Adropin is a peptide hormone that was discovered in 2008 by Kumar et al. This protein consists of 76 amino acids, and it was originally described as a secreted peptide, with residues 1-33 encoding a secretory signal peptide sequence. The amino acid sequence of this protein in humans, mice and rats is identical. While our knowledge of the exact physiological roles of this poorly understood peptide continues to evolve, recent data suggest a role in energy homeostasis and the control of glucose and fatty acid metabolism. This protein is encoded by the Enho gene, which is expressed primarily in the liver and the central nervous system. The regulation of adropin secretion is controversial. Adropin immunoreactivity has been reported by several laboratories in the circulation of humans, non-human primates and rodents. However, more recently it has been suggested that adropin is a membrane-bound protein that modulates cell-cell communication. Moreover, adropin has been detected in various tissues and body fluids, such as brain, cerebellum, liver, kidney, heart, pancreas, small intestine, endothelial cells, colostrum, cheese whey and milk. The protein level, as shown by previous research, changes in various physiological and pathophysiological conditions. Adropin is involved in carbohydrate-lipid metabolism, metabolic diseases, central nervous system function, endothelial function and cardiovascular disease. The knowledge of this interesting protein, its exact role and mechanism of action is insufficient. This article provides an overview of the existing literature about the role of adropin, both in physiological and pathophysiological conditions.

Fatty acid (FA) profiles in the plasma of patients with metabolic syndrome and chronic kidney disease (CKD) seem to be identical despite their different etiology (dietary mistakes vs. cachexia). The aim of this study was to compare both profiles and to highlight the differences that could influence the improvement of the treatment of patients in both groups. The study involved 73 women, including 24 patients with chronic kidney disease treated with haemodialysis, 19 patients with metabolic syndrome (MetS), and 30 healthy women in the control group. A total of 35 fatty acids and derivatives were identified and quantified by gas chromatography. Intensified elongation processes from acid C10:0 to C16:0 were noted in both groups (more intense in MetS), as well as an increased synthesis of arachidonic acid (C20:4n6), which was more intense in CKD. Significant correlations of oleic acid (C18:1n9), gamma linoleic acid (C18:3n6), and docosatetraenoate acid (C22:4n6) with parameters of CKD patients were observed. In the MetS group, auxiliary metabolic pathways of oleic acid were activated, which simultaneously inhibited the synthesis of eicosapentanoic acid (EPA) and docosahexaenoic acid (DHA) from alpha lipoic acid (ALA). On the other hand, in the group of female patients with CKD, the synthesis of EPA and DHA was intensified. Activation of the synthesis of oleic acid (C18: 1n9 ct) and trans-vaccinic acid (C18:1) is a protective mechanism in kidney diseases and especially in MetS due to the increased concentration of saturated fatty acid (SFA) in plasma. The cause of the increased amount of all FAs in plasma in the CKD group, especially in the case of palmitic (C16:0) and derivatives stearic (C18:0) acids, may be the decomposition of adipose tissue and the progressing devastation of the organism, whereas, in the MetS group, dietary intake seems to be the main reason for the increase in SFA. Moreover, in MetS, auxiliary metabolic pathways are activated for oleic acid, which cause the simultaneous inhibition of EPA and DHA synthesis from ALA, whereas, in the CKD group, we observe an increased synthesis of EPA and DHA. The higher increase of nervonic acid (C24:1) in CKD suggests a higher degree of demyelination and loss of axons.

Recently there has been heightened interest in the potential significance of interleukin (IL)-17 and IL-23 in the development/progression of human malignancies. Here, we analyzed the systemic levels of these cytokines in 75 patients with different types of gastric neoplasms (carcinoma, gastrointestinal stromal tumors, neuroendocrine neoplasms, and lymphomas) and 42 healthy volunteers. We found that patients with all types of gastric neoplasms have significantly lower IL-23 levels. However, in comparison to the levels in healthy individuals, IL-17 concentrations were lower only in patients with types of gastric neoplasms other than carcinoma. Interestingly, IL-17 levels significantly differed between patients with early and advanced gastric carcinoma. No significant associations were detected between the systemic levels of examined interleukins and TNM staging. However, peripheral levels of IL-23 were correlated with the absolute numbers of circulating populations of bone marrow-derived mesenchymal and very small embryonic/epiblast-like stem cells in patients with gastric carcinoma. ROC curve analyses demonstrated that systemic levels of IL-17 seem to meet basic criteria for consideration as a helpful diagnostic marker in the detection of gastric carcinoma. In conclusion, our study provides translational evidence confirming the clinical significance of IL-17 and IL-23 in the pathogenesis of different types of gastric neoplasms in humans.

