There is ample scientific evidence to suggest a link between the fatty acid-binding protein 4 (FABP4) and insulin resistance, gestational (GDM), and type 2 (T2DM) diabetes mellitus. This novel proinflammatory adipokine is engaged in the regulation of lipid metabolism at the cellular level. The molecule takes part in lipid oxidation, the regulation of transcription as well as the synthesis of membranes. An involvement of FABP4 in the pathogenesis of obesity and insulin resistance seems to be mediated via FABP4-dependent peroxisome proliferator-activated receptor γ (PPARγ) inhibition. A considerable number of studies have shown that plasma concentrations of FABP4 is increased in obesity and T2DM, and that circulating FABP4 levels are correlated with certain clinical parameters, such as body mass index, insulin resistance, and dyslipidemia. Since plasma-circulating FABP4 has the potential to modulate the function of several types of cells, it appears to be of extreme interest to try to develop potential therapeutic strategies targeting the pathogenesis of metabolic diseases in this respect. In this manuscript, representing a detailed review of the literature on FABP4 and the abovementioned metabolic disorders, various mechanisms of the interaction of FABP4 with insulin signaling pathways are thoroughly discussed. Clinical aspects of insulin resistance in diabetic patients, including women diagnosed with GDM, are analyzed as well.

The aim of the study was the assessment of right ventricular (RV) structure and diastolic function in hypertensive subjects. The study group consisted of 44 patients with untreated, mild to moderate essential systemic hypertension. All the patients were in sinus rhythm, no symptoms of congestive heart failure, ischaemic or valvular heart disease and lung disorders were found. Twenty-six healthy subjects were the control group. M-mode echocardiographic measurements of the right ventricular wall (RVW) diastolic thickness, right ventricular outflow tract diameter (RVOTD), left ventricular (LV) structure and LV systolic function were performed. Pulsed Doppler echocardiography was used to measure peak early (TE) and peak atrial (TA) right ventricular diastolic filling velocities as well as velocity-time integrals (VTI-TE and VTI-TA). TE:TA and VTI-TE:VTI-TA ratios were calculated. Similar parameters of the left ventricular diastolic filling were recorded at the level of mitral annulus. Mean pulmonary artery pressure (MPAP) was measured non-invasively by the estimation of pulmonary artery systolic flows. We demonstrated in hypertensive patients significantly thicker RVW (3.94 vs 2.8 mm, P < 0.001) and increased LV mass. In the hypertensive, increased TA and VTI-TA and diminished TE:TA and VTI-TE:VTI-TA ratios were recorded, indicating the abnormalities of RV diastolic function. RV diastolic filling parameters correlated positively with corresponding parameters of LV filling. The results of our study demonstrate that impairment of LV diastolic function, the common finding in systemic hypertension, is associated with diastolic disturbances of the right ventricle. RVW thickening and hypertrophy of interventricular septum seem to be major factors influencing RV diastolic function.

