities.
Time frame: Baseline to 12 months after bariatric surgery
Change in nerve fiber density
Time frame: Baseline to 12 months after bariatric surgery
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