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Hyperglycaemia and central obesity disrupt conditioned pain modulation: A single-blind cross-over randomised controlled trial
Journal article   Open access   Peer reviewed

Hyperglycaemia and central obesity disrupt conditioned pain modulation: A single-blind cross-over randomised controlled trial

Di Ye, Timothy Fairchild, Dr Lechi Vo and Peter Drummond
The Journal of Pain, Vol.25(9), 104553
2024
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Abstract

Hyperglycaemia and high adiposity are risk factors for pain in diabetes. To clarify these links with pain, the effects of a glucose load on sensory detection, pain sensitivity, conditioned pain modulation (primary aims), and autonomic and endothelial functions (secondary aims) were examined in 64 pain-free participants: 22 with normal adiposity (determined by dual-energy X-ray absorptiometry), 29 with high adiposity, and 13 with combined high adiposity and elevated glycated haemoglobin (HbA1c; including prediabetes and type 2 diabetes). Participants ingested either 37.5-g glucose or 200-mg sucralose (taste-matched) in the first session and crossed over to the other substance in the second session one month later. At baseline, painful temple cooling (the conditioning stimulus) inhibited pressure- and heat-pain in the ipsilateral arm (the test stimuli) immediately after cooling ceased (partial η2’s >.32). Glucose ingestion weakened pressure-pain inhibition irrespective of HbA1c levels (partial η2 =.11). However, a larger reduction in pressure-pain inhibition after ingesting glucose was associated with a higher waist/hip ratio (r =.31), suggesting a role of central obesity. Heat-pain inhibition was absent at baseline in unmedicated participants with elevated HbA1c, and these participants reported more occlusion-induced pain after ingesting glucose (partial η2’s >.17). Glucose ingestion interfered with parasympathetic activity in all participants (partial η2 =.11) but did not affect endothelial function (measured by reactive hyperaemia) or alter other sensations (e.g., feet vibration detection). The disruptive effect of hyperglycaemia on conditioned pain modulation increases in line with central obesity, which might facilitate pain in diabetes. Lay summary: Ingesting 37.5-g glucose (approximately 350-mL soft drink) interfered with pain processing in pain-free, normal-weight adults as well as those with combined overweight and high blood glucose levels. The interference was stronger alongside increasing waistline, suggesting that controlling blood glucose and body fat mass might reduce risk of chronic pain.

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