IntroductionEarly atherosclerotic changes in the endothelium associated with metabolic syndrome are generated with the participation of inflammatory cells, cytokines and enzymes of the extracellular matrix. The study is aimed at a comparison between the activity of inflammatory agents, tumour necrosis factor α (TNF-α) and the enzymes of the connective tissue matrix in the blood of healthy female patients as well as those suffering from the metabolic syndrome.Material and methodsThe examination included 35 women with metabolic syndrome (MS). The control group (C) comprised 35 healthy women. Lipidogram, C-reactive protein level (CRP), fasting glucose level (FGL), matrix metalloproteinase (MMP)-8 and -9 activity, tissue inhibitor of metalloproteinase-1 (TIMP-1) and TNF-α levels in blood were determined.ResultsAs compared with the control group, the level of inflammatory factors and the activity of extracellular matrix enzymes in the metabolic syndrome were statistically higher (p < 0.05) and concerned the following parameters: TNF-α (pg/ml): MS 6.59 ±3.18, C 4.78 ±2.91; CRP (mg/dl): MS 2.18 ±2.04, C 1,26 ±1.35; TIMP-1 (ng/ml): MS 265.5 ±2.9, C 205.4 ±72.6; MMP-9 (ng/ml): MS 198.2 ±138.6, C 138.6 ±116.1. Statistically significant correlations were also found between TIMP-1 and the following factors: BMI (R = 0.400, p < 0.001), waist/hip ratio (WHR) (R = 0.278, p < 0.05), waistline (R = 0.417, p < 0.001), FGL (R = 0.290, p < 0.05), HDL cholesterol (R = –0.253, p < 0.05) and triglycerides (R = 0.269, p < 0.05).There were positive correlations of MMP-9 with FGL (R = 0.446, p < 0.001) and waistline (R = 0.260, p < 0.05); MMP-8 with FGL (R = 0.308, p < 0.05); and CRP with BMI (R = 0.370, p < 0.01), WHR (R = 0.325, p < 0.01) and waistline (R = 0.368, p < 0.01).ConclusionsMetabolic syndrome is connected with higher activity of cytokines (TNF-α), inflammatory markers (CRP) and matrix enzymes (MMP-9, MMP-8, TIMP-1).

Psoriasis represents a common skin disease which is clinically manifested by chronic cutaneous lesions. It has been observed that psoriasis is associated with an increased risk of cardiovascular diseases, which is contributed to the inappropriate lipid metabolism. Statins are commonly used in clinical practice to lower cholesterol concentration and, accordingly, decrease the individual risk of developing a cardiovascular episode. There have been reports that statin administration could also result in better management of psoriasis. The observed beneficial effects are contributed to the effects on lipid metabolism, including that in skin, as well as anti-inflammatory and immunomodulatory properties of statins. Simvastatin and atorvastatin were found to improve the clinical outcome in patients with psoriatic skin lesions. Clinically, the effectiveness of this novel treatment was confirmed by the significant reduction in PASI score. To date several cases have been reported in which atorvastatin or pravastatin worsened psoriasis. Based on these results, it seems that statins represent a promising class of medications which could be extensively used in psoriasis.

Obstructive sleep apnoea (OSA) induces thrombophilia and reduces fibrinolysis. Alpha-2-antiplasmin (a-2-AP) and plasminogen activator inhibitor 1 (PAI-1) are major inhibitors of the fibrinolytic system. Increased concentrations of these factors are associated with a higher risk of cardiovascular diseases. The aim of this study was to assess plasma a-2-AP and PAI-1 in patients with OSA and evaluate correlations with the polysomnographic record and selected risk factors of cardiovascular diseases. The study group comprised 45 patients with OSA, and the control group consisted of 19 patients who did not meet the diagnostic criteria of OSA. Plasma a-2-AP and PAI-1 concentrations were assessed by enzyme-linked immunosorbent assay (ELISA). In the study group, the median value of plasma a-2-AP was higher than that of the control group (157.34 vs. 11.89 pg/ml, respectively, P<0.0001). A-2-AP concentration increased proportionally to the severity of OSA. The concentration of a-2-AP was positively correlated with the apnoea-hypopnoea index (AHI), apnoea index (AI), respiratory disturbances time (RDT), and desaturaion index (DI), and negatively correlated with mean and minimal oxygen saturation (SpO2 mean, SpO2 min, respectively). The median value of PAI-1 was higher in the study group than the control group (12.55 vs. 5.40 ng/ml, respectively, P = 0.006) and increased along with OSA severity. PAI-1 concentration was positively correlated with AHI, AI, RDT, DI, and body mass index (BMI) and negatively correlated with SpO2 mean and SpO2 min. Higher plasma concentrations of a-2-AP and PAI-1 in patients with OSA indicated that these patients had increased prothrombotic activity. OSA increases the risk of cardiovascular complications as it enhances prothrombotic activity.