Influence of leaf damage by the horse chestnut leafminer (Cameraria ohridella Deschka & Dimic) on mycorrhiza of Aesculus hippocastanum L.

In many parts of Europe, the white horse chestnut (Aesculus hippocastanum L.) has been attacked by the horse chestnut leafminer (Cameraria ohridella Deschka & Dimic), which causes premature leaf dieback. A. hippocastanum L. establishes mutualistic symbiosis with arbuscular mycorrhizal (AM) fungi. This study involved a comparison of mature A. hippocastanum individuals susceptible to C. ohridella and individuals resistant to this insect after a one-time treatment with a chemical preparation injected into the tree trunks 7 years before the investigation began. Concentration of macronutrients in soil and the activity of soil nonspecific dehydrogenase did not differ between soils under canopies of the treated and untreated trees. Concentrations of C and N were significantly higher in leaves of the treated than those of the untreated trees. The infestation by C. ohridella and defoliation of leaves of the untreated trees did not significantly influence the frequency and intensity of AM colonization compared to the chemically treated trees, although a tendency towards higher average AM colonization of roots of the untreated trees, infested by the herbivores, than roots of the non-infested trees was observed. The results also indicated a tendency for higher biomass of fine roots per soil volume under the trees treated against C. ohridella than under the trees invaded by the insect.

TRPV6 channel modulates proliferation of insulin secreting INS-1E beta cell line.

Transient receptor potential channel vanilloid type 6 (TRPV6) is a non-selective cation channel with high permeability for Ca²âº ions. So far, the role of TRPV6 in pancreatic beta cells is unknown. In the present study, we characterized the role of TRPV6 in controlling calcium signaling, cell proliferation as well as insulin expression, and secretion in experimental INS-1E beta cell model. TRPV6 protein production was downregulated using siRNA by approx. 70%, as detected by Western blot. Intracellular free Ca²âº ([Ca²âº]i) was measured by fluorescence Ca²âº imaging using fura-2. Calcineurin/NFAT signaling was analyzed using a NFAT reporter assay as well as a calcineurin activity assay. TRPV6 downregulation resulted in impaired cellular calcium influx. Its downregulation also reduced cell proliferation and decreased insulin mRNA expression. These changes were companied by the inhibition of the calcineurin/NFAT signaling. In contrast, insulin exocytosis was not affected by TRPV6 downregulation. In conclusion, this study demonstrates for the first time the expression of TRPV6 in INS-1E cells and rat pancreatic beta cells and describes its role in modulating calcium signaling, beta cell proliferation and insulin mRNA expression. In contrast, TRPV6 fails to influence insulin secretion.

TPM3 deletions cause a hypercontractile congenital muscle stiffness phenotype.

OBJECTIVE: Mutations in TPM3, encoding Tpm3.12, cause a clinically and histopathologically diverse group of myopathies characterized by muscle weakness. We report two patients with novel de novo Tpm3.12 single glutamic acid deletions at positions ΔE218 and ΔE224, resulting in a significant hypercontractile phenotype with congenital muscle stiffness, rather than weakness, and respiratory failure in one patient. METHODS: The effect of the Tpm3.12 deletions on the contractile properties in dissected patient myofibers was measured. We used quantitative in vitro motility assay to measure Ca(2+) sensitivity of thin filaments reconstituted with recombinant Tpm3.12 ΔE218 and ΔE224. RESULTS: Contractility studies on permeabilized myofibers demonstrated reduced maximal active tension from both patients with increased Ca(2+) sensitivity and altered cross-bridge cycling kinetics in ΔE224 fibers. In vitro motility studies showed a two-fold increase in Ca(2+) sensitivity of the fraction of filaments motile and the filament sliding velocity concentrations for both mutations. INTERPRETATION: These data indicate that Tpm3.12 deletions ΔE218 and ΔE224 result in increased Ca(2+) sensitivity of the troponin-tropomyosin complex, resulting in abnormally active interaction of the actin and myosin complex. Both mutations are located in the charged motifs of the actin-binding residues of tropomyosin 3, thus disrupting the electrostatic interactions that facilitate accurate tropomyosin binding with actin necessary to prevent the on-state. The mutations destabilize the off-state and result in excessively sensitized excitation-contraction coupling of the contractile apparatus. This work expands the phenotypic spectrum of TPM3-related disease and provides insights into the pathophysiological mechanisms of the actin-tropomyosin complex.

