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Metabolic signals and innate immune activation in obesity and exercise
Robert Ringseis, Klaus Eder, Frank Christoph Mooren, Karsten Krüger. Exercise immunology review, 2015-01-01
Topic: Brain proteins, microglia and lab models
The combination of a sedentary lifestyle and excess energy intake has led to an increased prevalence of obesity which constitutes a major risk factor for several co-morbidities including type 2 diabetes and cardiovascular diseases. Intensive research during the last two decades has revealed that a characteristic feature of obesity linking it to insulin resistance is the presence of chronic low-grade inflammation being indicative of activation of the innate immune system. Recent evidence suggests that activation of the innate immune system in the course of obesity is mediated by metabolic signals, such as free fatty acids (FFAs), being elevated in many obese subjects, through activation of pattern recognition receptors thereby leading to stimulation of critical inflammatory signaling cascades, like IκBα kinase/nuclear factor-κB (IKK/NF- κB), endoplasmic reticulum (ER) stress-induced unfolded protein response (UPR) and NOD-like receptor P3 (NLRP3) inflammasome pathway, that interfere with insulin signaling. Exercise is one of the main prescribed interventions in obesity management improving insulin sensitivity and reducing obesity- induced chronic inflammation. This review summarizes current knowledge of the cellular recognition mechanisms for FFAs, the inflammatory signaling pathways triggered by excess FFAs in obesity and the counteractive effects of both acute and chronic exercise on obesity-induced activation of inflammatory signaling pathways. A deeper understanding of the effects of exercise on inflammatory signaling pathways in obesity is useful to optimize preventive and therapeutic strategies to combat the increasing incidence of obesity and its comorbidities.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Ringseis, R., Eder, K., Mooren, F. C., & Krüger, K. (2015). Metabolic signals and innate immune activation in obesity and exercise. Exercise immunology review. https://doi.org/10.22029/eir.2015.1696
Vancouver
Ringseis R, Eder K, Mooren FC, Krüger K. Metabolic signals and innate immune activation in obesity and exercise. Exercise immunology review. 2015. doi:10.22029/eir.2015.1696. PMID: 25825956.
BibTeX
@article{ringseis2015-25825956,
author = {Ringseis, Robert and Eder, Klaus and Mooren, Frank Christoph and Krüger, Karsten},
title = {{Metabolic signals and innate immune activation in obesity and exercise}},
journal = {Exercise immunology review},
year = {2015},
doi = {10.22029/eir.2015.1696},
pmid = {25825956},
url = {https://doi.org/10.22029/eir.2015.1696}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- Intensive research during the last two decades has revealed that a characteristic feature of obesity linking it to insulin resistance is the presence of chronic low-grade inflammation being indicative of activation of the innate immune system.
- Recent evidence suggests that activation of the innate immune system in the course of obesity is mediated by metabolic signals, such as free fatty acids (FFAs), being elevated in many obese subjects, through activation of pattern recognition receptors thereby leading to stimulation of critical inflammatory signaling cascades, like IκBα kinase/nuclear factor-κB (IKK/NF- κB), endoplasmic reticulum (ER) stress-induced unfolded protein response (UPR) and NOD-like receptor P3 (NLRP3) inflammasome pathway, that interfere with insulin signaling.
Why it matters
This review is about metabolic signals and innate immune activation in obesity and exercise, and it does not address Alzheimer's disease. It describes how free fatty acids can trigger inflammatory signaling that interferes with insulin signaling, and how exercise improves insulin sensitivity and reduces obesity-induced chronic inflammation.
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Study details
- Evidence strengthLow
How this study scored 35/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it. We have no data on journal's citation record, so that was left out: it earned 34 of the 96 points we could judge it on, which is 35 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Exercise immunology review) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2015 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 123 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 9.5 citations a year over 13 year(s) since 2015 |
| Impact for its field and year | 0 / 6 | Cited 0.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 1 / 4 | Cited 8 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Karsten Krüger: h-index 40 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Justus-Liebig-Universität Gießen: institution h-index 661 (OpenAlex) |
| Multicenter collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 25825956) |
| Free to read | 2 / 2 | Free to read |
| Points | 34 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 34 of the 96 points we could judge it on is 35 out of 100. |
| Total | 35 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.22029/eir.2015.1696
- PubMed: 25825956
- Original source →
- Free full text: Universitätsbibliothek Gießen →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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