Defective glucose and lipid metabolism in rheumatoid arthritis is determined by chronic inflammation in metabolic tissues
Journal of Internal Medicine, ISSN: 1365-2796, Vol: 284, Issue: 1, Page: 61-77
2018
- 40Citations
- 39Captures
- 8Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations40
- Citation Indexes40
- 40
- CrossRef31
- Captures39
- Readers39
- 39
- Mentions8
- News Mentions8
- 8
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Article Description
Background: Rheumatoid arthritis (RA) patients are at increased risk of insulin resistance (IR); however, the specific mechanisms mediating this association are currently unknown. Objective: To investigate whether the inflammatory activity associated with RA accounts for the observed defective glucose metabolism and lipid metabolism in these patients. Methods: We followed two main strategies: (i) extensive metabolic profiling of a RA cohort of 100 patients and 50 healthy control subjects and (ii) mechanistic studies carried out in both a collagen-induced arthritis mouse model and 3T3-L1 adipocytes treated with conditioned serum from RA patients. Results: Following the exclusion of obese and diabetic subjects, data from RA patients demonstrated a strong link between the degree of systemic inflammation and the development of IR. These results were strengthened by the observation that induction of arthritis in mice resulted in a global inflammatory state characterized by defective carbohydrate and lipid metabolism in different tissues. Adipose tissue was most susceptible to the RA-induced metabolic alterations. These metabolic effects were confirmed in adipocytes treated with serum from RA patients. Conclusions: Our results show that the metabolic disturbances associated with RA depend on the degree of inflammation and identify inflammation of adipose tissue as the initial target leading to IR and the associated molecular disorders of carbohydrate and lipid homeostasis. Thus, we anticipate that therapeutic strategies based on tighter control of inflammation and flares could provide promising approaches to normalize and/or prevent metabolic alterations associated with RA.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85043469292&origin=inward; http://dx.doi.org/10.1111/joim.12743; http://www.ncbi.nlm.nih.gov/pubmed/29532531; https://onlinelibrary.wiley.com/doi/10.1111/joim.12743; http://doi.wiley.com/10.1111/joim.12743; https://onlinelibrary.wiley.com/doi/abs/10.1111/joim.12743
Wiley
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