Potrava, některé její složky, nápoje a potravinové doplňky často ovlivňují metabolismus a transport léčiv v organismu nebo přímo farmakodynamické účinky léčiv. V důsledku těchto interakcí dochází ke změnám v biologické dostupnosti léčiv, ke snížení účinku nebo selhání terapie nebo ke zvýšení rizika výskytu nežádoucích účinků, výjimečně dokonce může dojít k projevům toxicity. Cílem přehledu je podat základní informaci o rozsahu aktuálních znalostí o interakcích potravy a nápojů s léčivy. Zejména pak ukázat na léčiva, která je z různých důvodů nezbytné užívat bud' nalačno, nebo po jídle a současně upozornit na skutečnost, že se léčiva mají zapíjet vodou.

Food, some of its ingredients, drinks and dietary supplements often affect the metabolism and transport of drugs in the body or directly the pharmacodynamic effects of drugs. As a result of these interactions, there is a change in the bioavailability of the drugs, in reducing the effect or failure of the therapy, or in increasing the risk of adverse reactions, and in exceptional cases there may be signs of toxicity. The aim of the review is to provide basic information about the extent of current knowledge about food and drink interactions with drugs. In particular, point to medicines that, for various reasons, need to be taken either on an empty stomach or after a meal, and at the same time to draw attention to the fact that medicines should be swallowed with water.

• MeSH
• ABC transportéry agonisté   antagonisté a inhibitory   fyziologie   MeSH
• abirateron terapeutické užití   MeSH
• absorpce v žaludku fyziologie   MeSH
• alkoholické nápoje škodlivé účinky   MeSH
• aplikace orální MeSH
• biologická dostupnost MeSH
• čaj enzymologie   fyziologie   MeSH
• enterocyty enzymologie   fyziologie   metabolismus   MeSH
• farmakoterapie metody   MeSH
• fyziologie výživy fyziologie   MeSH
• glukagonu podobný peptid 1 fyziologie   MeSH
• interakce bylin a léků fyziologie   MeSH
• interakce mezi potravou a léky * fyziologie   MeSH
• lidé MeSH
• mléko MeSH
• nežádoucí účinky léčiv MeSH
• ovocné a zeleninové šťávy škodlivé účinky   MeSH
• SLC transportéry agonisté   antagonisté a inhibitory   fyziologie   MeSH
• sycené nápoje škodlivé účinky   MeSH
• systém (enzymů) cytochromů P-450 fyziologie   MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• Publikační typ
• kazuistiky MeSH
• přehledy MeSH

• MeSH
• diabetes mellitus 1. typu farmakoterapie   MeSH
• diabetes mellitus 2. typu farmakoterapie   MeSH
• enterocyty metabolismus   účinky léků   MeSH
• hepatocyty enzymologie   metabolismus   účinky léků   MeSH
• játra enzymologie   metabolismus   účinky léků   MeSH
• léková kontraindikace MeSH
• lidé MeSH
• metformin farmakokinetika   farmakologie   terapeutické užití   MeSH
• nežádoucí účinky léčiv MeSH
• těhotenství účinky léků   MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• Check Tag
• lidé MeSH
• těhotenství účinky léků   MeSH

• MeSH
• enterocyty metabolismus   MeSH
• enteroendokrinní buňky metabolismus   MeSH
• kyselina ursodeoxycholová farmakologie   terapeutické užití   MeSH
• lidé MeSH
• metabolismus lipidů MeSH
• metabolismus sacharidů MeSH
• žlučové kyseliny a soli * metabolismus   terapeutické užití   MeSH
• Check Tag
• lidé MeSH

