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Biologiczna rola neuronostatyny, hormonu kodowanego przez gen somatostatyny
Neuronostatyna jest hormonem peptydowym kodowanym przez gen somatostatyny. Neuronostatyna została odkryta w 2008 roku dzięki zastosowaniu metod bioinformatycznych. Badania na gryzoniach wykazały, że wywiera ona szerokie działanie w centralnym układzie nerwowym, jak również w tkankach obwodowych. Wykazano, że neuronostatyna zmniejsza pobieranie pokarmu oraz wody, spowalnia pasaż żołądkowo-jelitowy, a także może mieć ważne znaczenie w procesie adipogenezy. Peptyd ten powoduje również zwiększenie wydzielania glukagonu z komórek alfa wysp trzustkowych. Ponad to, dowiedziono, że neuronostatyna wpływa na kurczliwość serca oraz na ciśnienie krwi, a także bierze udział w procesach związanych z zapamiętywaniem, odczuwaniem bólu oraz lęku, a także może wywoływać efekt zbliżony do depresji. W niniejszej pracy dokonano aktualnego stanu na temat biologicznej roli neuronostatyny w organizmie.
The Effects of Neuropeptide B on Proliferation and Differentiation of Porcine White Preadipocytes into Mature Adipocytes
Neuropeptide B (NPB) affects energy homeostasis and metabolism by binding and activating NPBWR1 and NPBWR2 in humans and pigs. Recently, we reported that NPB promotes the adipogenesis of rat white and brown preadipocytes as well as 3T3-L1 cells. In the present study, we evaluated the effects of NPB on the proliferation and differentiation of white porcine preadipocytes into mature adipocytes. We identified the presence of NPB, NPBWR1, and NPBWR2 on the mRNA and protein levels in porcine white preadipocytes. During the differentiation process, NPB increased the mRNA expression of PPARγ, C/EBPβ, C/EBPα, PPARγ, and C/EBPβ protein production in porcine preadipocytes. Furthermore, NPB stimulated lipid accumulation in porcine preadipocytes. Moreover, NPB promoted the phosphorylation of the p38 kinase in porcine preadipocytes, but failed to induce ERK1/2 phosphorylation. NPB failed to stimulate the expression of C/EBPβ in the presence of the p38 inhibitor. Taken together, we report that NPB promotes the differentiation of porcine preadipocytes via a p38-dependent mechanism.
Expression of adropin in the reproductive organs of healthy female dogs and those with cystic endometrial hyperplasia, pyometra, and ovarian cysts
The Action of Cannabidiol on Doxycycline Cytotoxicity in Human Cells—In Vitro Study
Improper use of drugs in both animal and human therapy, such as doxycycline (DOX), lead to the accumulation of residues in edible animal tissues as well as in the environment. Plant-derived compounds reduce the adverse effects of drugs. This study aimed to evaluate the effect of cannabidiol (CBD) in two concentrations: lower (1.56 µg/mL) (DOX + C1) and higher (3.125 µg/mL) (DOX + C2) on the cytotoxicity of doxycycline in human cells. The toxicity of DOX and its CBD-containing mixtures was assessed after 72 h of exposure in three human cell lines: neural (SH-SY5Y), hepatic (HepG2), and kidney (HEK-293). The exposure to DOX resulted in inhibition of mitochondrial activity (SH-SY5Y) and inhibition of DNA synthesis (HepG2 and HEK-293). IC50 values for DOX ranged from 9.8 to >200 µg/mL in SH-SY5Y cells, 13.4 to 200 µg/mL in HepG2 cells, and 8.9 to 30.4 µg/mL in HEK-293 cells. The nature of the interaction depended on both the cell lines and the concentration of CBD in the mixture. Both CBD mixtures demonstrated a synergistic interaction in neuronal cells. In HepG2 cells, both mixtures showed additive and antagonistic interactions. In HEK-293 cells, the DOX + C1 mixture exhibited an antagonistic (protective) effect, while the DOX + C2 mixture showed an additive effect. There were no changes in oxidative stress levels; however, alterations in apoptosis levels and cell morphology were observed following exposure to the mixtures. The presence of doxycycline in the diet and the environment poses a health risk to consumers. The increasing consumption of CBD-containing products may reduce the risk associated with the presence of this drug in food. It is worth emphasizing the need for research aimed at minimizing the adverse effects of pharmaceuticals on the health of humans and animals.