[Cognitive Behavioral Therapy for Anxiety and Depression in Patients with Parkinson's Disease]. / Kognitive Verhaltenstherapie von Angst und Depression bei Patienten mit Morbus Parkinson.

Non-motor symptoms in patients with Parkinson's disease (PD) are gaining more and more interest. Diagnosis of mental disorders in particular, such as anxiety and depression, are often not a part of the professional's diagnostic procedure in spite of the high prevalence rate. To provide these patients with comprehensive treatment, proper diagnosis and appropriate therapy are required. Cognitive Behavioral Therapy (CBT) has been one of the most efficient therapies for anxiety and depression, also in a group setting. This review compares studies that examined patients with PD diagnosed with anxiety disorders and/or depression. In eight studies, CBT in an individual setting was assessed. Three of these had a single case study design, three did not have a control group and two were randomized controlled trials. Two interventions were telephone-based and two were in a group therapy setting. Several results indicate that there is a decline in depressive symptoms as well as anxiety after CBT. There are very few randomized controlled studies on this issue. The efficacy of group treatment needs to be investigated better in order to offer patients effective treatment, keeping in kind their special circumstances.

Takotsubo cardiomyopathy: serious early complications and two-year mortality - a 101 case study.

BACKGROUND: Takotsubo cardiomyopathy (TTC) is characterised by transient contractility disturbances of the apex of the left ventricle. METHODS: We enrolled 101 patients from the northern-eastern part of Poland in the years 2008-2012 who were hospitalised for TCC. The control group consisted of female patients diagnosed with anterior myocardial infarction with ST-segment elevation (anterior STEMI) (n = 101). RESULTS: 89 % of the study group were women. Patients with TTC had diabetes (12.6 % vs 29.7 %; p = 0.002) and hyperlipidaemia (36.8 % vs 64.4 %; p = 0.0001) significantly less frequently, and better kidney function assessed by estimated glomerular filtration rate versus patients with anterior STEMI (74.52 % vs 64.30 %; p = 0.004). In the TTC group there were more patients with chronic obstructive pulmonary disease (11.6 % vs 1.0 %; p = 0.002) and thyroid disturbances, especially hyperthyroidism (23.4 % vs 11.0 %; p = 0.021). In patients with TTC sudden cardiac arrest, pulmonary oedema and cardiogenic shock were observed less frequently than in the control group (14.7 % vs 30.7 %; p = 0.0078). Hospitalisations in TTC patients were less frequently complicated by pneumonia (20.0 % vs 35.6 %; p = 0.0148) and urinary infection (4.2 % vs 21.8 %; p = 0.0003). Cardiac rupture occurred in 3 patients with TTC and in 1 with anterior STEMI. In-hospital mortality was significantly lower in the group with TTC. Also, mortality at 30 days, 3 months, 1 year and 2.5 years was significantly lower in patients with TTC than in patients with MI (p = 0.035; p = 0.0226; p = 0.0075; p = 0.009). CONCLUSIONS: Previously considered to be a benign syndrome, TTC should be reconsidered as a clinical condition at risk for serious complications such as cardiac arrest, cardiogenic shock, pulmonary oedema and cardiac rupture leading to death and causing substantial early hazard. The prognosis in TTC is significantly better than in patients with anterior STEMI.

Ischemic and injured bowel evaluation by Fluorescence imaging.

AIM: Although fluorescence has been proposed for estimation of bowel perfusion decades ago it is still not widely used. In emergency situations like mesenteric ischemia, fluorescence might give objective criteria to evaluate the perfusion and guide the decisions of surgeons. METHOD: The use of near-inrafrared angiography by PinPoint (Novadaq) in a serial of four emergency situations of acute mesenteric ischemia has been evaluated in a university hospital setting. RESULTS: The use of the near-infrared tool is in emergency situations easy to handle and little time-consuming. The angiography showed clearly the perfusion in regions that were not estimated as recoverable by the surgeons. In one of the cases a significant amount of bowel could be spared by use of the system. CONCLUSION: Although the assessment of the perfusion with the applied system is comprehensible, it would be desirable to evaluate a threshold level in order to further objectify it. While the surgeons who used the tool were subjectively assured by the expressiveness it would need a randomized and maybe experimental setting to evaluate objectively the amount of spared bowel length.

Glucagon increases circulating fibroblast growth factor 21 independently of endogenous insulin levels: a novel mechanism of glucagon-stimulated lipolysis?

