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Metabolic syndrome (MS), defined as central obesity, hyperinsulinemia, insulin resistance, hypertension, dyslipidemia and glucose intolerance, has been associated with inflammatory biomarkers and cardiovascular diseases. This study was carried out on three groups of women; lean controls, moderately obese with MS (OB-MS) and morbidly obese with MS (MOB-MS). The main objectives were: 1. to analyze the plasma levels of total and acylated ghrelin, peptide YY(3-36) (PYY(3-36)), cholecystokinin (CCK), gastrin and insulin levels under basal conditions and in response to a standard mixed meal, and 2. to elucidate the relationship between the plasma levels of these gut peptides and metabolic syndrome parameters. Plasma levels of the gut hormones were measured by radioimmunoassays at time 0 just before the meal and at 30, 60 and 120 min after a meal ingestion. Traditional lipid profile and high-sensitivity C reactive protein (hs-CRP), the strongest biomarker of inflammation were also determined in OB-MS and MOB-MS. When compared to OB-MS, MOB-MS exhibited much higher anthropometric parameters such as waist circumference, higher fat mass and higher plasma levels of low density lipoprotein-cholesterol (LDL-C) and hs-CRP. Both these obese groups revealed significantly higher values of body mass index (BMI), fat mass, total cholesterol (TC), LDL-C, fasting glucose, fasting insulin, insulin resistance (IR) calculated from homeostatic model assessment (HOMA) and hs-CRP compared to the values recorded in lean subjects. Fasting PYY(3-36) level was lower, while fasting acylated ghrelin was higher in MOB-MS than in OB-MS. Plasma total and acylated ghrelin levels were significantly lower in OB-MS compared to lean women. In MOB-MS women the fasting PYY(3-36) levels were lower compared to lean controls and OB-MS, whilst postprandially in both OB-MS and MOB-MS, it was much lower than in lean women. The fasting plasma levels of total and acylated ghrelin and their postprandial decrease were significantly smaller in both obese groups compared to lean subjects. Plasma hs-CRP levels correlated positively with BMI, waist circumference, fat mass, fasting glucose, HOMA IR and fasting active ghrelin, whilst it negatively correlated with plasma fasting and total ghrelin. Moreover, plasma fasting acylated ghrelin correlated positively with fat mass. Fasting total ghrelin correlated positively with BMI, HDL-C and negatively with HOMA IR. We conclude that MS features of obesity are closely related to fasting and postprandial alterations of concentrations of PYY(3-36), CCK and ghrelin, suggesting that determination of gut hormones controlling food intake might be considered as a valuable tool to assess the progression of MS to comorbidities of obesity.

The aim of the work was to compare two analytical methods of trace analysis in respect to their applicability in heavy metals determination in biological samples. Atomic absorption spectrometry (AAS) may be considered as the method of choice in such analyses due to its accuracy, precision and low detection limit. On the other hand, voltammetric methods seem to be as useful, but rarely applied. Having in mind that there is no universal analytical method, we have compared two AAS and voltammetric methods as the tools for Zn and Cu determination in the samples collected from rat gastric juice and gastric mucosa. Construction of the renewable silver amalgam film electrode (Hg(Ag)FE) for stripping voltammetry was described. Detailed optimization of measurements procedure and sample preparation for differential pulse anodic stripping voltammetry (DP ASV) and AAS were also performed and presented. The obtained results of quantitative analysis of the chosen parameters by means of both methods are discussed.

