• Adipocytes
• IL-6
• Irisin
• Osteogenesis
• TLR4/MyD88/NF-κB

• Animals
• Fibronectins/metabolism
• Fibronectins/genetics
• Toll-Like Receptor 4/metabolism
• Myeloid Differentiation Factor 88/metabolism
• Interleukin-6/metabolism
• Interleukin-6/genetics
• Obesity/complications
• Obesity/metabolism
• Mice
• Adipocytes/metabolism
• NF-kappa B/metabolism
• Mice, Knockout
• Diet, High-Fat/adverse effects
• Signal Transduction
• Male
• Osteogenesis
• Mice, Inbred C57BL
• Mesenchymal Stem Cells/metabolism
• Cell Differentiation

• Adipokines
• inflammation
• omentin-1
• psoriasis
• resistin
• vaspin

• Humans
• Animals
• GPI-Linked Proteins/genetics
• GPI-Linked Proteins/metabolism
• Lectins/genetics
• Lectins/metabolism
• Cytokines/genetics
• Cytokines/metabolism
• Adiponectin/genetics
• Adiponectin/metabolism
• Psoriasis/genetics
• Psoriasis/metabolism
• Psoriasis/pathology
• Serpins/genetics
• Serpins/metabolism
• Signal Transduction

• autoimmunity
• biologics
• imiquimod
• macrophages
• modern dermatological treatment
• mouse models
• psoriasiform dermatitis
• psoriasis
• rodent disease models
• skin diseases

• Psoriasis/immunology
• Psoriasis/pathology
• Animals
• Macrophages/immunology
• Macrophages/metabolism
• Disease Models, Animal
• Mice
• Humans
• Langerhans Cells/immunology
• Langerhans Cells/pathology
• Immunity, Innate
• Skin/pathology
• Skin/immunology
• Skin/metabolism

• N41/DBS/001026 Ministry of Science and Higher Education
• N41/DBS/001119 Ministry of Science and Higher Education

• Autoimmunity
• Enteropathy
• In vitro osteoclastogenesis
• Osteoclast
• Rheumatic disease

• adipokines
• axial spondyloarthritis
• bone erosion
• rheumatoid arthritis
• syndesmophyte

• Bone loss
• Exercise
• Glucocorticoid
• Kefir
• Osteoporosis

We aimed to evaluate the association between adipose tissue (AT) dysfunction, autoimmunity, and disease activity in rheumatoid arthritis (RA). A cross-sectional study including 150 RA patients and 50 healthy donors and longitudinal study with 122 RA patients treated with anti-tumor necrosis factor (TNF)-α, anti-interleukin 6 receptor (IL6R) or anti-CD20 therapies for 6 months were carried out. In vitro experiments with human AT and adipocyte and macrophage cell lines were performed. A collagen-induced arthritis mouse model was developed. The insulin resistance and the altered adipocytokine profile were associated with disease activity, the presence of anti-citrullinated proteins anti-bodies (ACPAs), and worse response to therapy in RA. AT in the context of arthritis is characterized by an inflammatory state alongside the infiltration of macrophages and B/plasmatic cells, where ACPAs can have a direct impact, inducing inflammation and insulin resistance in macrophages and promoting a defective adipocyte differentiation, partially restored by biologicals.

•

IR is related to disease activity, inflammation, and autoimmunity in RA patients

• Adipokines
• Arthritis
• Atherosclerosis
• Inflammation
• MACE
• Sarcopenia
• Visceral fat

• Adipokines/blood
• Adult
• Arthritis, Psoriatic/complications
• Arthritis, Psoriatic/physiopathology
• Body Mass Index
• Cardiovascular Diseases/etiology
• Carotid Intima-Media Thickness
• Cross-Sectional Studies
• Female
• Heart Disease Risk Factors
• Humans
• Male
• Middle Aged
• Spondylarthritis/complications
• Spondylarthritis/physiopathology

