Cord Blood Spexin Level in Mothers with Obesity-Forecast of Future Obesity?

Spexin (SPX) is a peptide that plays an important role in the regulation of food intake and body weight (BW) by the effect on carbohydrate-lipid metabolism. However, the role of SPX in fetal life, in children, and in adolescent metabolism is limited. Therefore, we decided to check whether obesity affects the concentration of SPX in the mother's peripheral blood (MB) and umbilical cord blood (UCB). Using MB and UCB sera on the day of delivery obtained from 48 women (24 non-obese and 24 obese) and commercially available Elisa kits and colorimetric assays, we determined changes in SPX and the relationship between SPX concentration and other metabolic and anthropometric markers (body weight and BMI) on the day of delivery and in children at the age of 36 months. We found lower concentrations of SPX in MB (p < 0.05) and UCB (p < 0.01) derived from obese women (BMI > 30) and a moderate linear correlation (r = 0.4429; p < 0.01) between SPX concentrations in MB and UCB. We also noted that the concentration of SPX is not correlated with the child's body weight on the day of birth (r = -0.0128). However, there is a relationship between SPX at birth and body weight at 3 years of age (r = -0.3219; p < 0.05). Based on the obtained results, it can be assumed that spexin is one of the factors modulating the child's metabolism already in the fetal period and can be considered a potential marker of future predisposition to obesity. However, confirmation of this thesis requires additional research.

METHODS FOR DIAGNOSING DENTAL CARIES LESIONS.

Tooth decay (dental caries) commonly occurs throughout the world and is one of the most widespread infectious diseases of lifestyle, globally affecting all age groups; up to 90% schoolchildren and almost 100% adults in both developing and developed countries. When left untreated, it can lead to disease outbreaks resulting in advere-health and life-threatening conditions such as endocarditis or sepsis. Undoubtedly, basic measures are thus required in both dental and GP practice to ensure that dental caries are detected early. This article presents the various diagnostic methods used to identify these disease outbreaks.

30-Day spexin treatment of mice with diet-induced obesity (DIO) and type 2 diabetes (T2DM) increases insulin sensitivity, improves liver functions and metabolic status.

Spexin (SPX) is a 14 aa peptide discovered in 2007 using bioinformatics methods. SPX inhibits food intake and regulates lipid, and carbohydrate metabolism. Here, we evaluate the ability of SPX at improving metabolic control and liver function in obese and type 2 diabetic animals. The effects of 30 days SPX treatment of mice with experimentally induced obesity (DIO) or type 2 diabetes (T2DM) on serum glucose and lipid levels, insulin sensitivity and hormonal profile (insulin, glucagon, adiponectin, leptin, TNF alpha, IL-6 and IL-1ß) are characterized. In addition, alterations of hepatic lipid and glycogen contents are evaluated. We report that SPX decreases body weight in healthy and DIO mice, and reduces lipid content in all three animal groups. SPX improves insulin sensitivity in DIO and T2DM animals. In addition, SPX modulates hormonal and metabolic profile by regulating the concentration of adiponectin (concentration increase) and leptin (concentration decrease) in the serum blood of DIO and T2DM mice. Lastly, SPX decreases lipid content as well as IL-6 and TNF-α protein levels in liver of DIO and T2DM mice, and reduces IL-6 and TNF-alpha concentrations in the serum derived from T2DM mice. Based on our results, we conclude that SPX could be involved in the development of obesity and type 2 diabetes mellitus and it can be further evaluated as a potential target for therapy of DIO and T2DM.

Infantile Colic-The Perspective of German and Polish Pediatricians in 2020.

The objective of the study was to characterize how infantile colic is perceived and managed by German and Polish pediatricians. Data in both countries were collected by using a paper questionnaire with seven questions and predefined and free text fields for the answers. Answers from 160 German and 133 Polish pediatricians were collected. The average of the occurrence rates estimated by both responder groups were at the higher end of published rates. The majority of pediatricians from both countries rated the parental burden caused by infantile colic to be high or very high. Pediatricians' awareness about the association between infantile colic and maternal depression and premature termination of breastfeeding is relatively well established in both countries. While more than 90% of German pediatricians stated knowledge of infantile colic being a major risk factor for shaken baby syndrome, this knowledge was only declared by half of the Polish responders. Pharmacological interventions, pro-/synbiotics or simethicone, are part of the treatment repertoire of nearly all responding pediatricians. In addition, non-pharmacological interventions (e.g., change of feeding, change of parental behavior) are also among the employed interventions. Results of this study will allow to better design and prioritize communication about infantile colic directed at pediatricians.

Serum RBP4 positively correlates with triglyceride level but not with BMI, fat mass and insulin resistance in healthy obese and non-obese individuals.