Impairment of mucosal barrier integrity of small intestine might be causative in immune-mediated gastrointestinal diseases. We tested the markers of epithelial apoptosis - cytokeratin 18 caspase-cleaved fragment (cCK-18), and enterocyte damage - intestinal fatty acid-binding protein (I-FABP) and soluble CD14 (sCD14) in sera of patients with untreated celiac disease (CLD), those on gluten-free diet (CLD-GFD), patients with autoimmune diabetes mellitus (T1D), T1D with insulitis (T1D/INS), and diabetes mellitus type 2 (T2D). We found elevated levels of cCK-18 (P<0.001), I-FABP (P<0.01) and sCD14 (P<0.05) in CLD when compared to healthy controls. However, the levels of cCK-18 (P<0.01) and I-FABP (P<0.01) in CLD-GFD were higher when compared with controls. Interestingly, elevated levels of cCK-18 and I-FABP were found in T2D and T1D (P<0.001), and T1D/INS (P<0.01, P<0.001). Twenty-two out of 43 CLD patients were seropositive for cCK-18, 19/43 for I-FABP and 11/43 for sCD14; 9/30 of T2D patients were positive for cCK-18 and 5/20 of T1D/INS for sCD14, while in controls only 3/41 were positive for cCK-18, 3/41 for I-FABP and 1/41 for sCD14. We documented for the first time seropositivity for sCD14 in CLD and potential usefulness of serum cCK-18 and I-FABP as markers of gut damage in CLD, CLD-GFD, and diabetes.

• MeSH
• apoptóza MeSH
• biologické markery krev   MeSH
• celiakie krev   epidemiologie   patologie   MeSH
• cytokiny krev   MeSH
• diabetes mellitus 1. typu krev   epidemiologie   patologie   MeSH
• diabetes mellitus 2. typu krev   epidemiologie   patologie   MeSH
• dospělí MeSH
• enterocyty metabolismus   patologie   MeSH
• komorbidita MeSH
• lidé středního věku MeSH
• lidé MeSH
• mladiství MeSH
• mladý dospělý MeSH
• nemoci jater krev   epidemiologie   patologie   MeSH
• prevalence MeSH
• reprodukovatelnost výsledků MeSH
• rizikové faktory MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• senzitivita a specificita MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mladiství MeSH
• mladý dospělý MeSH
• mužské pohlaví MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Geografické názvy
• Česká republika MeSH

Post-translational modification of histones is fundamental to the regulation of basic nuclear processes and subsequent cellular events, including differentiation. In this study, we analyzed acetylated forms of histones H2A, H2B, and H4 during induced differentiation in mouse (mESCs) and human (hESCs) embryonic stem cells and during induced enterocytic differentiation of colon cancer cells in vitro. Endoderm-like differentiation of mESCs induced by retinoic acid and enterocytic differentiation induced by histone deacetylase inhibitor sodium butyrate were accompanied by increased mono-, di-, and tri-acetylation of histone H2B and a pronounced increase in di- and tri-acetylation of histone H4. In enterocytes, mono-acetylation of histone H2A also increased and tetra-acetylation of histone H4 appeared only after induction of this differentiation pathway. During differentiation of hESCs, we observed increased mono-acetylation and decreased tri-acetylation of H2B. Mono-, di-, and tri-acetylation of H4 were reduced, manifested by a significant increase in nonacetylated H4 histones. Levels of acetylated histones increased during induced differentiation in mESCs and during histone deacetylase (HDAC) inhibitor-induced enterocytic differentiation, whereas differentiation of human ESCs was associated with reduced acetylation of histones H2B and H4.