• ACPA = anti‐cyclic citrullinated peptide antibodies
• ACR = American college of rheumatology
• ACTB = actin beta
• BMI = body mass index
• CRP = C-reactive protein
• CV = cardiovascular
• DAPSA = disease activity in psoriatic arthritis
• DAS28 = disease activity score 28
• DMARDs = disease-modifying anti-rheumatic drugs
• ESR = erythrocyte sedimentation rate
• EULAR = European league against rheumatism
• HAQ = health assessment questionnaire
• HC = healthy controls
• HDL = high density lipoprotein
• HMW = high molecular weight
• IGF = insulin-like growth factor
• IL = interleukin
• LDL = low density lipoprotein
• LMW = low molecular weight
• MAPK = mitogen-activated protein kinase
• MMW = medium molecular weight
• NF‐κB = nuclear factor κB
• NSAIDs = non-steroidal anti-inflammatory drugs
• OA = osteoarthritis
• PASI = psoriasis area severity index
• PBMCs = peripheral blood mononuclear cells
• PsA = psoriatic arthritis
• RA = rheumatoid arthritis
• RF = rheumatoid factor
• SIRT‐1 = silencing the gene for sirtuin
• SNORD-25 = small nucleolar RNA = C/D Box 25
• TGF-β = activity and in transforming growth factor
• TNF = tumor necrosis factor
• VAS = visual analogue scale
• VEGF = vascular endothelial growth factor
• miRNA = microRNA

• Axial spondyloarthritis
• cardiometabolic comorbidity
• interleukin-17A; treatment
• psoriatic arthritis

Greater than 90% of patients with psoriatic arthritis (PsA) first develop their arthritis on a background of known psoriasis (Pso). Thus, having skin/nail Pso certainly is an important risk factor for PsA but as PsA develops in <30% of those affected with Pso, the presence of Pso alone is insufficient as a means of identifying which patients with Pso will develop PsA. It is hoped that with further molecular assessment of Pso patients who do not have any evidence of inflammatory musculoskeletal disease compared to those with early PsA features, that the “at risk” profile of Pso patients destined to develop PsA can be refined such that disease prevention studies can be designed and a new era of treatment for PsA can emerge. In this article, the early stages in the development of PsA are outlined and what is currently known about clinical features, genetic factors and soluble or tissue biomarkers associated with the development of PsA in patients with Pso is reviewed in detail. Finally, proposals are outlined regarding the approaches required in order to address this important research area.

• biomarkers
• genomics
• proteomics
• psoriasis
• psoriatic arthritis
• risk factors

Recent studies suggest a role of adipokines in the pathogenesis of hidradenitis suppurativa (HS). Omentin-1 and apelin are two recently identified adipokines that have been involved in the regulation of metabolic and inflammatory responses.

To investigate serum omentin-1 and apelin levels in patients with HS and to assess their associations with metabolic parameters, disease severity and HS risk.

This case-control study included 139 non-diabetic individuals (78 HS patients and 61 ageand sex-matched controls). Serum concentrations of omentin-1 and apelin and the homeostasis model assessment of insulin resistance (HOMA-IR) were measured in all participants.

Serum omentin-1 concentrations were significantly higher in HS patients compared to controls, whereas apelin serum levels did not significantly differ between both groups. These differences in omentin-1 concentrations remained significant even after adjusting for age, sex, and body mass index (BMI). The results of logistic regression analysis showed that increased omentin-1 plasma levels were an independent risk factor for HS. However, we found no association between serum levels of both omentin-1 and apelin with HS severity.

Our results show that patients with HS have raised omentin-1 serum levels, which are associated with HS risk.