The higher values of disordered angiogenesis markers, endothelial damage markers and inflammatory markers both in the PE and the intrauterine growth restriction (IUGR) groups suggest the existence of shared disorders in the development of these pathologies. The correlations between disordered angiogenesis markers and endothelial damage markers argue in favor of a mutual relationship between these two processes in the development of pathologies evolving as secondary to placental ischemia. The results obtained confirm that the lesion profiles are the same in both PE and IUGR patients, which can be utilized in developing common diagnostic criteria.

The aim of this study was to verify whether eight-week-long swimming exercise training would evaluate the level of selected indicators of the pro-oxidant/antioxidant status in response to cold water in comparison with swimming under thermoneutral conditions in sedentary male and female elderly rats. The exercise-trained groups swam four min/day and five days a week during eight weeks of housing. Exercise was performed by swimming in glass tanks containing tap water maintained according to group at 5 °C and 36 °C. At the end of treatment (48 h after the last session), all rats were anaesthetized. The level of chosen biomarkers of oxidative stress and antioxidant enzyme activity was determined in the red blood cells and plasma. The results of study show that female rats seem to be better adapted to changing thermal conditions of the environment, developing not only morphological, but also antioxidant, defense mechanisms, mainly in the form of increased erythrocyte superoxide dismutase (SOD) activity and glutathione (GSH) concentration to restore the pro-oxidant/oxidant balance of the organism. Significantly higher concentrations of GSH were observed in the female rats of the group swimming in cold water (by 15.4% compared to the control group and by 20.5% in relation to the group of female rats swimming at 36 °C). In the group exposed to swimming training exercise in cold water, a significantly higher activity of SOD1 (by 13.4%) was found compared to the control group. On the other hand, the organs of ageing male rats show a reduced capacity to increase the metabolic response to low temperatures compared to female ones. In addition, it was demonstrated that cold exposure leads to an increase in lipid peroxidation in tissues. On the other hand, the repeated exposure to low levels of oxidative stress may result in some adaptive changes in organisms that help them to resist stress-induced damage.

(1) Analyses of disordered angiogenesis markers in early- and late-onset preeclampsia patients and patients with physiological pregnancies allow for a suggestion that natural "ageing of the placenta" and placental hypoperfusion lesions exacerbating with the advancing gestational age are some of the causes of late-onset preeclampsia. (2) Cases of early-onset preeclampsia are associated with more severe changes of disordered angiogenesis marker concentrations, which may be indicative of a more considerable impairment of placental perfusion in such patients. (3) In the course of the physiological pregnancy, there is a gradual increase in sFlt-1 and decrease in PlGF, which implies an elevated angiogenesis disorder that progresses with the gestational age.

The aim of the study was comparison of levels of resistin (RE), soluble receptor for advanced glycation end products (sRAGE), soluble receptor activator for nuclear factor-κB ligand (sRANKL), osteoprotegerin (OPG), glucose (GL), total protein (TP), and albumin (AL) between women with preterm and term rupture of fetal membranes and evaluation of prognostic values of all above in diagnostic of premature labor. Ninety-eight women in singleton pregnancy presenting with premature rupture of fetal membranes were included and divided into two groups: A -49 women after 37 weeks and B -49 women before 36 weeks of gestation. Plasma levels of sRAGE, OPG, TP, and AL were significantly lower in group B, and RE and GL plasma levels were higher in this group. The high prognostic values for sRAGE and sRANKL in the prognosis of spontaneous delivery after preterm rupture of membranes (pPROM) were found. The authors concluded that sRAGE and sRANKL serum levels could be a useful prognostic factors after pPROM. Resistin can play role in pathogenesis of rupture of membranes in premature pregnancy.