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2019
DOI: 10.1038/s41598-019-53149-7
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The analgesic effect of refeeding on acute and chronic inflammatory pain

Abstract: Pain is susceptible to various cognitive factors. Suppression of pain by hunger is well known, but the effect of food intake after fasting (i.e. refeeding) on pain remains unknown. In the present study, we examined whether inflammatory pain behavior is affected by 24 h fasting and 2 h refeeding. In formalin-induced acute inflammatory pain model, fasting suppressed pain behavior only in the second phase and the analgesic effect was also observed after refeeding. Furthermore, in Complete Freund’s adjuvant-induce… Show more

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Cited by 15 publications
(15 citation statements)
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“…Additionally, with LitLab™, we found strong associations between the genes that comprised our organ network and pain signaling and physiological response to pain. In line with this, fasting and calorie restriction have an analgesic effect in murine models [ [77] , [78] , [79] ], and intermittent fasting was proposed as a non-invasive, inexpensive, and implementable strategy to chronic pain treatment (reviewed in [ 80 ]). Key underlying mechanisms in fasting-enhanced neuroplasticity include a short-term corticosterone increase, a reduction in GABAergic inhibition, and an increase in protein chaperons and neurotrophic growth factors such as brain-derived neurotrophic factor (BDNF), which exerts positive effects on neuronal survival and synaptogenesis [ [81] , [82] , [83] ].…”
Section: Discussionmentioning
confidence: 99%
“…Additionally, with LitLab™, we found strong associations between the genes that comprised our organ network and pain signaling and physiological response to pain. In line with this, fasting and calorie restriction have an analgesic effect in murine models [ [77] , [78] , [79] ], and intermittent fasting was proposed as a non-invasive, inexpensive, and implementable strategy to chronic pain treatment (reviewed in [ 80 ]). Key underlying mechanisms in fasting-enhanced neuroplasticity include a short-term corticosterone increase, a reduction in GABAergic inhibition, and an increase in protein chaperons and neurotrophic growth factors such as brain-derived neurotrophic factor (BDNF), which exerts positive effects on neuronal survival and synaptogenesis [ [81] , [82] , [83] ].…”
Section: Discussionmentioning
confidence: 99%
“…Additionally, with LitLab™, we found strong associations between the genes comprised in our organ network and pain signaling and physiological response to pain. In line with this, fasting and calorie restriction have an analgesic effect in murine models [64][65][66], and intermittent fasting was proposed as a non-invasive, inexpensive, and implementable strategy to chronic pain treatment (reviewed in [67]). Key underlying mechanisms in fasting-enhanced neuroplasticity include activation of short-term corticosterone increase, reduction in GABAergic inhibition, and increase in protein chaperons and neurotrophic growth factors such as brain-derived neurotrophic factor (BDNF), which exerts positive effects on neuronal survival and synaptogenesis [68][69][70].…”
Section: A Brain-liver-fats Organ Network Modulated By Stfmentioning
confidence: 96%
“…This type of pain usually appears after an illness or injury, however it is not understood as a symptom but as a characteristic of the condition [ 4 ]. Chronic pain can be classified as nociceptive or neuropathic [ 2 ], with the central and the peripheral nervous systems being affected by the multiple etiologies that cause pain [ 5 , 6 ]. It can vary greatly from one person to another and even within the same individual depending on the context [ 6 , 7 ].…”
Section: Introductionmentioning
confidence: 99%