• adipokines
• apelin
• hidradenitis suppurativa
• omentin

Deregulation of adiponectin is found in systemic autoimmune rheumatic diseases (SARDs). Its expression is downregulated by various inflammatory mediators, but paradoxically, elevated serum levels are present in SARDs with high inflammatory components, such as rheumatoid arthritis and systemic lupus erythematosus. Circulating adiponectin is positively associated with radiographic progression in rheumatoid arthritis as well as with cardiovascular risks and lupus nephritis in systemic lupus erythematosus. However, in SARDs with less prominent inflammation, such as systemic sclerosis, adiponectin levels are low and correlate negatively with disease activity. Regulators of adiponectin gene expression (PPAR-γ, Id3, ATF3, and SIRT1) and inflammatory cytokines (interleukin 6 and tumor necrosis factor α) are differentially expressed in SARDs and could therefore influence total adiponectin levels. In addition, anti-inflammatory therapy could also have an impact, as tocilizumab treatment is associated with increased serum adiponectin. However, anti-tumor necrosis factor α treatment does not seem to affect its levels. Our review provides an overview of studies on adiponectin levels in the bloodstream and other biological samples from SARD patients and presents some possible explanations why adiponectin is deregulated in the context of therapy and gene regulation.

• PPAR-γ
• adiponectin
• gene regulation
• interleukin 6
• systemic autoimmune rheumatic diseases
• therapy
• tumor necrosis factor α

The goals of our study were to determine the possible association of interleukin (IL)-31 with Th17 cytokine profile in serum and to quantify retinoic acid-related orphan receptor C (RORC) mRNA expression in psoriatic arthritis (PsA) patients. This cross-sectional study was conducted in 50 patients with PsA and 30 control subjects (CS) matched by age and gender. The cytokine serum levels were quantified by magnetic bead–based assay using the Bio-Plex MAGPIX system, and RORC mRNA expression was determined by quantitative polymerase chain reaction (qPCR). As a result, significant differences in IL-31 were observed between study groups (77.23 pg/mL in PsA vs 64.4 pg/mL in CS, P < 0.001) and Th17 cytokine profile serum levels (IL-17A: 6.36 pg/mL in PsA vs 2.97 pg/mL in CS, P = 0.02; IL-17F: 44.15 pg/mL in PsA vs 23.36 pg/mL in PsA, P = 0.01; IL-17E: 3.03 pg/mL in PsA vs 0.82 pg/mL in CS, P < 0.001; IL-21: 36.45 pg/mL in PsA vs 12.44 pg/mL in CS, P = 0.02); however, significant differences were not observed for IL-23 (31.2 pg/mL in PsA vs 53.26 pg/mL in CS, P = 0.58). Furthermore, positive correlations between IL-31 and Th17 cytokine profile serum levels were found (IL-17A: r_s = 0.64, P < 0.001; IL-17F: r_s = 0.73, P < 0.001; IL-17E: r_s = 0.70, P < 0.001; IL-21: r_s = 0.54, P = 0.002; IL-23: r_s = 0.5, P < 0.01). Regarding RORC gene expression, the PsA group showed an increase of 6.85-fold compared to the CS group. We did not find any association between the serum levels of cytokines and RORC gene expression. In conclusion, in PsA, there are increased serum levels of IL-31, IL-17A, IL-17F, IL-17E, and IL-21, but not IL-23. Moreover, there was a positive correlation of IL-31 with the Th17 cytokine profile and a high RORC gene expression. Altogether, these findings suggest a proinflammatory contribution of IL-31 in close association with the Th17 cytokine profile in PsA.

• IL-31
• RORC
• Th17 cytokine profile
• mRNA expression
• psoriatic arthritis

• LEPR (ObR), osteoarthritis (OA)
• articular cartilage
• chondrocyte
• leptin
• rheumatoid arthritis (RA)

• Animals
• Cartilage, Articular/metabolism
• Cartilage, Articular/physiopathology
• Humans
• Leptin/metabolism
• Osteoarthritis/metabolism
• Osteoarthritis/pathology
• Receptors, Leptin/metabolism
• Signal Transduction