AIMS/HYPOTHESIS: Glucagon reduces body weight by modifying food intake, glucose/lipid metabolism and energy expenditure. All these physiological processes are also controlled by fibroblast growth factor 21 (FGF-21), a circulating hepatokine that improves the metabolic profile in obesity and type 2 diabetes. Animal experiments have suggested a possible interaction between glucagon and FGF-21 however, the metabolic consequences of this crosstalk are not understood. METHODS: The effects of exogenous glucagon on plasma FGF-21 levels and lipolysis were evaluated in healthy volunteers and humans with type 1 diabetes, as well as in rodents with streptozotocin (STZ)-induced insulinopenic diabetes. In vitro, the role of glucagon on FGF-21 secretion and lipolysis was studied using isolated primary rat hepatocytes and adipocytes. Fgf-21 expression in differentiated rat pre-adipocytes was suppressed by small interfering RNA and released FGF-21 was immunoneutralised by polyclonal antibodies. RESULTS: Glucagon induced lipolysis in healthy human volunteers, patients with type 1 diabetes, mice and rats with STZ-induced insulinopenic diabetes, and in adipocytes isolated from diabetic and non-diabetic animals. In addition, glucagon increased circulating FGF-21 in healthy humans and rodents, as well as in patients with type 1 diabetes, and insulinopenic rodents. Glucagon stimulated FGF-21 secretion from isolated primary hepatocytes and adipocytes derived from animals with insulinopenic diabetes. Furthermore, FGF-21 stimulated lipolysis in primary adipocytes isolated from non-diabetic and diabetic rats. Reduction of Fgf-21 expression (by approximately 66%) or immunoneutralisation of released FGF-21 markedly attenuated glucagon-stimulated lipolysis in adipocytes. CONCLUSIONS/INTERPRETATION: These results indicate that glucagon increases circulating FGF-21 independently of endogenous insulin levels. FGF-21 participates in glucagon-induced stimulation of lipolysis.

Obestatin inhibits lipogenesis and glucose uptake in isolated primary rat adipocytes.

Ghrelin and obestatin are encoded by the preproghrelin gene and originate from post-translational processing of the preproghrelin peptide. Obestatin is mainly present in the stomach, but its action is focused on appetite inhibition in opposition to ghrelin function. Recently, it has been presented that obestatin may regulate adipocyte metabolism and influence fat content. However, obestatin action is still poorly understood. Therefore, we aimed to investigate obestatin function on adipocyte metabolism in the rat. We studied changes in the mRNA expression of active and inactive isoforms of obestatin receptors. In addition, we analyzed influence of obestatin on lipogenesis, lipolysis and glucose transport in isolated adipocytes. Moreover, we also performed analysis of obestatin action on lipolysis in differentiated rat preadipocytes with silenced obestatin receptor. We found significantly higher expression of the obestatin receptor Gpr39-1a active form at an mRNA level following adipocytes incubation with obestatin. We did not observe expression changes in the inactive form of obestatin receptor Gpr39-1b. Additionally, we found significant changes in Gpr39-1a expression following obestatin receptor silencing in cells incubated with obestatin in comparison to control. Obestatin inhibited both, basal and insulin-stimulated lipogenesis and glucose transport in adipocytes. Furthermore, obestatin potentiated adrenalin-stimulated lipolysis. We also found reduced glycerol release following obestatin incubation in adipocytes with silenced Gpr39 gene. Our results indicate that obestatin acts via the GPR39 receptor in isolated adipocytes, and that through this mechanism obestatin influences lipid accumulation, glucose uptake and lipolysis.

Mutations in the skeletal muscle alpha-actin gene in patients with actin myopathy and nemaline myopathy.

Muscle contraction results from the force generated between the thin filament protein actin and the thick filament protein myosin, which causes the thick and thin muscle filaments to slide past each other. There are skeletal muscle, cardiac muscle, smooth muscle and non-muscle isoforms of both actin and myosin. Inherited diseases in humans have been associated with defects in cardiac actin (dilated cardiomyopathy and hypertrophic cardiomyopathy), cardiac myosin (hypertrophic cardiomyopathy) and non-muscle myosin (deafness). Here we report that mutations in the human skeletal muscle alpha-actin gene (ACTA1) are associated with two different muscle diseases, 'congenital myopathy with excess of thin myofilaments' (actin myopathy) and nemaline myopathy. Both diseases are characterized by structural abnormalities of the muscle fibres and variable degrees of muscle weakness. We have identified 15 different missense mutations resulting in 14 different amino acid changes. The missense mutations in ACTA1 are distributed throughout all six coding exons, and some involve known functional domains of actin. Approximately half of the patients died within their first year, but two female patients have survived into their thirties and have children. We identified dominant mutations in all but 1 of 14 families, with the missense mutations being single and heterozygous. The only family showing dominant inheritance comprised a 33-year-old affected mother and her two affected and two unaffected children. In another family, the clinically unaffected father is a somatic mosaic for the mutation seen in both of his affected children. We identified recessive mutations in one family in which the two affected siblings had heterozygous mutations in two different exons, one paternally and the other maternally inherited. We also identified de novo mutations in seven sporadic probands for which it was possible to analyse parental DNA.