Nesfatin-1 expression and blood plasma concentration in female dogs suffering from cystic endometrial hyperplasia and pyometra and its possible interaction with phoenixin-14
Abstract Background Nesfatin-1 is a neuropeptide that regulates the hypothalamic-pituitary-gonadal axis and may play a role in uterus function. It is co-expressed with other peptides, such as phoenixin, which can influence sex hormone secretion. Our previous research has confirmed that phoenixin-14 is involved in the development of cystic endometrial hyperplasia (CEH) and pyometra in dogs. Therefore, based on the similarities and interactions between these neuropeptides, we hypothesized that nesfatin-1 might also regulate the reproductive system in dogs. This study aimed to determine the expression of nesfatin-1 and its interaction with phoenixin-14 in dogs with CEH or pyometra compared to healthy females, and concerning animals’ body condition score (BCS 4–5/9 vs. BCS > 5/9). Results The analysis of nesfatin-1 in the uterus of bitches consisted of qPCR, western blot and immunofluorescence assays, and ELISAs. The results showed significantly higher nesfatin-1 encoding gene, nucleobindin-2 mRNA (Nucb2) and nesfatin-1 protein expression in overweight females and those suffering from CEH or pyometra compared to healthy animals. The immunoreactivity of nesfatin-1 was elevated in the uteri of bitches with higher BCS > 5/9. Moreover, nesfatin-1 blood concentrations increased in all examined overweight bitches. In the case of phoenixin signals, we found opposite results, regardless of the female body condition score. Conclusion The etiology of CEH and pyometra are not fully known, although we have expanded the level of knowledge with respect to the possible interaction of nesfatin-1 and phoenixin in female dogs’ uteri. They interact oppositely. With increasing female body weight, the expression of nesfatin-1 in the uterus and its peripheral blood concentration increased. However, for female dogs affected by CEH and pyometra, a decreased level of phoenixin-14, irrespective of their body condition score is characteristic. This knowledge could be crucial in the development of biomarkers for these conditions, which may lead to earlier recognition.
Raw data to article - Neuronostatin regulates proliferation and differentiation of rat brown primary preadipocytes
GIP_HUMAN [22–51] Peptide Encoded by the Glucose-Dependent Insulinotropic Polypeptide (GIP) Gene Suppresses Insulin Expression and Secretion in INS-1E Cells and Rat Pancreatic Islets
GIP_HUMAN [22–51] is a recently discovered peptide that shares the same precursor molecule with glucose-dependent insulinotropic polypeptide (GIP). In vivo, chronic infusion of GIP_HUMAN [22–51] in ApoE−/− mice enhanced the development of aortic atherosclerotic lesions and upregulated inflammatory and proatherogenic proteins. In the present study, we evaluate the effects of GIP_HUMAN [22–51] on insulin mRNA expression and secretion in insulin-producing INS-1E cells and isolated rat pancreatic islets. Furthermore, we characterize the influence of GIP_HUMAN [22–51] on cell proliferation and death and on Nf-kB nuclear translocation. Rat insulin-producing INS-1E cells and pancreatic islets, isolated from male Wistar rats, were used in this study. Gene expression was evaluated using real-time PCR. Cell proliferation was studied using a BrdU incorporation assay. Cell death was quantified by evaluating histone-complexed DNA fragments. Insulin secretion was determined using an ELISA test. Nf-kB nuclear translocation was detected using immunofluorescence. GIP_HUMAN [22–51] suppressed insulin (Ins1 and Ins2) in INS-1E cells and pancreatic islets. Moreover, GIP_HUMAN [22–51] promoted the translocation of NF-κB from cytoplasm to the nucleus. In the presence of a pharmacological inhibitor of NF-κB, GIP_HUMAN [22–51] was unable to suppress Ins2 mRNA expression. Moreover, GIP_HUMAN [22–51] downregulated insulin secretion at low (2.8 mmol/L) but not high (16.7 mmol/L) glucose concentration. By contrast, GIP_HUMAN [22–51] failed to affect cell proliferation and apoptosis. We conclude that GIP_HUMAN [22–51] suppresses insulin expression and secretion in pancreatic β cells without affecting β cell proliferation or apoptosis. Notably, the effects of GIP_HUMAN [22–51] on insulin secretion are glucose-dependent.
Neuronostatin regulates proliferation and differentiation of rat brown primary preadipocytes
AbstractHigh variations in juvenile wood properties in the radial direction and its worse performance than mature wood make it less suitable for some applications and often treated as waste material. This study aimed to assess how thermal modification affects the chemical composition and the physical, mechanical and swelling properties of Scots pine juvenile and mature wood. An additional goal was to evaluate if the modification can equalise the differences in selected properties of juvenile wood to those of mature wood so that from waste material, juvenile wood can become a fully-fledged raw material for various industrial applications. Thermal treatment at 220 °C influenced wood chemical composition, degrading mainly hemicelluloses but also affecting cellulose and lignin, which resulted in a reduction of hydroxyls and carbonyl/carboxyl groups. These changes were more pronounced for mature than juvenile wood. It reduced mass loss and swelling rate, and increased swelling pressure in the tangential and radial directions to a higher degree for juvenile than mature wood. Changes in mechanical properties in compression were statistically significant only for mature wood, while wood hardness remained unaffected. Although the applied heat treatment improved the performance of juvenile wood by reducing its swelling rate, it did not equalise the examined properties between juvenile and mature wood. Since higher juvenile wood proportion is expected in the wood supply from the future intensively managed forests, there is still a need to find suitable modification methods or better processing techniques so that instead of being thrown away as waste, it could be used broadly in various industrial applications.
The role of the orexin (hypocretin) system in controlling energy homeostasis, endocrine system, and reproduction in pigs and other living organisms
Expression and localization of the neuropeptide phoenixin-14 and its receptor GRP173 in the canine reproductive organs and periovarian adipose tissue
The tissue distribution of nucleobindin-2/nesfatin-1 in the reproductive organs of bitches with regard to the animal’s age and body weight
Abstract Introduction Neuropeptide nesfatin-1, a nucleobindin-2 derivative, plays a role in regulating food intake, energy metabolism and body weight. It also interacts with the hypothalamic-pituitary-gonadal axis and has functions in the reproductive system. However, its impact on the canine reproductive tract has not been well documented. This study aimed to investigate the potential role of nesfatin-1 in canine ovarian activity and uterine function. Material and Methods Tissue and peripheral blood samples were collected from 60 bitches of various ages and body condition scores (BCS). Analyses included real-time PCR, immunofluorescence examinations and ELISA tests. Results Higher level of nucleobindin-2 mRNA were found in the ovarian tissue of both younger and elderly overweight dogs (BCS > 5/9). The elevated expression of nesfatin-1 was observed in the uterine tissues of overweight dogs (BCS > 5/9) compared to its expression in animals in optimal body condition (BCS = 4/9). This finding was consistent with higher nesfatin-1 levels in the peripheral blood of overweight dogs. Conclusion The distribution and expression of nesfatin-1 in canine reproductive organs vary depending on the animal’s age and body weight. The role of nesfatin-1 in the reproductive system is influenced by the animal’s body condition and the extent of surplus adipose tissue, which may have significant implications for reproductive functions.
The levels of adropin and its therapeutic potential in diabetes
Adropin, a peptide hormone encoded by the energy homeostasis-associated gene, is expressed in various tissues, including the brain. Accumulating evidence from in vivo and in vitro studies highlights adropin's pivotal role in modulating carbohydrate and lipid metabolism. Notably, circulating adropin levels are lower in overweight and obese humans, and experimental interventions involving adropin overexpression or synthetic administration demonstrate promising outcomes in mitigating obesity-related metabolic abnormalities and preventing weight gain. This review comprehensively summarizes the current understanding of adropin's potential implications in diverse types of diabetes. Specifically, it explores adropin's utility as a biomarker for different types of diabetes and elucidates its significance as a potential predictor of diabetic adverse outcomes. Furthermore, the review delves into the beneficial effects of adropin treatment in animal models of experimentally induced diabetes, shedding light on its mechanisms of action in modulating glucose metabolism. In this comprehensive overview, we aim to provide a nuanced understanding of multifaceted role of adropin in diabetes pathogenesis and its therapeutic potential in combating this global health challenge.
Protective Action of Cannabidiol on Tiamulin Toxicity in Humans—In Vitro Study
The growing awareness and need to protect public health, including food safety, require a thorough study of the mechanism of action of veterinary drugs in consumers to reduce their negative impact on humans. Inappropriate use of veterinary drugs in animal husbandry, such as tiamulin, leads to the appearance of residues in edible animal tissues. The use of natural substances of plant origin, extracted from hemp (Cannabis sativa L.), such as cannabidiol (CBD), is one of the solutions to minimize the negative effects of tiamulin. This study aimed to determine the effect of CBD on the cytotoxicity of tiamulin in humans. The cytotoxic activity of tiamulin and the effect of its mixtures with CBD were tested after 72 h exposure to three human cell lines: SH-SY5Y, HepG2 and HEK-293. Cytotoxic concentrations (IC50) of the tested drug and in combination with CBD were assessed using five biochemical endpoints: mitochondrial and lysosomal activity, proliferation, cell membrane integrity and effects on DNA synthesis. Oxidative stress, cell death and cellular morphology were also assessed. The nature of the interaction between the veterinary drug and CBD was assessed using the combination index. The long-term effect of tiamulin inhibited lysosomal (SH-SY5SY) and mitochondrial (HepG2) activity and DNA synthesis (HEK-293). IC50 values for tiamulin ranged from 2.1 to >200 µg/mL (SH-SY5SY), 13.9 to 39.5 µg/mL (HepG2) and 8.5 to 76.9 µg/mL (HEK-293). IC50 values for the drug/CBD mixtures were higher. Reduced levels of oxidative stress, apoptosis and changes in cell morphology were demonstrated after exposure to the mixtures. Interactions between the veterinary drug and CBD showed a concentration-dependent nature of tiamulin in cell culture, ranging from antagonistic (low concentrations) to synergistic effects at high drug concentrations. The increased risk to human health associated with the presence of the veterinary drug in food products and the protective nature of CBD use underline the importance of these studies in food toxicology and require further investigation.