Psoriatic arthritis is a chronic inflammatory disease with skin and joint pathology as the dominant characteristics. Scientific evidence supports its systemic nature and relevant relationship with obesity, metabolic syndrome, and associated conditions. Metabolic syndrome and obesity share common signaling pathways with joint inflammation, reinforcing the idea that adipose tissue is a major contributor to disease development and severity. The adipose tissue is not a mere energy store but also an endocrine organ participating in the immune response. In the search for the best therapeutic strategy for a patient, we should appraise the adipose tissue as an endocrine and immune organ responsible for mild chronic inflammation. Today, our challenge is not only to achieve disease remission but to control the associated comorbidities as well. In light of the high prevalence of obesity in psoriatic arthritis patients and the importance of the adipose tissue in the development of chronic inflammation, we aimed to identify the most relevant articles in this regard published in English until June 2020 using the PubMed database. Search terms included psoriatic arthritis, in combination with metabolic syndrome, obesity, adipokines, cardiovascular disease, and treatment. This review summarizes the current evidence regarding the role of adipose tissue as an adipokine-secreting endocrine organ, discussing its influence on disease development and severity, and ultimately in meeting successful disease management.

• adipokines
• cardiovascular risk
• metabolic syndrome
• obesity
• pathophysiology
• psoriatic arthritis
• treatment

• ankylosing spondylitis
• biomarker
• proximity extension assay
• psoriasis
• psoriatic arthritis
• spondyloarthritis

• adipocytokines
• adipokines
• autoimmunity
• rheumatic diseases
• rheumatoid arthritis

Background. This study investigated the effect of non-surgical periodontal treatment on clinical indices and salivary levels of visfatin, chemerin, and progranulin in diabetic patients with periodontitis.

Methods. This interventional clinical trial was performed on 20 patients with type II diabetes mellitus (T2DM) with moderate to severe chronic periodontitis (periodontitis stages II or III according to the new classification of periodontal diseases). Clinical indices, including gingival index (GI), probing pocket depth (PPD), clinical attachment level (CAL) and plaque index (PI), were recorded and visfatin, chemerin, and progranulin adipokines levels were also measured in unstimulated saliva by ELISA technique at baseline and twelve weeks after non-surgical periodontal treatment.

Results. GI dropped from 1.92±0.27 to 0.71±0.14 after the intervention (P<0.001). Also, there were significant changes in the PPD and PI (P<0.001). However, no significant changes were observed in the CAL (P<0.05). The concentrations of all three salivary adipokines decreased after treatment, but this change was statistically significant only for progranulin (P<0.05).

Conclusion. Non-surgical periodontal therapy resulted in improvements in the clinical indices of GI, PPD, and PI in T2DM patients with periodontitis. Moreover, the significant reduction in the salivary level of progranulin after treatment suggests that it might be considered a target inflammatory marker in periodontal diseases.

• Adipokines
• Human chemerin protein
• Non-surgical periodontal debridement
• Periodontitis
• Type 2 diabetes mellitus
• Visfatin
• progranulin

• adipokines
• adiponectin
• autoimmune
• leptin
• rheumatology

• Adipokines/immunology
• Animals
• Humans
• Inflammation/immunology
• Musculoskeletal Diseases/immunology

• adipokines
• inflammation
• rheumatoid arthritis
• spondyloarthritis
• structural damage

• Adipokines/metabolism
• Animals
• Arthritis/metabolism
• Arthritis/pathology
• Humans
• Inflammation/metabolism
• Inflammation/pathology
• Joints/metabolism
• Joints/pathology
• Rheumatic Diseases/metabolism
• Rheumatic Diseases/pathology

• metabolic syndrome
• omentin
• psoriasis
• psoriatic arthritis
• visfatin

• Adipokine
• Attack
• Colchicine resistance
• Familial Mediterranean fever
• Omentin

• Genomics
• Microbiome
• Multi-omics
• Personalized medicine
• Precision medicine
• Proteomics
• Psoriasis
• Psoriatic arthritis
• Seronegative spondyloarthritis
• Transcriptomics