• MeSH
• acetylace MeSH
• buněčná diferenciace MeSH
• embryonální kmenové buňky cytologie   metabolismus   MeSH
• endoderm cytologie   metabolismus   MeSH
• enterocyty cytologie   metabolismus   MeSH
• epigeneze genetická MeSH
• histonacetyltransferasy metabolismus   MeSH
• histony metabolismus   MeSH
• lidé MeSH
• myši MeSH
• nádorové buněčné linie MeSH
• posttranslační úpravy proteinů * MeSH
• spektrometrie hmotnostní - ionizace laserem za účasti matrice MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

There is substantial clinical and experimental evidence that ammonia is a major factor in the pathogenesis of hepatic encephalopathy. In the article is demonstrated that in hepatocellular dysfunction, ammonia detoxification to glutamine (GLN) in skeletal muscle, brain, and likely the lungs, is activated. In addition to ammonia detoxification, enhanced GLN production may exert beneficial effects on the immune system and gut barrier function. However, enhanced GLN synthesis may exert adverse effects in the brain (swelling of astrocytes or altered neurotransmission) and stimulate catabolism of branched-chain amino acids (BCAA; valine, leucine, and isoleucine) in skeletal muscle. Furthermore, the majority of GLN produced is released to the blood and catabolized in enterocytes and the kidneys to ammonia, which due to liver injury escapes detoxification to urea and appears in peripheral blood. As only one molecule of ammonia is detoxified in GLN synthesis whereas two molecules may appear in GLN breakdown, these events can be seen as a vicious cycle in which enhanced ammonia concentration activates synthesis of GLN leading to its subsequent catabolism and increase in ammonia levels in the blood. These alterations may explain why therapies targeted to intestinal bacteria have only a limited effect on ammonia levels in patients with liver failure and indicate the needs of new therapeutic strategies focused on GLN metabolism. It is demonstrated that each of the various treatment options targeting only one the of the ammonia-lowering mechanisms that affect GLN metabolism, such as enhancing GLN synthesis (BCAA), suppressing ammonia production from GLN breakdown (glutaminase inhibitors and alpha-ketoglutarate), and promoting GLN elimination (phenylbutyrate) exerts substantial adverse effects that can be avoided if their combination is tailored to the specific needs of each patient.

• MeSH
• amoniak metabolismus   MeSH
• enterocyty metabolismus   MeSH
• fenylbutyráty škodlivé účinky   farmakologie   terapeutické užití   MeSH
• glutamin metabolismus   MeSH
• glutaminasa antagonisté a inhibitory   MeSH
• hyperamonemie farmakoterapie   etiologie   metabolismus   MeSH
• jaterní encefalopatie dietoterapie   farmakoterapie   metabolismus   MeSH
• játra metabolismus   MeSH
• kosterní svaly metabolismus   MeSH
• kritický stav MeSH
• kyselina glutamová metabolismus   farmakologie   terapeutické užití   MeSH
• kyseliny ketoglutarové škodlivé účinky   farmakologie   terapeutické užití   MeSH
• ledviny metabolismus   MeSH
• lékové interakce MeSH
• lidé MeSH
• mikrobiota MeSH
• mozek metabolismus   MeSH
• orgánová specificita MeSH
• střeva mikrobiologie   MeSH
• větvené aminokyseliny metabolismus   terapeutické užití   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH

BACKGROUND: Citrulline is an amino acid produced by enterocytes. Serum citrulline concentration has been proposed as a marker of enterocyte mass and function. Our study focused on evaluation of citrulline levels in patients with diarrhea related to toxic intestinal damage (mucositis), intestinal graft versus host disease (GVHD), and other etiology of diarrhea (e.g., dysmicrobia) after allogeneic stem cells transplantation (SCT). MATERIAL AND METHODS: This was a prospective study in 11 adults (18 blood samples) with diarrhea developed after allogeneic SCT in 4/2011-1/2012 compared to twenty healthy control samples. RESULTS: The median (interquartile range) of citrulline levels was significantly lower in the transplanted patients group compared to healthy controls: 9.3 (3.62-15.38) vs. 33.3 (26.82-36.23) µmol/L, p<0.0001. The median values of citrulline in patients with post-transplant toxic intestinal mucositis (n=8, days 1-22 post-transplant) vs. intestinal GVHD (n=7, day 43-142) vs. other etiology of diarrhea (e.g., dysmicrobia) (n=3, day 120-127) were: 9.55 (2.95-12.03) vs. 5 (3.85-9.05) vs. 15.6 (15.45-18.3) mol/L resp. Serum citrulline levels were significantly higher in other (eg, dysmicrobic) etiology of diarrhea in comparison with mucositis (p=0.0336) and GVHD (p=0.0152). CONCLUSIONS: Citrulline levels are very low shortly after the myeloablative FLU/MEL or BuCY2 conditioning allogeneic SCT due to the toxic intestinal damage. Significantly low levels of citrulline were also in patients with intestinal GVHD later on. Other observations in larger groups of patients are necessary before any specific recommendation for citrulline levels monitoring in intestinal GVHD can be made.

