Dietary supplementation with phytohemagglutinin in combination with alpha-ketoglutarate limits the excretion of nitrogen via urinary tract

The aim of the study was to evaluate the effect of both phytohaemagglutinin (PHA) alone, and in combination with alpha-ketoglutaric acid (AKG), on nitrogen elimination via the urinary tract as opposed to the gastrointestinal tract of rats. In experiment I, rats were assigned to one of two experimental groups, (1) Control and (2) PHA, whilst in experiment 2, rats were assigned to one of three experimental groups, (1) Control, (2) AKG, and (3) AKG+PHA. AKG was administered via drinking water, while PHA was administered via a stomach tube. The stock solution of crude PHA in 0.9% NaCl, was (20% w/v) in water: 50 mg PHA/ml, 20 ml/kg body wt. Rats were 7 weeks old at the start of the experiments. Significantly lower daily weight gains in the AKG+PHA and PHA groups (p<0.05) were observed compared to the Control and AKG groups. Increased duodenal crypt depth (138%; p<0.05) was noticeable in the AKG+PHA group of Controls; however, there was no significant difference in the thickness of the tunica mucosa. In the AKG+PHA group, the expression of neuropeptide Y (NPY) in the granula of neuronal cells of the submucosal parasympathetic ganglia was noticeable, although no expression was found in goblet cells. Finally, significant reduction in N excretion in urine was observed in the AKG+PHA, compared with the Control groups (p<0.05). It is concluded that a combined PHA and AKG treatment stimulated the small bowel growth via enhanced epithelial turnover, reduced the N excreted in urine and increased the N in faeces

Absorption of Polyunsaturated Fatty Acid (PUFA) Is Related to IgG Blood Levels of Neonatal Pigs during the First 48 Hours Postpartum

The current study is aimed at highlighting the impact of enterally or parenterally applied immunoglobulins (Igs) on polyunsaturated fatty acid (PUFA) absorption in newborn pigs. Piglets were chosen as the appropriate model since they are born agammaglobulinemic and any effects of Ig addition can thus be easily monitored. Twenty-one, new born piglets were used in the study. Plasma levels of PUFAs, ARA, DHA, and EPA dropped (similarly to that seen in human infants) by between 40 and 50% in newborn, unsuckled piglets fed an infant formula for 48 h. However, piglets fed the same infant formula but supplied with immunoglobulins (Igs) either orally, by feeding piglets with swine or bovine colostrum, or intravenously, by i.u.a. (intraumbilical artery) infusion of swine or human Ig preparations or swine serum, demonstrated improved growth and PUFA levels similar to those observed at birth. The significant positive correlation was found between the body weight gain, as well as levels of ARA and EPA, and plasma immunoglobulins concentration. These results indicate the importance of the presence of Ig in the blood for appropriate absorption of dietary PUFAs and probably other nutrients in newborn piglets. This may have an impact on the dietary guidelines for human neonates, especially those born prematurely with low plasma Ig levels, since PUFAs are important factors for brain development in early life

The Immature Gut Barrier and Its Importance in Establishing Immunity in Newborn Mammals

The gut is an efficient barrier which protects against the passage of pathogenic microorganisms and potential harmful macromolecules into the body, in addition to its primary function of nutrient digestion and absorption. Contrary to the restricted macromolecular passage in adulthood, enhanced transfer takes place across the intestines during early life, due to the high endocytic capacity of the immature intestinal epithelial cells during the fetal and/or neonatal periods. The timing and extent of this enhanced endocytic capacity is dependent on animal species, with a prominent non-selective intestinal macromolecular transfer in newborn ungulates, e.g., pigs, during the first few days of life, and a selective transfer of mainly immunoglobulin G (IgG), mediated by the FcRn receptor, in suckling rodents, e.g., rats and mice. In primates, maternal IgG is transferred during fetal life via the placenta, and intestinal macromolecular transfer is largely restricted in human neonates. The period of intestinal macromolecular transmission provides passive immune protection through the transfer of IgG antibodies from an immune competent mother; and may even have extra-immune beneficial effects on organ maturation in the offspring. Moreover, intestinal transfer during the fetal/neonatal periods results in increased exposure to microbial and food antigens which are then presented to the underlying immune system, which is both naïve and immature. This likely stimulates the maturation of the immune system and shifts the response toward tolerance induction instead of activation or inflammation, as usually seen in adulthood. Ingestion of mother's milk and the dietary transition to complex food at weaning, as well as the transient changes in the gut microbiota during the neonatal period, are also involved in the resulting immune response. Any disturbances in timing and/or balance of these parallel processes, i.e., intestinal epithelial maturation, luminal microbial colonization and mucosal immune maturation due to, e.g., preterm birth, infection, antibiotic use or nutrient changes during the neonatal period, might affect the establishment of the immune system in the infant. This review will focus on how differing developmental processes in the intestinal epithelium affect the macromolecular passage in different species and the possible impact of such passage on the establishment of immunity during the critical perinatal period in young mammals

Decreased plasma concentrations of a-ketoglutarate in patients with chronic symptomatic coronary heart disease compared with healthy controls