• Ankylosing spondylitis
• heart failure with preserved ejection fraction
• psoriatic arthritis
• rheumatoid arthritis
• systemic lupus erythematosus

• Adipokines
• Association
• Leptin
• Sarcoidosis

• Pathogenesis
• Psoriatic arthritis
• Treatment

Rheumatic diseases encompass a diverse group of chronic disorders that commonly affect musculoskeletal structures. Osteoarthritis (OA) and rheumatoid arthritis (RA) are the two most common, leading to considerable functional limitations and irreversible disability when patients are unsuccessfully treated. Although the specific causes of many rheumatic conditions remain unknown, it is generally accepted that immune mechanisms and/or uncontrolled inflammatory responses are involved in their etiology and symptomatology. In this regard, the bidirectional communication between neuroendocrine and immune system has been demonstrated to provide a homeostatic network that is involved in several pathological conditions. Adipokines represent a wide variety of bioactive, immune and inflammatory mediators mainly released by adipocytes that act as signal molecules in the neuroendocrine-immune interactions. Adipokines can also be synthesized by synoviocytes, osteoclasts, osteoblasts, chondrocytes and inflammatory cells in the joint microenvironment, showing potent modulatory properties on different effector cells in OA and RA pathogenesis. Effects of adiponectin, leptin, resistin and visfatin on local and systemic inflammation are broadly described. However, more recently, other adipokines, such as progranulin, chemerin, lipocalin-2, vaspin, omentin-1 and nesfatin, have been recognized to display immunomodulatory actions in rheumatic diseases. This review highlights the latest relevant findings on the role of the adipokine network in the pathophysiology of OA and RA.

• adipokine
• inflammation
• osteoarthritis
• rheumatic diseases
• rheumatoid arthritis

• Puerarin
• hypercalcemia
• meta-analysis
• murine model
• ovariectomy
• postmenopausal osteoporosis.

• biomarkers
• osteoarthritis
• psoriatic arthritis

• Adult
• Aged
• Arthritis, Psoriatic/diagnosis
• Biomarkers/blood
• Cartilage Oligomeric Matrix Protein/blood
• Chemokine CCL2/blood
• Diagnosis, Differential
• Female
• Humans
• Male
• Middle Aged
• Nerve Growth Factor/blood
• Osteoarthritis/diagnosis
• ROC Curve
• Reproducibility of Results
• Resistin/blood
• Severity of Illness Index
• Solubility

• Adipocytes/metabolism
• Aging/metabolism
• Aging/pathology
• Animals
• Body Weight/physiology
• Bone Resorption/metabolism
• Bone Resorption/pathology
• Bone Resorption/therapy
• Exercise/physiology
• Humans
• Muscle, Skeletal/metabolism
• Muscle, Skeletal/pathology
• Obesity/metabolism
• Obesity/pathology
• Obesity/therapy
• Osteoblasts/metabolism
• Osteoporosis/metabolism
• Osteoporosis/pathology
• Osteoporosis/therapy
• Stem Cells/metabolism

• P2C HD086843 NICHD NIH HHS
• R01 AR073264 NIAMS NIH HHS
• P30 DK056350 NIDDK NIH HHS
• U01 HL127522 NHLBI NIH HHS
• R01 AR075803 NIAMS NIH HHS
• R01 AR066616 NIAMS NIH HHS

Secretion from adipose tissue of adipokines or adipocytokines, comprising of bioactive peptides or proteins, immune molecules and inflammatory mediators, exert critical roles in inflammatory arthritis and obesity. This review considers the evidence generated over the last decade regarding the effects of several adipokines including leptin, adiponectin, visfatin, resistin, chemerin and apelin, in cartilage and bone homeostasis in the pathogenesis of rheumatoid arthritis and osteoarthritis, which has important implications for obesity.