• MeSH
• biologické markery krev   MeSH
• citrulin krev   MeSH
• dospělí MeSH
• enterocyty metabolismus   MeSH
• homologní transplantace škodlivé účinky   MeSH
• lidé středního věku MeSH
• lidé MeSH
• pilotní projekty MeSH
• studie případů a kontrol MeSH
• transplantace hematopoetických kmenových buněk škodlivé účinky   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Many physiological functions exhibit a diurnal rhythmicity that is influenced by biological clocks and feeding rhythms. In this review, we discuss the growing evidence showing the important role of circadian rhythms in regulating intestinal mucosa. First, we introduce the molecular timing system and the interrelationship between the master biological clock in the suprachiasmatic nuclei of the brain and the peripheral intestinal clock and provide evidence that the intestinal clock is entrained with the external environment. Second, we review the circadian rhythmicity of enterocyte proliferation and the largely unknown regulatory mechanisms behind these rhythms. Finally, we focus on the circadian clock control of food processing that functions by regulating the expression of digestive enzymes and intestinal nutrient and salt transporters. The concepts to be discussed highlight the ability of the intestinal epithelium to utilize self-sustained clock signals together with signals associated with changes in the cellular environment and to use endogenous temporal control of the gastrointestinal functions to meet varying physiological and pathophysiological demands. The fact that internal de-synchronizations within the body, such as those that occur in shift workers or with changes in food intake behaviour, are often associated with malfunctions of the gastrointestinal tract indicates that more information about the connections between the circadian clock and intestinal mucosa/transporting enterocytes could provide clues for future therapies.

• MeSH
• časové faktory MeSH
• cirkadiánní rytmus * MeSH
• enterocyty metabolismus   MeSH
• gastrointestinální nemoci metabolismus   patofyziologie   MeSH
• intestinální absorpce MeSH
• lidé MeSH
• membránové transportní proteiny metabolismus   MeSH
• nucleus suprachiasmaticus metabolismus   patofyziologie   MeSH
• podněty MeSH
• přijímání potravy MeSH
• proliferace buněk MeSH
• signální transdukce MeSH
• střevní nervový systém metabolismus   patofyziologie   MeSH
• střevní sliznice inervace   metabolismus   patofyziologie   MeSH
• trávení MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH

PURPOSE: To examine the p38 mitogen-activated protein kinase (p38) phosphorylation and transforming growth factor beta 1 (TGF-β1) expression in rat colon enterocytes after irradiation and their contribution to pathology of intestinal radiation disease. MATERIALS AND METHODS: Male Wistar rats were irradiated with whole body γ-radiation of 0.5, 1, 2, 3, 4, 5, 6, 7, 8, 9, and 10 Gy ((60)Co, 1.44 Gy.min(-1)). Samples were taken 4 and 24 h after irradiation, immunohistochemically stained, then p38 phosphorylation and TGF-β1 expression were measured in apical and cryptal enterocytes using computer image analysis. In selected groups, morphometric parameters, mitosis and apoptosis were evaluated. RESULTS: P38 phosphorylation integrated optical density (IOD)-based levels increased 2.4-fold (p ≤ 0.01) and 3.6 to 22.8-fold (p ≤ 0.001) in apical enterocytes 4 h after 0.5 Gy and 24 h after 3-10 Gy, respectively. TGF-β1 IOD-based expression increased 3.3- to 6.9-fold (p ≤ 0.001) and 1.6- to 4.9-fold (p ≤ 0.001) in apical cells 4 h after 0.5-2, 4, 5 Gy and 24 h after 6-10 Gy, respectively. No changes were observed in crypts. CONCLUSIONS: We found a chronological and dose-dependent order of p38 activation and TGF-β1 expression in apical enterocytes. Transient up-regulation of p38 and TGF-β1 signalling observed 4 h after low-dose irradiation may participate in molecular mechanisms creating cellular over-expression in apical compartment, while persistent patterns measured 24 h after high-dose irradiation might provide protection of remaining cells in order to maintain tissue integrity.

