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The exact roles of adipokines in the pathogenesis of type 2 diabetes and obesity are still unclear. The aim of the study was to evaluate fatty acid binding protein 4 (FABP4) concentrations in the serum and urine of women with excessive gestational weight gain (EGWG) and gestational diabetes mellitus (GDM) in the early post-partum period, with reference to their laboratory test results, body composition, and hydration status. The study subjects were divided into three groups: 24 healthy controls, 24 mothers with EGWG, and 22 GDM patients. Maternal body composition and hydration status were evaluated by the bioelectrical impedance analysis (BIA) method. Concentrations of FABP4, leptin, and ghrelin were determined via enzyme-linked immunosorbent assay (ELISA). Healthy women were characterized by the lowest serum leptin concentrations and by a negative correlation between the serum and urine FABP4 levels. Serum FABP4 levels were the highest in the GDM group. Serum FABP4 and leptin concentrations correlated positively in the GDM group. The EGWG group had the highest degree of BIA disturbances in the early puerperium and positive correlations between the urine FABP4 and serum leptin and ghrelin concentrations. The physiological and pathological significance of these findings requires further elucidation.

Bystander Me45 Melanoma Cells Increase Damaging Effect in UVC-irradiated Cells

Posted by A Krzywon, M Widel. on 2019-03-29 10:38:00



The aim of our study was to investigate the possible mechanism(s) of the bystander effect induced by UVC light in malignant melanoma Me45 cells that were co‐incubated with irradiated cells of the same line. We have found that the UVC band effectively generated apoptosis, premature senescence, single and double DNA strand breaks and reduced clonogenic survival of bystander cells. However, in the feedback response, the bystander cells intensified damage in directly irradiated cells, especially seen at the level of apoptosis and survival of clonogenic cells. Pretreatment of bystander cells with inhibitor of inducible nitric oxide synthase blocks this signaling. It seems that the mediators of this phenomenon produced and secreted by neighboring cells are superoxide, nitric oxide and TGF‐β. The reverse deleterious effect caused by cells not exposed to UVC in directly exposed cells is opposed to the protective/rescue effect exerted by the bystander cells in the case of ionizing radiation known in the literature. Whether this opposite adverse effect is a feature of only Me45 melanoma cells or whether it is a general phenomenon occurring between cells of other types exposed to ultraviolet radiation requires further research.


The  aim of the study was to evaluate the hypoglycaemic potential of  supplementary Cr in the form of chromium(III) glycinate (CrGly) in the  diabetic model of rats. The experiment was conducted on 40 male Wistar  rats, of which 30 were made diabetic by injection of a single dose of  streptozotocin (55 mg/kg b.m.), while the remaining 10 rats served as  the healthy control. After inducing hyperglycaemia, 2 groups of diabetic  rats (10 rats each) were supplemented with Cr either as CrGly or  chromium(III) picolinate (CrPic) given orally at a dose of 10 mg/kg diet  (about 0.75 mg Cr/kg b.m.) with adequate AIN-93M diet for 7 weeks. At  the termination of experiment, all animals were sacrificed to collect  blood and internal organs for biochemical assays. Blood biochemical  indices and tissular trace element contents (Fe, Zn, Cu, Cr) were  measured and compared with the values of the untreated groups. It was  found that CrGly significantly decreased blood glucose, total  cholesterol, HDL cholesterol and triacylglycerol levels more efficiently  than CrPic. Furthermore, both Cr compounds normalized disturbed the  serum, renal and cardiac molar Cu/Zn ratio, as well as restored the  kidney Zn and Cu levels in rats with hyperglycaemia. Supplementary Cr  did not increase the tissular Cr levels in diabetic rats. The study  confirmed the hypoglycaemic potential of CrGly in the diabetic model of  rats.


Long-term memory impairment is reported in more than 50% of cardiac arrest survivors. Monosialoganglioside (GM1) provided neuroprotection in experimental models of stroke but failed to replicate its promise clinically for unknown reasons. GM1 stimulates the release of nerve growth factor (NGF), which is synthesized as a precursor protein (pro-NGF) that either mediates apoptosis through the p75 neurotrophin receptor (p75NTR) or is cleaved by the protease furin (FUR) to yield mature NGF, the latter supporting survival through tropomyosin kinase receptor (Trk). The flavanol epicatechin (EPI) inhibits p75NTR-mediated signaling and apoptosis by pro-NGF. The aim of the current work is to test whether these two drugs affect, or communicate with, each other in the setting of CNS injuries. Using the two-vessel occlusion model of global ischemia/reperfusion (I/R), we tested if pharmacological modulation of Trk, p75NTR, and NGF balance with GM1, EPI, and their combination, can correct the memory deficit that follows this insult. Finally, we tested if FUR insufficiency and/or p75NTR-mediated apoptosis negatively affect the neurotherapeutic effect of GM1. Key proteins for Trk and p75NTR, FUR, and both forms of NGF were assessed. All treatment regiments successfully improved spatial memory retention and acquisition. A week after the insult, most Trk and p75NTR proteins were normal, but pro/mature NGF ratio remained sharply elevated and was associated with the poorest memory performance. Pharmacological correction of this balance was achieved by reinforcing Trk and p75NTR signaling. GM1 increased FUR levels, while concomitant administration of EPI weakened GM1 effect on pro-survival Trk and p75NTR mediators. GM1 neuroprotection is therefore not limited by FUR but could be dependent on p75NTR.

Decreased circulating levels of ANGPTL8 in Graves’ disease patients

Posted by HX Li, MJ Xu, L Zhao, et al. on 2019-03-28 11:07:00



Angiopoietin-like protein 8 (ANGPTL8), a newly identified hormone, has been recently characterized as a metabolic regulator which can affect energy homeostasis and has interesting potentials as a metabolic disease therapy. However, little is as yet known as to whether circulating ANGPTL8 levels are altered in thyroid dysfunction. This study measured serum ANGPTL8 levels in patients with Graves’ disease and explored the correlations between its serum levels and thyroid index in Graves’ disease.


The concentration of ANGPTL8 was analyzed in blood samples of 128 well-characterized individuals whose anthropometric parameters, biochemical parameters, and thyroid index were measured. The participants were divided into Graves’ disease patients (n?=?60) and healthy control subjects (n?=?68). Logistic regression was used to evaluate the relationship between ANGPTL8 and Graves’ disease.


Serum ANGPTL8 levels were more significantly decreased in Graves’ disease patients than in healthy control subjects (177.67 ±?135.07 vs 326.41?±?194.72 pg/mL; p?<?0.001). Serum ANGPTL8 was negatively correlated with free triiodothyronine (FT3), free thyroxine (FT4), and thyroid peroxidase antibodies (TPOAb) while being positively correlated with thyrotropin (TSH). Logistic regression analyses demonstrated that serum ANGPTL8 was significantly associated with Graves’ disease (p <?0.05).


Circulating concentrations of ANGPTL8 showed a significant reduction in Graves’ disease patients. Thus, it is suggested that thyroid function should be taken into consideration when evaluating the results of ANGPTL8.

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