WSTĘP: Wyniki dotychczasowych badań sugerują, że już od najwcześniejszych etapów rozwoju miażdżycy naczyń krwionośnych zachodzą zmiany w funkcjonowaniu mitochondriów komórek. Wyniki badań eksperymentalnychsugerują, że dysfunkcja śródbłonka, podwyższone stężenia cytokin prozapalnych, jak równieżnadmierne wytwarzanie wolnych rodników tlenowych, obserwowane w przebiegu miażdżycy, znacząco zaburzają reakcje cyklu Krebsa. Obecnie jednak mało jest danych z badań klinicznych na temat wpływu miażdżycy na stężenia metabolitów cyklu Krebsa u ludzi. Celem niniejszej pracy było określenie wpływu niedokrwienia mięśnia sercowego u pacjentów z chorobą wieńcową na osoczowe stężenie a-ketoglutaranu.MATERIAŁ I METODY: Do badania włączono 53 pacjentów z potwierdzoną w badaniu koronarograficznym chorobą niedokrwienną serca, którzy zostali przyjęci do szpitala z powodu utrzymywania się, mimo zastosowania farmakoterapii, objawów stabilnej dławicy piersiowej, bez towarzyszącego wzrostu stężenia markerów martwicy mięśnia sercowego we krwi. Do grupy kontrolnej włączono 20 zdrowych osób. Wartości osoczowych stężeń a-ketoglutaranu określono z zastosowaniem wysokosprawnej chromatografii cieczowej (HLPC).WYNIKI: Pacjenci z utrzymującymi się objawami stabilnej przewlekłej choroby wieńcowej charakteryzowali się istotnie niższymi wartościami stężeń a-ketoglutaranu w osoczu w porównaniu z osobami z grupy kontrolnej. Obie grupy nie wykazywały istotnych statystycznie różnic pod względem innych analizowanych parametrów klinicznych i biochemicznych.WNIOSKI: 1. Wartości osoczowych stężeń a-ketoglutaranu u pacjentów ze stabilnym niedokrwieniem mięśnia sercowego są niższe w porównaniu z osobami zdrowymi. 2. Spadek zawartości a-ketoglutaranu w osoczu u tych pacjentów może być rezultatem zaburzeń przebiegu reakcji cyklu Krebsa spowodowanych dysfunkcją śródbłonka i procesami zapalnymi w naczyniach zaangażowanych w rozwój miażdżycy, chociaż do potwierdzenia tej tezy potrzebne są dalsze badania.BACKGROUND: Recent studies revealed that mitochondrial function is altered since the earliest stages of atherosclerosis development. Experimental studies results revealed that endothelial dysfunction, elevated levels of inflammatory cytokines, such as excessive reactive oxygen species production, which underlie atherosclerosis, result in significant disruptions in the Krebs cycle flux. However, there is little data about the influence of atherosclerosis on the Krebs cycle intermediates concentrations in people. The aim of the study was to evaluate a possible influence of chronic cardiac ischemia on plasma concentrations of a-ketoglutarate in people with stable symptomatic coronary heart disease. MATERIAL AND METHODS: Blood samples were collected from 53 patients, with stable, symptomatic coronary heart disease confirmed in coronarography, who were admitted to the hospital due to persistent severe angina despite pharmacological treatment, without the elevation of cardiac enzymes blood level. The control group included 20 healthy people. Plasma concentrations of a-ketoglutarate were determined using an high-performance liquid chromatography (HPLC). RESULTS: Patients with stable coronary heart disease had significantly lower a-ketoglutarate plasma concentrations compared to healthy controls. There were no statistically significant differences in other analyzed clinical and biochemical parameters between both groups. CONCLUSIONS: 1. Patients with chronic myocardial ischemia have lower plasma concentrations of a-ketoglutarate comparing to healthy controls. 2. The decrease of plasma a-ketoglutarate concentrations in these patients may be a consequence of the Krebs cycle disruption due to the influence of endothelial dysfunction and inflammatory processes involved in the development of atherosclerosis, however further investigations are required

Aspects of gastrointestinal motility in relation to the development of digestive function in neonates

Abstract Gastrointestinal motility is responsible for mixing and transport of digesta and elimination of undigested residues. The basis for the motility is the electrical activity of the gastrointestinal smooth muscle, which has a recurring pattern. In the small intestine of mature animals, this pattern is associated with periodic fluctuations of mesenteric blood flow, and gastric, pancreatic and biliary secretion, and with intestinal absorption. In general, feeding disrupts the cyclic pattern in the stomach and small intestine, replacing it with a continuous post-feeding pattern, and the duration of the post-feeding pattern is dependent on animal species, composition of the diet and feeding regime. The perinatal and weaning periods manifest drastic changes in digestive function and, thus, in gastrointestinal motility. Due to difficulties in performing studies in perinatal and neonatal animals, only few data on the development of gastrointestinal motility, and its synchronisation with other digestive functions, are available. Whereas some studies in the literature indicate that the development of gastrointestinal motility follows the maturation of the regulatory mechanisms, recent data also suggest that changes in gastrointestinal motility around birth and weaning reflect changes in nutrient supply. This paper deals with some aspects of gastrointestinal motility, primarily in the gastric antrum and small intestine, of neonatal animals. Certainly, changes in gastrointestinal motility in early life could be of paramount importance for proper digestive function and this research area requires further attention

Hyaluronate and total hyaluronate-binding capacity of proteins under experimental chronic hepatitis C and treatment with alpha-ketoglutarate

The increase of hyaluronic acid concentration in the blood serum of rats during modelling of chronic hepatitis C is presented. The research of changes in the absolute and relative hyaluronate-binding activity of cytosolic proteins in the rats’ cerebellum and hippocampus under normal condition, experimental chronic hepatitis C and with the alfa-ketoglutarate treatment was carried out