• MeSH
• aktivace enzymů účinky záření   MeSH
• apoptóza účinky záření   MeSH
• časové faktory MeSH
• celotělové ozáření škodlivé účinky   MeSH
• enterocyty cytologie   enzymologie   metabolismus   účinky záření   MeSH
• fosforylace účinky záření   MeSH
• kolon cytologie   účinky záření   MeSH
• krysa rodu rattus MeSH
• mitogenem aktivované proteinkinasy p38 metabolismus   MeSH
• mitóza účinky záření   MeSH
• polarita buněk účinky záření   MeSH
• potkani Wistar MeSH
• regulace genové exprese účinky záření   MeSH
• záření gama škodlivé účinky   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

The intestinal transport of nutrients exhibits distinct diurnal rhythmicity, and the enterocytes harbor a circadian clock. However, temporal regulation of the genes involved in colonic ion transport, i.e., ion transporters and channels operating in absorption and secretion, remains poorly understood. To address this issue, we assessed the 24-h profiles of expression of genes encoding the sodium pump (subunits Atp1a1 and Atp1b1), channels (α-, β-, and γ-subunits of Enac and Cftr), transporters (Dra, Ae1, Nkcc1, Kcc1, and Nhe3), and the Na(+)/H(+) exchanger (NHE) regulatory factor (Nherf1) in rat colonic mucosa. Furthermore, we investigated temporal changes in the spatial localization of the clock genes Per1, Per2, and Bmal1 and the genes encoding ion transporters and channels along the crypt axis. In rats fed ad libitum, the expression of Atp1a1, γEnac, Dra, Ae1, Nhe3, and Nherf1 showed circadian variation with maximal expression at circadian time 12, i.e., at the beginning of the subjective night. The peak γEnac expression coincided with the rise in plasma aldosterone. Restricted feeding phase advanced the expression of Dra, Ae1, Nherf, and γEnac and decreased expression of Atp1a1. The genes Atp1b1, Cftr, αEnac, βEnac, Nkcc1, and Kcc1 did not show any diurnal variations in mRNA levels. A low-salt diet upregulated the expression of βEnac and γEnac during the subjective night but did not affect expression of αEnac. Similarly, colonic electrogenic Na(+) transport was much higher during the subjective night than the subjective day. These findings indicate that the transporters and channels operating in NaCl absorption undergo diurnal regulation and suggest a role of an intestinal clock in the coordination of colonic NaCl absorption.

• MeSH
• aldosteron krev   MeSH
• cirkadiánní proteiny Period genetika   MeSH
• cirkadiánní rytmus genetika   MeSH
• elektrolyty farmakokinetika   MeSH
• enterocyty metabolismus   MeSH
• intestinální absorpce genetika   MeSH
• iontové kanály genetika   MeSH
• kolon cytologie   fyziologie   MeSH
• krysa rodu rattus MeSH
• kuchyňská sůl farmakokinetika   MeSH
• potkani Wistar MeSH
• přijímání potravy genetika   MeSH
• stanovení celkové genové exprese MeSH
• střevní sliznice metabolismus   MeSH
• transportní proteiny genetika   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH