Filters
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.
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.
Daily Treatment of Mice with Type 2 Diabetes with Adropin for Four Weeks Improves Glucolipid Profile, Reduces Hepatic Lipid Content and Restores Elevated Hepatic Enzymes in Serum
Adropin is a peptide hormone encoded by Energy Homeostasis Associated gene. Adropin modulates energy homeostasis and metabolism of lipids and carbohydrates. There is growing evidence demonstrating that adropin enhances insulin sensitivity and lowers hyperlipidemia in obese mice. The aim of this study was to investigate the effects of daily administration of adropin for four weeks in mice with experimentally induced type 2 diabetes (T2D). Adropin improved glucose control without modulating insulin sensitivity. Adropin reduced body weight, size of adipocytes, blood levels of triacylglycerol and cholesterol in T2D mice. T2D mice treated with adropin had lower liver mass, reduced hepatic content of triacylglycerol and cholesterol. Furthermore, adropin attenuated elevated blood levels of hepatic enzymes (ALT, AST, GGT and ALP) in T2D mice. In T2D mice, adropin increased the circulating adiponectin level. Adropin had no effects on circulating insulin and glucagon levels and did not alter pancreatic islets morphology. These results suggest that adropin improves glucose control, lipid metabolism and liver functions in T2D. In conjunction with reduced lipid content in hepatocytes, these results render adropin as an interesting candidate in therapy of T2D.
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.
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.