New Tanaidacea (Crustacea: Peracarida) from the Gulf of Guinea

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Składniki technologiczne i wartość odżywcza pieczywa bezglutenowego®

The basis of a gluten-free diet is the exclusion of all products containing gluten, which is obtained from wheat, rye, barley and oats and their derivatives. The quality of gluten-free bread is shaped by additives, including hydrocolloids, which affect its structure, improve palatability and affect the nutritional value. Gluten-free bread can be low in protein and contain more total fat and salt, compared to wheat bread. When choosing gluten-free bread, you should make a particularly careful selection of products and diversify dishes prepared with their use.Podstawą diety bezglutenowej jest wykluczenie wszystkich produktów zawierających gluten, który otrzymywany jest z pszenicy, żyta, jęczmienia i owsa oraz z ich pochodnych. Ja-kość pieczywa bezglutenowego jest kształtowana przez dodat-ki m.in. hydrokoloidy, które wpływają na jego strukturę, po-prawiają smakowitość oraz wpływają na wartość odżywczą. Pieczywo bezglutenowe może być ubogie w białko i zawierać więcej tłuszczu ogółem oraz soli, w porównaniu do pieczywa pszennego. Wybierając pieczywo bezglutenowe należy doko-nywać szczególnie starannego doboru produktów i urozmai-cania potraw przygotowywanych z ich udziałem

Expression Profile of Brain Aging and Metabolic Function are Altered by Resveratrol or α-Ketoglutarate Supplementation in Rats Fed a High-Fat Diet

The aim of this study was to examine the impact of different dietary interventions started at middle age on the metabolic phenotype and gene expression profiling in the hypothalamus. One-year old rats were fed either a control diet, high-fat diet (HFD), HFD supplemented with resveratrol (HFD+RESV), or HFD supplemented with α-ketoglutarate (HFD+AKG). A 6-week HFD feeding led to significant changes in concentrations of plasma glucose, insulin, lipids, and thyroid hormones. Moreover, 32% of the 84 analyzed genes correlated with aging were differentially expressed compared to the control group, with the largest functional class being related to inflammatory response. Dietary RESV ameliorated the changes in plasma glucose, total cholesterol, and triiodothyronine concentrations induced by HFD feeding and significantly downregulated 60% of the surveyed genes compared to the control group, resulting in a major molecular shift compared to HFD alone. In contrast, AKG supplementation did not affect the metabolic phenotype, but prevented the gene expression pattern caused by HFD consumption, mimicking the effects observed in the control group. HFD feeding induces metabolic dysfunction and age-related genetic alterations in the hypothalamus of middle-aged rats, while dietary RESV or AKG may partially retard these effects, even though these compounds act in a different and specific manner

Impact of Human Adenovirus 36 on Embryonated Chicken Eggs: Insights into Growth Mechanisms

Human adenovirus 36 (HAdV-D36) is presently the sole virus identified to be associated with an elevated risk of obesity in both humans and animals. However, its impact on embryonated chicken eggs (ECEs) remains unexplored. This study endeavoured to examine the influence of HAdV-D36 on embryonic development by utilizing embryonated chicken eggs as a dynamic model. To simulate various infection routes, the allantoic cavity and the yolk sac of ECEs were inoculated with HAdV-D36. Subsequently, embryos from both the experimental (inoculated with virus) and control (inoculated with PBS) groups were weighed and subjected to daily histological examination. The daily embryo weights were assessed and compared between groups using the Shapiro–Wilk test. Histopathological changes in tissues were examined and compared between the tested and control groups to ascertain physiological alterations induced by the virus. Our study confirmed a significant increase in the body weight of ECEs. However, this phenomenon was not attributable to adipose tissue development; rather, it was characterized by an augmented number of cells in all observed tissues compared to control subjects. We posit that HAdV-D36 may impact developing organisms through mechanisms other than enhanced adipose tissue development. Specifically, our findings indicate an increased number of cells in all tissues, a phenomenon that occurs through an as-yet-unexplored pathway

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

Difference in Performance of EPI Pigs Fed Either Lipase-Predigested or Creon®-Supplemented Semielemental Diet

Pancreatic enzyme replacement therapy (PERT) and fat predigestion are key in ensuring the optimal growth of patients with cystic fibrosis. Our study attempted to highlight differences between fat predigestion and conventional PERT on body composition of young pigs with exocrine pancreatic insufficiency (EPI). EPI and healthy pigs were fed with high-fat diet for six weeks. During the last two weeks of the study, all pigs received additional nocturnal alimentation with Peptamen AF (PAF) and were divided into three groups: H - healthy pigs receiving PAF; P - EPI pigs receiving PAF+PERT; and L - EPI pigs receiving PAF predigested with an immobilized microbial lipase. Additional nocturnal alimentation increased the body weight gain of EPI pigs with better efficacy in P pigs. Humerus length and area in pigs in groups L and P were lower than that observed in pigs in group H (p value 0.005-0.088). However, bone mineral density and strength were significantly higher in P and L as compared to that of H pigs (p value 0.0026-0.0739). The gut structure was improved in P pigs. The levels of neurospecific proteins measured in the brain were mainly affected in P and less in L pigs as compared to H pigs. The beneficial effects of the nocturnal feeding with the semielemental diet in the prevention of EPI pigs' growth/development retardation are differently modified by PERT or fat predigestion in terms of growth, bone properties, neurospecific protein distribution, and gut structure

A PDE10A inhibitor CPL500036 is a novel agent modulating striatal function devoid of most neuroleptic side-effects

Background: Phosphodiesterase 10A (PDE10A) is expressed almost exclusively in the striatum and its inhibition is suggested to offer potential treatment in disorders associated with basal ganglia. We evaluated the selectivity, cytotoxicity, genotoxicity, pharmacokinetics and potential adverse effects of a novel PDE10A inhibitor, CPL500036, in vivo. Methods: The potency of CPL500036 was demonstrated by microfluidic technology, and selectivity was investigated in a radioligand binding assay against 44 targets. Cardiotoxicity in vitro was evaluated in human ether-a-go-go related gene (hERG)-potassium channel-overexpressing cells by the patch-clamp method and by assessing key parameters in 3D cardiac spheroids. Cytotoxicity was determined in H1299, HepG2 and SH-SY5Y cell lines. The Ames test was used for genotoxicity analyses. During in vivo studies, CPL500036 was administered by oral gavage. CPL500036 exposure were determined by liquid chromatography–tandem mass spectrometry and plasma protein binding was assessed. The bar test was employed to assess catalepsy. Prolactin and glucose levels in rat blood were measured by ELISAs and glucometers, respectively. Cardiovascular safety in vivo was investigated in dogs using a telemetry method. Results: CPL500036 inhibited PDE10A at an IC(50) of 1 nM, and interacted only with the muscarinic M2 receptor as a negative allosteric modulator with an IC(50) of 9.2 µM. Despite inhibiting hERG tail current at an IC(25) of 3.2 μM, cardiovascular adverse effects were not observed in human cardiac 3D spheroids or in vivo. Cytotoxicity in vitro was observed only at > 60 μM and genotoxicity was not recorded during the Ames test. CPL500036 presented good bioavailability and penetration into the brain. CPL500036 elicited catalepsy at 0.6 mg/kg, but hyperprolactinemia or hyperglycemic effects were not observed in doses up to 3 mg/kg. Conclusion: CPL500036 is a potent, selective and orally bioavailable PDE10A inhibitor with a good safety profile distinct from marketed antipsychotics. CPL500036 may be a compelling drug candidate