Neuropeptide B promotes differentiation of rodent white preadipocytes into mature adipocytes.

Neuropeptide B (NPB) modulates energy homeostasis and metabolism through activation of NPBWR1 and NPBWR2 in humans and NPBWR1 in rodents. Recently, we reported that NPB promotes adipogenesis in rat brown preadipocytes. In the present study, we evaluated the effects of NPB on proliferation and differentiation into mature adipocytes of white rat preadipocytes and 3T3-L1 cells. We found the expression of NPBWR1 and NPB on mRNA and protein level in rat white preadipocytes and 3T3-L1 cells. NPB increased expression of mRNA and protein production of adipogenic genes (PPARγ, C/EBPß, CEBPα and FABP4) in rat preadipocytes and 3T3-L1 cells during the differentiation process. Furthermore, NPB stimulated lipid accumulation in rat preadipocytes and 3T3-L1 cells. In addition, we found that NPB promotes phosphorylation of p38 kinase in rat preadipocytes and 3T3-L1 cells. NPB failed to stimulate expression of proadipogenic genes in the presence of p38 inhibitor. NPB failed to modulate viability and proliferation of rat preadipocytes and 3T3-L1 cells. Taken together, we report that NPB promotes differentiation of rodent preadipocytes via p38-dependent mechanism. NPB does not modulate viability and proliferation of rat preadipocytes and 3T3-L1 cells.

Ostarine does not enhance the metabolic effect of exercise in obese rats.

Overweight and obesity are associated with severe metabolic disorders and an increased risk of cardiovascular diseases. It is a known fact that physical activity has a positive effect on metabolic parameters, and also reduces the risk of diseases such as diabetes. Some products can enhance the rate of lipolysis and help in improving fat loss. One of these are selective androgen receptor modulators (SARMs) which act as anabolic agents and are also believed to aid in fat-burning. In this study, we investigated whether 30 days of ostarine administration could potentially improve metabolic parameters using the rat model of obesity combined with exercise. We assessed the levels of biochemical and hormonal parameters in serum samples as well as insulin sensitivity indices of tissues. There were significant changes in the metabolic parameters with exercise. However, we did not find any additive effects of ostarine and exercise on most of the parameters tested. Similar results were obtained from the analysis of gene expression and the concentration of leptin and adiponectin. Our results indicated that ostarine had a lowering effect on cholesterol concentration in the serum (P<0.05). Moreover, when combining ostarine and exercise, additive changes were only observed in the levels of total and HDL cholesterol. No significant change was observed in the metabolic parameters of obese rats with the use of ostarine at the dose of 0.4 mg/kg body weight. Since ostarine is known to enhance performance, further research on its effects is needed.

The role of the orexin (hypocretin) system in controlling energy homeostasis, endocrine system, and reproduction in pigs and other living organisms.

Orexins A (OXA) and B (OXB) (hypocretin 1 and 2) are neuropeptides produced in the brain and peripheral tissues. Biological activities of orexins are mediated through activation of two G-protein coupled receptors termed as orexin 1 receptor (OX1R) and orexin 2 receptor (OX1R). Orexin system (OXA, OXB, OX1R, OX2R) was implicated in controlling sleep, energy expenditure, appetite, reproduction as well as metabolism and energy homeostasis. In this review, we summarize the current knowledge regarding the role of the orexin system in controlling porcine physiology. Particularly, we review and discuss evidence indicating that in pig and other living organisms, orexins and their receptors modulate the energy homeostasis, reproduction as well as functions of peripheral tissues including the pancreas, adrenal glands, gastro-intestinal tract and adipose tissue.

Evidence for a smooth onset of deformation in the neutron-rich Kr isotopes.

