The role of leptin in the pathophysiology of rheumatoid arthritis

Toussirot, Éric; Michel, Fabrice; Binda, Delphine; Dumoulin, Gilles

doi:10.1016/j.lfs.2015.05.001

Cited by 42 publications

(38 citation statements)

References 100 publications

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“…Leptin, a key regulator of appetite, by inducing the expression of anorexigenic factors and inhibiting the production of orexigenic peptides, stimulates the production of TNFα, IL‐6, and IL‐12. In turn, TNFα and IL1 up‐regulate leptin production 38. While elevated serum and synovial fluid leptin levels were reported in RA,38 conventional DMARDs and TNF blockers did not modify the levels of leptin 38.…”

Section: Discussionmentioning

confidence: 97%

“…37 However, many authors consider leptin, resistin, and visfatin as pro-inflammatory mediators, whereas adiponectin can have pro-inflammatory or antiinflammatory properties depending on the isoform studied. 38,39 Leptin, a key regulator of appetite, by inducing the expression of anorexigenic factors and inhibiting the production of orexigenic peptides, stimulates the production of TNFα, IL-6, and IL-12. In turn, TNFα and IL1 upregulate leptin production.…”

Section: Discussionmentioning

confidence: 99%

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Changes in body composition and metabolic profile during interleukin 6 inhibition in rheumatoid arthritis

Tournadre

Pereira

Dutheil

et al. 2017

J cachexia sarcopenia muscle

145

132

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BackgroundRheumatoid arthritis (RA) is a chronic inflammatory disease characterized by increased mortality associated with cardiometabolic disorders including dyslipidaemia, insulin resistance, and cachectic obesity. Tumour necrosis factor inhibitors and interleukin 6 receptor blocker licensed for the treatment of RA decrease inflammation and could thus improve cardiovascular risk, but their effects on body composition and metabolic profile need to be clarified. We investigated the effects of tocilizumab (TCZ), a humanized anti‐interleukin 6 receptor antibody, on body composition and metabolic profile in patients treated for RA.MethodsTwenty‐one active RA patients treated with TCZ were included in a 1 year open follow‐up study. Waist circumference, body mass index, blood pressure, lipid profile, fasting glucose, insulin, serum levels of adipokines and pancreatic/gastrointestinal hormones, and body composition (dual‐energy X‐ray absorptiometry) were measured at baseline and 6 and 12 months of treatment. At baseline, RA patients were compared with 21 non‐RA controls matched for age, sex, body mass index, and metabolic syndrome.ResultsCompared with controls, body composition was altered in RA with a decrease in total and appendicular lean mass, whereas fat composition was not modified. Among RA patients, 28.6% had a skeletal muscle mass index below the cut‐off point for sarcopaenia (4.8% of controls). After 1 year of treatment with TCZ, there was a significant weight gain without changes for fat mass. In contrast, an increase in lean mass was observed with a significant gain in appendicular lean mass and skeletal muscle mass index between 6 and 12 months. Distribution of the fat was modified with a decrease in trunk/peripheral fat ratio and an increase in subcutaneous adipose tissue. No changes for waist circumference, blood pressure, fasting glucose, and atherogenic index were observed.ConclusionsDespite weight gain during treatment with TCZ, no increase in fat but a modification in fat distribution was observed. In contrast, muscle gain suggests that blocking IL‐6 might be efficient in treating sarcopaenia associated with RA.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Changes in body composition and metabolic profile during interleukin 6 inhibition in rheumatoid arthritis

Tournadre

Pereira

Dutheil

et al. 2017

J cachexia sarcopenia muscle

145

132

View full text Add to dashboard Cite

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“…Although the aetiology and pathogenesis of BD are not clear, increased serum levels of proinflammatory cytokines could be involved in the pathogenesis of BD, influencing factors such as inflammation, thrombosis of the small arteries and veins, increased neutrophil activity and chemotaxis, and activation of circulating T and B cells . Adipose tissues are a source of adipokines, which induce the expression of proinflammatory cytokines, which in turn increase concentrations of circulating adipokines . Individual studies have used different laboratory methods to detect these adipokines, and so each study's values may not be comparable with others or may need a correction factor applied.…”

Section: Discussionmentioning

confidence: 99%

Association of circulating resistin, leptin, adiponectin and visfatin levels with Behçet disease: a meta-analysis

Lee

Song

2018

Clin Exp Dermatol

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“…High levels of leptin both systemically and in the joints have been reported by some authors - also correlating with disease activity [121] - but other studies found no changes or even low levels of leptin and no correlations with disease biomarkers or activity scores [122]. …”

Section: Leptin and Autoimmunitymentioning

confidence: 99%

Leptin in inflammation and autoimmunity

2017

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After its discovery as a key controller of metabolic function, leptin has been later extensively implicated in additional function including important modulatory activities on the innate and adaptive immune responses. This review analyzes the known implications of leptin in multiple inflammatory conditions, including autoimmune diseases, and how this knowledge could be instrumental in the design of leptin-based manipulation strategies to help restoration of abnormal immune responses.

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The role of leptin in the pathophysiology of rheumatoid arthritis

Cited by 42 publications

References 100 publications

Changes in body composition and metabolic profile during interleukin 6 inhibition in rheumatoid arthritis

Changes in body composition and metabolic profile during interleukin 6 inhibition in rheumatoid arthritis

Association of circulating resistin, leptin, adiponectin and visfatin levels with Behçet disease: a meta-analysis

Leptin in inflammation and autoimmunity

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