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
“…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] ].…”
Objective
Fasting regimens can promote health, mitigate chronic immunological disorders, and improve age-related pathophysiological parameters in animals and humans. Several ongoing clinical trials are using fasting as a potential therapy for various conditions. Fasting alters metabolism by acting as a reset for energy homeostasis, but the molecular mechanisms underlying the beneficial effects of short-term fasting (STF) are not well understood, particularly at the systems or multiorgan level.
Methods
We performed RNA-sequencing in nine organs from mice fed
ad libitum
(0 h) or subjected to fasting five times (2–22 h). We applied a combination of multivariate analysis, differential expression analysis, gene ontology, and network analysis for an in-depth understanding of the multiorgan transcriptome. We used literature mining solutions, LitLab™ and Gene Retriever™, to identify the biological and biochemical terms significantly associated with our experimental gene set, which provided additional support and meaning to the experimentally derived gene and inferred protein data.
Results
We cataloged the transcriptional dynamics within and between organs during STF and discovered differential temporal effects of STF among organs. Using gene ontology enrichment analysis, we identified an organ network sharing 37 common biological pathways perturbed by STF. This network incorporates the brain, liver, interscapular brown adipose tissue, and posterior-subcutaneous white adipose tissue; hence, we named it the
brain-liver-fats
organ network. Using Reactome pathways analysis, we identified the immune system, dominated by T cell regulation processes, as a central and prominent target of systemic modulations during STF in this organ network. The changes we identified in specific immune components point to the priming of adaptive immunity and parallel the fine-tuning of innate immune signaling.
Conclusions
Our study provides a comprehensive multiorgan transcriptomic profiling of mice subjected to multiple periods of STF and provides new insights into the molecular modulators involved in the systemic immunotranscriptomic changes that occur during short-term energy loss.
“…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] ].…”
Objective
Fasting regimens can promote health, mitigate chronic immunological disorders, and improve age-related pathophysiological parameters in animals and humans. Several ongoing clinical trials are using fasting as a potential therapy for various conditions. Fasting alters metabolism by acting as a reset for energy homeostasis, but the molecular mechanisms underlying the beneficial effects of short-term fasting (STF) are not well understood, particularly at the systems or multiorgan level.
Methods
We performed RNA-sequencing in nine organs from mice fed
ad libitum
(0 h) or subjected to fasting five times (2–22 h). We applied a combination of multivariate analysis, differential expression analysis, gene ontology, and network analysis for an in-depth understanding of the multiorgan transcriptome. We used literature mining solutions, LitLab™ and Gene Retriever™, to identify the biological and biochemical terms significantly associated with our experimental gene set, which provided additional support and meaning to the experimentally derived gene and inferred protein data.
Results
We cataloged the transcriptional dynamics within and between organs during STF and discovered differential temporal effects of STF among organs. Using gene ontology enrichment analysis, we identified an organ network sharing 37 common biological pathways perturbed by STF. This network incorporates the brain, liver, interscapular brown adipose tissue, and posterior-subcutaneous white adipose tissue; hence, we named it the
brain-liver-fats
organ network. Using Reactome pathways analysis, we identified the immune system, dominated by T cell regulation processes, as a central and prominent target of systemic modulations during STF in this organ network. The changes we identified in specific immune components point to the priming of adaptive immunity and parallel the fine-tuning of innate immune signaling.
Conclusions
Our study provides a comprehensive multiorgan transcriptomic profiling of mice subjected to multiple periods of STF and provides new insights into the molecular modulators involved in the systemic immunotranscriptomic changes that occur during short-term energy loss.
“…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
Different fasting regiments are known to promote health, and chronic immunological disorders and mitigate age-related pathophysiological parameters in animals and humans. Indeed, several clinicals trials are currently ongoing using fasting as a potential therapy for a wide range of conditions. Fasting alters metabolism by acting as a reset for energy homeostasis, but the molecular mechanisms underlying the beneficial effects of short-term fasting (STF) are still not-well understood, particularly at a systems/multiorgan level. We investigated the dynamic gene expression patterns associated with periods of STF in nine different mouse organs. First, we identified both unique and shared transcriptional signatures at the organ and systemic levels. Second, we discovered differential temporal effects of STF among organs. Third, using gene ontology enrichment analysis, we identified an organ network, formed by the 63 common biological pathways perturbed by STF. This network incorporates the brain, liver, interscapular brown, and perigonadal white adipose tissue, hence we name it the brain-liver-fats organ network. Fourth, we identified that the immune system, dominated by T cell regulation processes, is a central and prominent target of systemic modulations during short-term energy loss in this organ network. The changes we identified in specific immune components point to the priming of adaptive immunity and parallel the fine-tuning of innate immune signaling. In conclusion, our study provides a comprehensive multi-organ transcriptomic profiling of mice subjected to multiple periods of STF and added new insights into the molecular modulators involved in the systemic immuno-transcriptomic changes that occur during short-term energy loss.
“…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 ].…”
Food strategies are currently used to improve inflammation and oxidative stress conditions in chronic pain which contributes to a better quality of life for patients. The main purpose of this systematic review is to analyze the effectiveness of different dietary strategies as part of the treatment plan for patients suffering from chronic pain and decreased health. PubMed, Web of Science, ProQuest, Scopus, Cumulative Index to Nursing & Allied Health Literature (CINAHL), Cambridge Core, and Oxford Academy databases were used to review and to appraise the literature. Randomized clinical trials (RCT), observational studies, and systematic reviews published within the last 6 years were included. The Physiotherapy Evidence Database (PEDro) scale, the PEDro Internal Validity (PVI), the Standard Quality Assessment Criteria for Evaluating Primary Research Papers from a variety of fields (QUALSYT), and the Quality Assessment Tool of Systematic Reviews scale were used to evaluate the risk of bias of the included studies. A total of 16 articles were included, of which 11 were RCTs and 5 were observational studies. Six of them showed an improvement in pain assessment, while two studies showed the opposite. Inflammation was shown to be decreased in four studies, while one did not show a decrease. The quality of life was shown to have improved in five studies. All of the selected studies obtained good methodological quality in their assessment scales. In the PVI, one RCT showed good internal validity, five RCTs showed moderate internal quality, while five of them were limited. Current research shows that consensus on the effects of an IF diet on pain improvement, in either the short or the long term, is lacking. A caloric restriction diet may be a good long term treatment option for people suffering from pain. Time restricted food and ketogenic diets may improve the quality of life in chronic conditions. However, more studies analyzing the effects of different nutritional strategies, not only in isolation but in combination with other therapies in the short and the long term, are needed.
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