• adipokines
• obesity
• osteoarthritis
• rheumatoid arthritis

Local priming of osteoclast precursors (OCp) has long been considered the main and obvious pathway that takes place in the human body, where local bone lining cells and RANKL-expressing osteocytes may facilitate the differentiation of OCp. However, priming of OCp away from bone, such as in inflammatory tissues, as revealed in peripheral blood, may represent a second pathway, particularly relevant in individuals who suffer from systemic bone loss such as prevalent in inflammatory diseases. In this review, we used a systematic approach to review the literature on osteoclast formation in peripheral blood in patients with inflammatory diseases associated with bone loss. Only studies that compared inflammatory (bone) disease with healthy controls in the same study were included. Using this core collection, it becomes clear that experimental osteoclastogenesis using peripheral blood from patients with bone loss diseases in prevalent diseases such as rheumatoid arthritis, osteoporosis, periodontitis, and cancer-related osteopenia unequivocally point toward an intrinsically increased osteoclast formation and activation. In particular, such increased osteoclastogenesis already takes place without the addition of the classical osteoclastogenesis cytokines M-CSF and RANKL in vitro. We show that T-cells and monocytes as OCp are the minimal demands for such unstimulated osteoclast formation. In search for common and disease-specific denominators of the diseases with inflammation-driven bone loss, we demonstrate that altered T-cell activity and a different composition—such as the CD14+CD16+ vs. CD14+CD16– monocytes—and priming of OCp with increased M-CSF, RANKL, and TNF- α levels in peripheral blood play a role in increased osteoclast formation and activity. Future research will likely uncover the barcodes of the OCp in the various inflammatory diseases associated with bone loss.

• CD14+CD16+
• T-cells
• inflammatory bone diseases
• osteoclast formation
• osteoclast precursor priming
• peripheral blood

Obesity is over-represented in patients with psoriatic arthritis (PsA) and associated with higher disease activity, poorer effect of treatment and increased cardiovascular morbidity. Studies on the effects of weight loss are however needed. This study aimed to prospectively study the effects of weight loss treatment with very low energy diet (VLED) on disease activity in patients with PsA (CASPAR criteria) and obesity (body mass index BMI ≥ 33 kg/m²).

VLED (640 kcal/day) was taken during 12–16 weeks, depending on pre-treatment BMI. Afterwards, an energy-restricted diet was gradually reintroduced. Weight loss treatment was given within a structured framework for support and medical follow-up.

Treatment with conventional synthetic and/or biologic disease-modifying anti-rheumatic drugs was held constant from 3 months before, until 6 months after baseline.

Patients were assessed with BMI, 66/68 joints count, Leeds enthesitis index, psoriasis body surface area (BSA), questionnaires and CRP at baseline, 3 and 6 months. Primary outcome was the percentage of patients reaching minimal disease activity (MDA) and secondary outcomes were reaching Psoriatic Arthritis Response Criteria (PsARC) and American College of Rheumatology (ACR) response criteria.

Totally 41/46 patients completed the study, 63% women, median age 54 years (IQR 48–62). At baseline increased BMI was associated with higher disease activity and poorer function.

The median weight loss was 18.7 kg (IQR 14.6–26.5) or 18.6% (IQR 14.7–26.3) of the baseline weight. A majority of the disease activity parameters improved significantly after weight loss, including 68/66 tender/swollen joints count, CRP, BSA, Leeds enthesitis index, HAQ and patient VAS for global health, pain and fatigue. A larger weight loss resulted in more improvement in a dose-response manner. The percentage of patients with MDA increased from 29 to 54%, (p = 0.002). PsARC was reached by 46.3%. The ACR 20, 50 and 70 responses were 51.2%, 34.1% and 7.3% respectively.

Short-term weight loss treatment with VLED was associated with significant positive effects on disease activity in joints, entheses and skin in patients with PsA and obesity. The study supports the hypothesis of obesity as a promotor of disease activity in PsA.