The neutron-rich nuclei 94,96Kr were studied via projectile Coulomb excitation at the REX-ISOLDE facility at CERN. Level energies of the first excited 2(+) states and their absolute E2 transition strengths to the ground state are determined and discussed in the context of the E(2(1)(+)) and B(E2;2(1)(+)→0(1)(+)) systematics of the krypton chain. Contrary to previously published results no sudden onset of deformation is observed. This experimental result is supported by a new proton-neutron interacting boson model calculation based on the constrained Hartree-Fock-Bogoliubov approach using the microscopic Gogny-D1M energy density functional.

Bovine neonatal pancytopenia in calves in Poland.

Bovine neonatal pancytopenia (BNP), a newly emerged syndrome of discussed etiology in calves, has been diagnosed since 2006. Here we describe first cases of BNP in Poland. Between September 2008 and April 2011, 62 cases of BNP were diagnosed in dairy calves. Bleeding skin lesions were mostly pronounced in summer and early autumn. Severe thrombocytopenia was observed in all sick animals. All calves came from herds vaccinated against BVDV infection with PregSure BVD vaccine (Pfizer). Substitution of colostrum from dams of BNP positive calves with colostrum from dams from herds free of BNP was the only effective measure to avoid new cases in affected herds.

Indigenous Health: ACTION on Prevention - 50th annual Australian Society for Medical Research National Scientific Conference.

The 50th annual National Scientific Conference of the Australian Society for Medical Research was held in Cairns, Queensland, 13-16 November 2011. The theme, 'Indigenous Health: ACTION on Prevention' highlighted the direct action being undertaken by health and medical researchers, as well as allied health professionals, to improve long-term health outcomes for Indigenous Australians.

Extent of the frontal sinuses in the aspect of neurosurgical craniotomy approaches.

BACKGROUND: Frontal sinuses within the frontal bone can be a potential obstacle in neurosurgical approach in this region. Their unintended opening during craniotomy is not beneficial due to the risk of brain infections by bacteria inhabiting the sinus mucosa. Therefore, such opening should be avoided whenever the surgical procedure does not involve the sinus itself. The aim of the study was the morphometric analysis of the frontal sinuses based on computed tomography imaging. MATERIALS AND METHODS: The width, height, projection surface area and location of the highest and most lateral points of the sinuses were determined. RESULTS: The vertical diameter of the sinuses was found to be greater in men compared with women. The most lateral point of the sinuses was located higher in men, and in men was located higher on the left side. The results obtained may indicate that the frontal sinuses tend to be larger in men and that air cells in men extend further in the upper-lateral direction on the left side of the frontal bone. CONCLUSIONS: This may cause an increased risk of unintentional opening of the left frontal sinus during frontal craniotomy or pterional craniotomy with frontal extension.

Orexin A stimulates glucose uptake, lipid accumulation and adiponectin secretion from 3T3-L1 adipocytes and isolated primary rat adipocytes.

AIMS/HYPOTHESIS: Orexin A (OXA) modulates body weight, food intake and energy expenditure. In vitro, OXA increases PPARγ (also known as PPARG) expression and inhibits lipolysis, suggesting direct regulation of lipid metabolism. Here, we characterise the metabolic effects and mechanisms of OXA action in adipocytes. METHODS: Isolated rat adipocytes and differentiated murine 3T3-L1 adipocytes were exposed to OXA in the presence or absence of phosphoinositide 3-kinase (PI3K) inhibitors. Pparγ expression was silenced using small interfering RNA. Glucose uptake, GLUT4 translocation, phosphatidylinositol (3,4,5)-trisphosphate production, lipogenesis, lipolysis, and adiponectin secretion were measured. Adiponectin plasma levels were determined in rats treated with OXA for 4 weeks. RESULTS: OXA PI3K-dependently stimulated active glucose uptake by translocating the glucose transporter GLUT4 from cytoplasm into the plasma membrane. OXA increased cellular triacylglycerol content via PI3K. Cellular triacylglycerol accumulation resulted from increased lipogenesis as well as from a decrease of lipolysis. Adiponectin levels in chow- and high-fat diet-fed rats treated chronically with OXA were increased. OXA stimulated adiponectin expression and secretion in adipocytes. Both pharmacological blockade of peroxisome proliferator-activated receptor γ (PPARγ) activity or silencing Pparγ expression prevented OXA from stimulating triacylglycerol accumulation and adiponectin production. CONCLUSIONS/INTERPRETATION: Our study demonstrates that OXA stimulates glucose uptake in adipocytes and that the evolved energy is stored as lipids. OXA increases lipogenesis, inhibits lipolysis and stimulates the secretion of adiponectin. These effects are conferred via PI3K and PPARγ2. Overall, OXA's effects on lipids and adiponectin secretion resemble that of insulin sensitisers, suggesting a potential relevance of this peptide in metabolic disorders.