Ghrelin, a novel peptide expressed in the gastrointestinal tract, especially in the gastric mucosa, exerts several biological activities including the stimulation of appetite and food intake, the stimulation of intestinal motility and the release of growth hormone. The aim of this study was to examine the expression of ghrelin in gastric mucosa after its exposure to ethanol and its effects on gastric lesions induced by ethanol with and without pretreatment with indomethacin. Acute gastric lesions were induced by intragastric administration of 75% ethanol in rats pretreated with saline-vehicle or ghrelin injected intraperitoneally (i.p.) without or with i.p. pretreatment with indomethacin. At the end of experiments, the rats were anesthetized, the stomach was exposed to measure gastric blood flow (GBF), to determine the area of gastric lesions and to take biopsy samples from the oxyntic mucosa for determination of transcripts of ghrelin, tumor necrosis alpha (TNF-alpha) and transforming growth factor alpha (TGFalpha) using RT-PCR and to assess the generation of PGE(2) by RIA. Exposure of gastric mucosa to 75% ethanol resulted in numerous mucosal lesions of an area of about 115 mm(2) and in the increase of mucosal expression of TNF-alpha, PGE(2), TGFalpha and ghrelin with concomitant decrease in GBF. Exogenous ghrelin reduced dose-dependently acute gastric lesions with simultaneous attenuation of GBF and a decrease in the expression of TNF-alpha but not TGFalpha. Pretreatment with indometahcin, which suppressed the generation of PGE(2) by about 85%, augmented ethanol-induced gastric lesions and eliminated the ghrelin-induced protection of mucosa against ethanol. We conclude that ghrelin, whose mucosal expression is enhanced after exposure to ethanol, exhibits a strong gastroprotection, at least in part, due to its anti-inflammatory action mediated by prostaglandins.

A biological activity of myokine irisin, has been intensively investigated in the context of a browning process occurring in white adipose tissue, but its role as a modulator of immune response has been little studied. The aim of our study was to determine the impact of irisin (0 - 100 nM) on pro-inflammatory activation of adipocyte 3T3 L1 cell line. Irisin reduced in a concentration-dependent manner the expression and activity of major proinflammatory cytokines, e.g. tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6) expression and their secretion into cell medium. Moreover, irisin enhanced adiponectin synthesis reversing the effect of the lipopolysaccharide (LPS)-induced attenuation of this adipokine expression. The opposite effect was observed for leptin whose expression increased by LPS and this effect was suppressed by irisin application. A decreased phosphorylation and activation of nuclear factor kappa B (NFκB) in the presence of irisin suggests that mechanism of action irisin involves the inhibition of an inflammatory transcription factor. Irisin exerts also an inhibitory effect on macrophage migration toward chemoattractants present in adipocyte supernatants. Among the specific molecules secreted by adipocytes was monocyte chemotactic protein 1 (MCP-1) whose expression was suppressed by irisn. In majority of experiments irisin was effective in 100 nM concentration but in some of them the inhibitory effects occurred already in a concentration of 50 nM of this peptide. This study for the first time showed that adipocytes are directly affected by irisin and provides an evidence on anti-inflammatory action of irisin on fat cells.

Crohn's disease and ulcerative colitis are both chronic inflammatory bowel diseases (IBDs) characterized by a cyclical nature, which alternates between active and quiescent states, ultimately impairing a patients' quality of life. The etiology of IBD is not known but it likely involves a combination of genetic predisposition and environmental risk factors. Physical exercise has been suggested to provide protection against the onset of IBD, but there are inconsistencies in the findings of the published literature. Current research recommends exercise to help counteract some IBD-specific complications and preliminary studies suggest that physical activity may be beneficial in reducing the symptoms of IBD. Obesity is becoming more prevalent in patients diagnosed with IBD and may be associated with higher disease activity. There is evidence that adipokines are involved in the inflammatory and metabolic pathways. Hypertrophy of the mesenteric white adipose tissue has been long recognized as a characteristic feature of Crohn's disease; however its importance is unknown. Recent data suggest that dysregulation of adipokine secretion by white adipose tissue is involved in the pathogenesis of Crohn's disease. Skeletal muscle was shown to produce biologically active myokines, which could be a important contributor to the beneficial effects of exercise. There is mounting evidence for the bi-directional endocrine cross talk between adipose tissue and skeletal muscle. The objective of the present review is to explore the role of exercise and its impact on IBD. Also, we discuss how current discoveries regarding the importance of adipokines and myokines and their cross talk expand our view of the pathological changes and the therapeutic options for IBD.