Evaluation of the relationship between leptin, resistin, adiponectin and natural regulatory T cells in relapsing-remitting multiple sclerosis

Kraszula, Łukasz; Jasińska, Anna; Eusebio, Makandjou-Ola; Kuna, Piotr; Głąbiński, Andrzej; Pietruczuk, Mirosława

doi:10.5114/ninp.2012.27211

Cited by 75 publications

(77 citation statements)

References 30 publications

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“…Previous studies have demonstrated that adiponectin increases insulin sensitivity, displays anti-atherogenic activity, and regulates the levels of glucose and fatty acids [10,11]. Recently, the association of adiponectin with neurological diseases, including both cerebrovascular diseases and NDDs, has attracted attention [48,53,55,61,64,67,72]. However, the exact role of adiponectin in the CNS is unclear.…”

Section: Discussion and Future Prospectsmentioning

confidence: 97%

“…Numerous studies have examined the association between adiponectin and neurological diseases [48,53,55,61,64,67,72]. Most of the available data are clinical [44,45] and do not fully provide insight regarding causality.…”

Section: Discussion and Future Prospectsmentioning

confidence: 97%

“…However, the adiponectin and adipsin levels in CSF did not correlate with their levels in plasma [70]. Kraszula et al [67] evaluated adiponectin and natural regulatory T (nTreg) cells in patients with relapsing-remitting MS (RRMS). RRMS patients were found to exhibit significantly decreased adiponectin levels, a reduced percentage of nTreg cells, and reduced mean fluorescence channel (MFC) of FoxP3, suggesting that adiponectin plays a role in the anti-inflammatory response and inhibits FoxP3 expression in RRMS patients.…”

Section: Warren Et Al 2012 [65]mentioning

confidence: 98%

“…MS is a chronic inflammatory disease of the brain and the spinal cord [67]. As such, researchers have evaluated the association of adiponectin with inflammatory mediators and cell types.…”

Section: Msmentioning

confidence: 99%

See 3 more Smart Citations

The emerging role of adiponectin in cerebrovascular and neurodegenerative diseases

Yang

Jiang

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Section: Discussion and Future Prospectsmentioning

confidence: 97%

Section: Discussion and Future Prospectsmentioning

confidence: 97%

Section: Warren Et Al 2012 [65]mentioning

confidence: 98%

“…MS is a chronic inflammatory disease of the brain and the spinal cord [67]. As such, researchers have evaluated the association of adiponectin with inflammatory mediators and cell types.…”

Section: Msmentioning

confidence: 99%

See 2 more Smart Citations

The emerging role of adiponectin in cerebrovascular and neurodegenerative diseases

Yang

Jiang

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

View full text Add to dashboard Cite

“…Leptin-deficiency also protects otherwise susceptible mice from developing other experimentally-induced inflammatory diseases including colitis, type I diabetes, hepatitis, and experimental autoimmune encephalomyelitis (EAE), where administration of leptin results in a shift in T cell response and restores disease susceptibility [66]. Leptin is increased in MS patients and this is associated with increased levels of immune mediators including IFNc, TNFa and IL-1b and decreased Tregs [67,68]. Additionally, increased leptin expression has also been reported in Behçet's disease [69], psoriasis [70], and during the acute phase of ulcerative colitis, but leptin levels are reportedly decreased in ankylosing spondylitis and ANCA-associated vasculitis [71][72][73].…”

Section: Leptinmentioning

confidence: 98%

Adipokines influence the inflammatory balance in autoimmunity

Hutcheson

2015

Cytokine

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Immunologic Effects of Metformin and Pioglitazone Treatment on Metabolic Syndrome and Multiple Sclerosis

Negrotto¹,

Farez²,

Correale³

2016

JAMA Neurol

153

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IMPORTANCE Metabolic syndrome (MetS) is thought to influence several autoimmune diseases, including multiple sclerosis (MS). Anti-inflammatory effects of treatments used for MetS, such as metformin hydrochloride and pioglitazone hydrochloride, have been demonstrated, although clinical evidence supporting use of these treatments in MS is lacking.OBJECTIVES To determine whether metformin and/or pioglitazone are associated with a reduction in disease activity as measured by brain magnetic resonance imaging in patients with MS and MetS and to evaluate the potential mechanisms underlying this anti-inflammatory effect. DESIGN, SETTING, AND PARTICIPANTSA prospective cohort study was conducted from March 1, 2012, to December 30, 2014, at a private MS referral center among 50 obese patients with MS who also developed MetS. Twenty patients received metformin hydrochloride, 850 to 1500 mg/d, and 10 patients received pioglitazone hydrochloride, 15 to 30 mg/d; 20 untreated patients served as controls. Groups were comparable in terms of sex, age, body mass index, Expanded Disability Status Scale score, disease duration, annual relapse rate, and treatment status. Patients were followed up for a mean (SD) of 26.7 (2.7) months (range, 24-33 months). MAIN OUTCOMES AND MEASURESMagnetic resonance imaging of the brain was performed at 6-month intervals, and the presence of new or enlarging T2 lesions or gadolinium-enhancing lesions was registered. Serum leptin and adiponectin levels were measured. The production of cytokines by peripheral blood mononuclear cells was assayed, as were regulatory T-cell numbers and function. RESULTSOf 50 patients, after 6 months of treatment, 20 patients with MS who were treated with metformin and 10 who received pioglitazone showed a significant decrease in the number of new or enlarging T2 lesions (metformin, 2.5 at study entry to 0.5 at month 24; pioglitazone, 2.3 at study entry to 0.6 at month 24), as well as of gadolinium-enhancing lesions (metformin, 1.8 at study entry to 0.1 at month 24; pioglitazone, 2.2 at study entry to 0.3 at month 24). Compared with controls, both treatments led to a decrease in mean (SD) leptin levels (metformin, 5.5 [2.4] vs 10.5 [3.4] ng/mL, P < .001; pioglitazone, 4.1 [0.8] vs 11.0 [2.6] ng/mL, P < .001) and increase in mean (SD) adiponectin serum levels (metformin, 15.4 [5.5] vs 4.5 [2.4] μg/mL, P < .001; pioglitazone, 12.6 [3.6] vs 4.8 [0.6] μg/mL, P < .001). Mean (SD) number of myelin basic protein peptide-specific cells secreting interferon γ and interleukin (IL)-17 were significantly reduced in patients receiving metformin compared with controls (interferon γ, 30.3 [11.5] vs 82.8 [18.8], P < .001; 212.4 [85.5] vs 553.8 [125.9], P < .001). Patients treated with pioglitazone showed significant decreases in the mean (SD) number of myelin basic protein peptide-specific cells secreting IL-6 and tumor necrosis factor compared with controls (IL-6, 361.6 [80.5] vs 1130.7 [149.21], P < .001; tumor necrosis factor, 189.9 [53.4] vs 341.0 [106.0], P < .001). Both metformin and...

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Evaluation of the relationship between leptin, resistin, adiponectin and natural regulatory T cells in relapsing-remitting multiple sclerosis

Cited by 75 publications

References 30 publications

The emerging role of adiponectin in cerebrovascular and neurodegenerative diseases

The emerging role of adiponectin in cerebrovascular and neurodegenerative diseases

Adipokines influence the inflammatory balance in autoimmunity

Immunologic Effects of Metformin and Pioglitazone Treatment on Metabolic Syndrome and Multiple Sclerosis

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