PURPOSE: Retinol binding protein 4 (RBP4) has recently been identified as an adipokine possibly involved in the development of impaired glucose metabolism. We aimed to test serum RBP4 in healthy non-obese individuals and in patients with well-characterized phenotype: obesity without confounding effects of diabetes, metabolic syndrome or dyslipidaemia. Additionally, we examined whether serum RBP4 is associated with anthropometric parameters, insulin resistance and blood lipid parameters. PATIENTS AND METHODS: Twenty-eight patients with obesity and no co-morbidities and twenty-five age-matched lean controls were recruited. Anthropometric parameters, body composition, fasting blood lipid profile, RBP4, glucose and insulin were assessed and HOMA-IR was calculated. RESULTS: Mean concentration of RBP4 did not differ between studied groups (in obese patients was 33.93 ± 4.46 µg/ml and 32.53 ± 2.53 µg/ml in non-obese controls). RBP4 positively correlated with serum triglycerides in obese and non-obese individuals (r = 0.74, p = 0.03 and r = 0.62, p = 0.02, respectively) and did not show any significant associations with HOMA-IR, anthropometric and body composition parameters. CONCLUSIONS: Excessive adiposity without co-morbidities is not associated with higher levels of circulating RBP4. Serum RBP4 cannot be considered as a direct predictive marker for impaired glucose metabolism. RBP4 possibly contributes to lipid metabolism.

Overexpression of Leap2 impairs Xenopus embryonic development and modulates FGF and activin signals.

Besides its widely described function in the innate immune response, no other clear physiological function has been attributed so far to the Liver-Expressed-Antimicrobial-Peptide 2 (LEAP2). We used the Xenopus embryo model to investigate potentially new functions for this peptide. We identified the amphibian leap2 gene which is highly related to its mammalian orthologues at both structural and sequence levels. The gene is expressed in the embryo mostly in the endoderm-derived tissues. Accordingly it is induced in pluripotent animal cap cells by FGF, activin or a combination of vegT/ß-catenin. Modulating leap2 expression level by gain-of-function strategy impaired normal embryonic development. When overexpressed in pluripotent embryonic cells derived from blastula animal cap explant, leap2 stimulated FGF while it reduced the activin response. Finally, we demonstrate that LEAP2 blocks FGF-induced migration of HUman Vascular Endothelial Cells (HUVEC). Altogether these findings suggest a model in which LEAP2 could act at the extracellular level as a modulator of FGF and activin signals, thus opening new avenues to explore it in relation with cellular processes such as cell differentiation and migration.

Phosphorylated ERK5/BMK1 transiently accumulates within division spindles in mouse oocytes and preimplantation embryos.

MAP kinases of the ERK family play important roles in oocyte maturation, fertilization, and early embryo development. The role of the signaling pathway involving ERK5 MAP kinase during meiotic and mitotic M-phase of the cell cycle is not well known. Here, we studied the localization of the phosphorylated, and thus potentially activated, form of ERK5 in mouse maturing oocytes and mitotically dividing early embryos. We show that phosphorylation/dephosphorylation, i.e. likely activation/inactivation of ERK5, correlates with M-phase progression. Phosphorylated form of ERK5 accumulates in division spindle of both meiotic and mitotic cells, and precisely co-localizes with spindle microtubules at metaphase. This localization changes drastically in the anaphase, when phospho-ERK5 completely disappears from microtubules and transits to the cytoplasmic granular, vesicle-like structures. In telophase oocytes it becomes incorporated into the midbody. Dynamic changes in the localization of phospho-ERK5 suggests that it may play an important role both in meiotic and mitotic division.

Spindle assembly checkpoint-related failure perturbs early embryonic divisions and reduces reproductive performance of LT/Sv mice.

The phenotype of the LT/Sv strain of mice is manifested by abnormalities in oocyte meiotic cell-cycle, spontaneous parthenogenetic activation, teratomas formation, and frequent occurrence of embryonic triploidy. These abnormalities lead to the low rate of reproductive success. Recently, metaphase I arrest of LT/Sv oocytes has been attributed to the inability to timely inactivate the spindle assembly checkpoint (SAC). As differences in meiotic and mitotic SAC functioning were described, it remains obscure whether this abnormality is limited to the meiosis or also impinges on the mitotic divisions of LT/Sv embryos. Here, we show that a failure to inactivate SAC affects mitoses during preimplantation development of LT/Sv embryos. This is manifested by the prolonged localization of MAD2L1 on kinetochores of mitotic chromosomes and abnormally lengthened early embryonic M-phases. Moreover, LT/Sv embryos exhibit elevated frequency of abnormal chromosome separation during the first mitotic division. These abnormalities participate in severe impairment of preimplantation development and significantly decrease the reproductive success of this strain of mice. Thus, the common meiosis and mitosis SAC-related failure participates in a complex LT/Sv phenotype.

Temporal regulation of the first mitosis in Xenopus and mouse embryos.

Cell cycle regulation in Eukaryotes is based on common molecular actors and mechanisms. However, the canonical cell cycle is modified in certain cells. Such modifications play a key role in oocyte maturation and embryonic development. They can be achieved either by introduction of new components, pathways, substrates, changed interactions between them, or by elimination of some factors inherited by the cells from previous developmental stages. Here we discuss a particular temporal regulation of the first embryonic M-phase of Xenopus and mouse embryos. These two examples help to understand better the general regulation of M-phase of the cell cycle.