Repeated use of powered hand-tools can result in the development of vibration-induced neuropathy in the hands of workers. It has been hypothesized that workers with metabolic syndrome or diabetes may be at greater risk of developing a vibration-induced neuropathy. However, these workers are usually excluded from epidemiological studies, so their risk of developing a vibration-induced neuropathy is unknown. The goal of this study was to use a rat-tail model of hand-arm vibration syndrome to characterize changes in sensory nerve function that occur in response to vibration exposure in fatty Zucker rats, an animal model of metabolic syndrome. Rats were exposed to tail vibration or restraintcontrol conditions 4 h/day for 10 days. A-beta, A-delta, and C-fiber function was assessed using transcutaneous electrical stimulation at 3 different frequencies. Average thresholds at each frequency were analyzed using mixed-model ANOVAs. Thresholds were measured before and after vibration exposure on days 1, 5 and 10. Previous data from our lab demonstrated that repeated exposure to vibration results in a reduction in A-beta and A-delta fiber thresholds and demyelination of tail nerves in Sprague Dawley rats. In this study vibration also resulted in a reduction in A-betafiber thresholds in lean (control) but not in fatty Zucker rats, suggesting vibration may have increased sensitivity to mechanical stimuli in lean rats. The increase in A-beta-fiber sensitivity was associated with an increase in circulating calcitonin-gene related peptide (CGRP) concentrations in lean rats. In contrast, circulating CGRP concentrations were reduced by vibration in fatty rats. Vibration did not affect A-delta- or C-fiber thresholds in either group of rats. These findings suggest that metabolic disorder or diabetes may not increase the risk of developing a vibration-induced neuropathy. They also suggest that changes in circulating CGRP levels may serve as an early biomarker for detecting vibration-induced nerve injuries in workers.