ClinicalTrials.gov identifier: NCT02917434, registered on September 21, 2016—retrospectively registered

The online version of this article (10.1186/s13075-019-1810-5) contains supplementary material, which is available to authorized users.

• Cardiovascular disease
• Metabolic syndrome
• Obesity
• Psoriasis
• Psoriatic arthritis
• VLED
• Weight loss

Osteoprotegerin (OPG) is a soluble glycoprotein that belongs to the tumor necrosis factor (TNF) receptor superfamily. OPG is mainly secreted by bone. The relationship between acute resistance training, serum OPG levels and metabolic syndrome, including insulin resistance, remains unclear. The purpose of this study was to determine the effect of resistance exercise on serum OPG levels and insulin resistance in middle-aged women with metabolic syndrome.

Twenty-four middle-aged women were divided into those with metabolic syndrome (n=12) and a normal control group without metabolic syndrome or insulin resistance (n=12). Metabolic syndrome was diagnosed according to the National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) criteria. The quantitative insulin-sensitivity check index (QUICKI) and the homeostatic model assessment (HOMA) index for assessing beta-cell function and insulin resistance were used. The intensity of the resistance exercise was 60–70% of the repetition maximum, for 40 minutes with 10–12 repetitions, performed three times per week. Venous blood samples were tested using standard laboratory procedures.

Before exercise, the metabolic syndrome group showed a significant increase in waist circumference (P=0.030) and serum triglyceride (TG) (P=0.014), and lower high-density lipoprotein-cholesterol (HDL-C) (P=0.010) compared with the control group. After the eight-week resistance exercise program, waist circumference, and the QUICKI decreased and OPG levels were significantly increased in the metabolic syndrome group compared with the normal control group.

A resistance exercise program was effective in reducing factors associated with metabolic syndrome including insulin resistance and increases serum levels of OPG in middle-aged women.

• Cardiovascular disease
• Inflammation
• Metabolic syndrome
• Obesity
• PsA
• RA

• body mass index
• disease activity
• inflammation
• obesity
• rheumatic and musculoskeletal diseases (RMDs)

• Adipokines
• Connective tissue diseases
• Inflammatory arthritis
• Leptin
• Vasculitis

Adipokines, secreted by the adipose tissue, are extensively involved in the regulation and maintenance of various physiological and pathological processes, including insulin sensitivity, energy expenditure, glucose and lipid metabolism, inflammatory activity, neuroendocrine activity, immunity, cancer, homeostasis, angiogenesis, cardiovascular function, breeding and bone metabolism, and all functions of the endocrine-reproductive system axis. Omentin is a recently identified adipokine, which has become a research hotspot due to its pleiotropic effects on various diseases. However, the specific receptor for omentin has not been identified so far. In this study, we report that omentin levels fluctuate in various diseases. In addition, we have focused on the pleiotropic roles of omentin in pulmonary diseases, as it may act as a biomarker for malignant pleural mesothelioma (MPM) and is related to disease severity. Omentin may play significant roles in other pulmonary diseases, such as asthma, obstructive sleep apnea syndrome (OSAS), pulmonary arterial hypertension (PAH), acute respiratory distress syndrome (ARDS), and chronic obstructive pulmonary disease (COPD). This review summarizes the advances in current knowledge and future trends, which may provide a concise and general view on omentin and its effects on pulmonary biology.