Microbial activity and metamitron degrading microbial communities differ between soil and water-sediment systems.

The herbicide metamitron is frequently detected in the environment, and its degradation in soil differs from that in aquatic sediments. In this study, we applied 13C6-metamitron to investigate the differences in microbial activity, metamitron mineralization and metamitron degrading microbial communities between soil and water-sediment systems. Metamitron increased soil respiration, whereas it suppressed respiration in the water-sediment system as compared to controls. Metamitron was mineralized two-fold faster in soil than in the water-sediment. Incorporation of 13C from 13C6-metamitron into Phospholipid fatty acids (PLFAs) was higher in soil than in sediment, suggesting higher activity of metamitron-degrading microorganisms in soil. During the accelerated mineralization of metamitron, biomarkers for Gram-negative, Gram-positive bacteria and actinobacteria dominated within the 13C-PLFAs in soil. Gram-negative bacteria dominated among the metamitron degraders in sediment throughout the incubation period. Actinobacteria, and actinobacteria and fungi were the main consumers of necromass of primary degraders in soil and water-sediment, respectively. This study clearly showed that microbial groups involved in metamitron degradation depend on the system (soil vs. water-sediment) and on time. It also indicated that the turnover of organic chemicals in complex environments is driven by different groups of synthropic degraders (primary degraders and necromass degraders) rather than by a single degrader.

Indocyanine Green Fluorescence Angiography Can Guide Intraoperative Localization During Parathyroid Surgery.

BACKGROUND AND AIMS: Intraoperative localization of pathologic parathyroid glands is of major importance for the hyperparathyroidism treatment. Based on the small size and the anatomic variability, the localization can be very challenging. The current practice is to compare preoperative ultrasonography with Technetium-99m sestamibi scintigraphy (MIBI) and plan the resection accordingly. In this study, we implemented indocyanine green angiography for the intraoperative localization of parathyroid glands. MATERIALS AND METHODS: This is a retrospective analysis of 37 patients with primary, secondary, or tertiary hyperparathyroidism who were operated using indocyanine green angiography for the intraoperative localization of pathological parathyroid glands. An indocyanine green solution of 2.5 mg was were intravenously administered for parathyroid gland visualization. Different fluorescence scores were correlated with changes in postoperative parathyroid hormone levels. RESULTS: Patients were divided into two groups depending on the presence of uniglandular or multiglandular disease. Sixty-four lesions were resected, and the final histopathologic analysis confirmed the parathyroid origin in 62 of them (96.8%). None of the patients with uniglandular disease developed postoperative hypoparathyroidism, whereas three patients in the multiglandular group developed temporary hypoparathyroidism symptoms. Indocyanine green imaging had higher sensitivity for the intraoperative detection of parathyroid glands compared with ultrasonography and MIBI (p < 0.001). CONCLUSION: Indocyanine green angiography indicated high sensitivity for the intraoperative identification of pathologic parathyroid glands leading to a resection rate of 95.16%. The modality was useful, especially in cases of revisional surgery or ectopic parathyroid glands. Randomized trials have already proven the value of indocyanine green imaging in predicting postoperative hypocalcemia. Our results support the regular use of this method during parathyroid surgery.

Obesity is associated with increased level of kisspeptin in mothers' blood and umbilical cord blood - a pilot study.

OBJECTIVE: Kisspeptin (KP) is a major regulator of reproductive functions. It has also been shown to be involved in the metabolic changes associated with obesity. According to the well-established concept of prenatal programming, environmental factors can influence physiological and behavioral systems at the early stages of development. Thus, we hypothesized that in pregnant women, obesity can be associated with alterations in the levels of KP. We also assumed that the observed changes in obese mothers' blood (MB) would be reflected in the umbilical cord blood (CB). MATERIALS AND METHODS: We collected MB and CB from obese and nonobese women and analyzed the differences in metabolic and hormonal profiles, including KP concentration, using commercially available assays. RESULTS: We found that the level of KP was increased in the MB and CB of obese patients compared to nonobese subjects (p<0.05). A strong correlation was observed between the concentration of KP in MB and CB (r=0.8343; p<0.01). Moreover, we detected that the differences in the adipokine profile observed in the MB were not reflected in CB. CONCLUSIONS: Our results indicate that blood KP concentration can serve as a valuable marker in pregnant women. However, further studies are needed to understand the alterations of this peptide in obese pregnant woman and their potential effects on offspring.