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Alterations in the resting state functional connectivity and hyperperfusion of pain processing areas of the brain have been demonstrated in painful-Diabetic Peripheral Neuropathy (DPN). However, the mechanisms underlying these abnormalities are poorly understood. There is thus a good rationale to explore if there is higher energy consumption in the pain processing areas of the brain. We performed a 31Phosphorus Magnetic Resonance Spectroscopy (31P-MRS) study to explore cellular energy usage (bioenergetics) in the primary somatosensory (S1) cortex in a wellcharacterised cohort of participants with painful- and painless-DPN. S1 PCr:ATP, a measure of energy consumption, was significantly reduced in painfulcompared with painless-DPN. This is indicative of greater S1 cortical energy consumption in painful-DPN. Furthermore, S1 PCr:ATP correlated with pain intensity during the MRI. S1 PCr:ATP was also significantly lower in painful-DPN individuals with moderate/severe pain compared to those with low pain. This is the first study to demonstrate higher S1 cortical energy metabolism in painfulcompared with painless-DPN. Moreover, the relationship between PCr:ATP and neuropathic pain measures shows that S1 bioenergetics is related to the severity of neuropathic pain. S1 cortical energetics may represent a biomarker of painful-DPN and could have the potential to serve as a target for therapeutic interventions.