• ARDS
• COPD
• MPM
• OSAS
• PAH
• adipokines
• adipose tissue
• asthma
• omentin
• respiratory diseases

• RANKL signaling pathways
• anti-psoriatic pharmacotherapy (APP)
• arthritis
• in silico screening
• multi-target
• natural compounds
• osteoclast
• preclinical study

• T cells
• adaptive immunity
• biologics
• skin inflammation
• systemic inflammation

• Adipokine
• meta-analysis
• omentin-1
• polycystic ovary syndrome

• Adult
• Cytokines/blood
• Down-Regulation
• Female
• GPI-Linked Proteins/blood
• Humans
• Insulin Resistance
• Lectins/blood
• Obesity/blood
• Obesity/complications
• Overweight/blood
• Overweight/complications
• Polycystic Ovary Syndrome/blood
• Polycystic Ovary Syndrome/complications
• Reproducibility of Results

The structure and physiological state of the local white adipose tissue (WAT) located underneath the lesional psoriatic skin and inside of the joints affected by psoriatic arthritis play an important role in the pathophysiology of these diseases. WAT pads associated with inflammatory sites in psoriasis and psoriatic arthritis are, correspondingly, dermal WAT and articular adipose tissue; these pads demonstrate inflammatory phenotypes in both diseases. Such local WAT inflammation could be the primary effect in the pathophysiology of psoriasis leading to the modification of the local expression of adipokines, a change in the structure of the basement membrane and the release of keratinocytes with consequent epidermal hyperproliferation during psoriasis. Similar articular adipose tissue inflammation can lead to the induction of structural modifications and synovial inflammation in the joints of patients with psoriatic arthritis.

• adipose tissue
• articular adipose tissue
• dermal adipocytes
• pathophysiology
• psoriasis
• psoriatic arthritis

• Adiponectin
• Chemerin
• Fetuin-A
• Obesity
• Omentin
• Psoriasis arthritis

• Adipokines/metabolism
• Humans
• Inflammation/immunology
• Inflammation/metabolism
• Psoriasis/immunology
• Psoriasis/metabolism

Psoriasis is a chronic, immune-mediated inflammatory disease predominantly affecting the skin, with a complex aetiology. Recently it has been suggested that the chronic inflammation of psoriasis may cause metabolic and vascular disorders. The relationship between obesity and psoriatic arthritis (PsA) is not clear, and there are insufficient prospective studies addressing this subject.

To investigate the relationship between psoriatic arthritis, severity of psoriasis and obesity in the Turkish population.

Patient data from psoriasis outpatient clinics from February 2007 to July 2013 were reviewed retrospectively using the Psoriasis-Turkey (PSR-TR) registration system. Patients’ age, onset age, body mass index (BMI), waist circumference, psoriasis area and severity index (PASI), and arthritis information were reviewed. In the outpatient clinics, patients who had joint pain consulted rheumatology clinics. The CASPAR criteria were used for the diagnosis of arthritis.

A total of 443 males and 495 females enrolled in this study. The mean age of females was 43.9 years (18–93 years) and the mean age of males was 44.6 years (18–89 years). A total of 231 (25%) patients had psoriatic arthritis. Investigation of the relationship between PASI, BMI, waist circumference (WC) and arthritis revealed a statistically significant relationship between each variable.

In this study we observed a relationship between PsA and high BMI, high WC and high PASI. Psoriatic arthritis is a chronic inflammatory disorder and a chronic inflammatory state induced by adiposity may lead to PsA.

• body mass index
• psoriasis
• psoriatic arthritis
• waist circumference

Leptin, an adipokine responsible for body weight regulation, may be involved in pathological processes related to inflammation in joint disorders including rheumatoid arthritis (RA), osteoarthritis, and psoriatic arthritis (PsA). These arthropathies have been associated with a wide range of systemic and inflammatory conditions including cardiovascular disease, obesity, and metabolic syndrome. As a potent mediator of immune responses, leptin has been found in some studies to play a role in these disorders. Furthermore, current potent biologic treatments effectively used in PsA including ustekinumab (an interleukin 12/23 blocker) and adalimumab (a tumor necrosis factor-alpha blocker also used in RA) have been found to increase leptin receptor expression in human macrophages. This literature review aims to further investigate the role leptin may play in the disease activity of these arthropathies.

• Psoriatic arthritis
• Rheumatoid arthritis
• Leptin
• Ustekinumab
• Tumor necrosis factor-alpha