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Kotunia A.,Katedra Nauk Fizjologicznych | Pietrzak P.,Katedra Nauk Fizjologicznych | Guilloteau P.,French National Institute for Agricultural Research | Zabielski R.,Katedra Nauk Fizjologicznych
Przeglad Gastroenterologiczny | Year: 2010

Sodium butyrate (NaB) dissociating to butyric acid is regarded as a molecule which may be potentially applied in gastrointestinal mucosa treatment. In humans, NaB is produced by colonic bacteria. In certain cases, NaB production may be diminished; hence supplementation with exogenous NaB is essential the more so as NaB is a major energy source for colonocytes. In this review, we would like to discuss present knowledge about the role of NaB in the gastrointestinal tract, in particular its trophic, proapoptotic, cytoprotective and anti-inflammatory role.


Banasiewicz T.,Katedra I Klinika Chirurgii Ogolnej | Borycka-Kiciak K.,Klinika Chirurgii Ogolnej I Przewodu Pokarmowego | Dobrowolska-Zachwieja A.,Katedra I Klinika Gastroenterologii | Friediger J.,Oddzial Chirurgii Ogolnej | And 7 more authors.
Przeglad Gastroenterologiczny | Year: 2010

This article presents the point of view of a group of experts in physiology, gastroenterology and surgery regarding effectiveness of butyric acid preparation in dietary treatment in patients with small and large bowel diseases. The literature review revealed that butyric acid given per os as sodium salt (sodium butyrate) has a number of beneficial effects on function and regeneration of intestines. The dietary product of special medicinal use Debutir™ (Polfa-Łódź) contains sodium butyrate as an active substance, protected in a triglyceride matrix, which allows slow release of sodium butyrate along the entire gastrointestinal tract, thereby permitting its positive effects to be exerted on the entire small and large bowel. Experts have pointed out the clinical need to introduce butyric acid and its salt in dietary treatment in patients with intestine diseases. Experts have specified several groups of patients who would gain special benefits from enriching the diet with butyric acid. Use of butyric acid preparations is recommended for elderly people, and for patients with irritable bowel disease (IBD), after intestine resection and pouchitis. The strong trophic effect of sodium butyrate justifies its use in patients with cancer cachexia, with chronic diseases and immunity disturbances.


Chlebowska-Smigiel A.,Katedra Biotechnologii | Gniewosz M.,Katedra Biotechnologii | Wilczak J.,Katedra Nauk Fizjologicznych | Kamola D.,Katedra Nauk Fizjologicznych
Zywnosc. Nauka. Technologia. Jakosc/Food. Science Technology. Quality | Year: 2014

The effect was studied of pullulan additive on the growth and fermentation capacity of nine strains of lactic acid bacteria of the genus Lactobacillus. Deep batch cultures were grown during a period of 24 h in an MRS control and experimental medium with 2.0 % of pullulan added. During that 24 h period, it was reported that the bacteria grew from the initial number of 104 cfu/cm ³ to the count of 107 ÷ 109 cfu/cm³ depending on the strain studied. No significant differences were reported between the count of bacteria cultured in the control medium and in the experimental medium with pullulan added. In order to compare the fermentation capacity of strains at time "0" and at the end of growing those bacteria in the two media, a content of short chain fatty acids (SCFA) was determined using an HPLC method. The following acids were found: formic acid, lactic acid, acetic acid, propionic acid, and hydroxybutyric acid. A higher total content of SCFA was reported in the MRS control medium compared to the MRS experimental medium. The pullulan additive added to the MRS medium contributed to an increased production of lactic acid by the two strains of LAB and of acetic acid by 5 of the 9 LAB strains analyzed. © by Polskie Towarzystwo Technologów Żywności, Kraków 2014.


Milewska M.,Katedra Nauk Fizjologicznych | Grabiec K.,Katedra Nauk Fizjologicznych | Grzelkowska-Kowalczyk K.,Katedra Nauk Fizjologicznych
Postepy Higieny i Medycyny Doswiadczalnej | Year: 2014

The commitment of myogenic cells in skeletal muscle differentiation requires earlier irreversible interruption of the cell cycle. At the molecular level, several key regulators of the cell cycle have been identified: cyclin-dependent kinases and their cyclins stimulate the cell cycle progress and its arrest is determined by the activity of cdk inhibitors (Cip/Kip and INK protein families) and pocket protein family: Rb, p107 and p130. The biological activity of cyclin/cdk complexes allows the successive phases of the cell cycle to occur. Myoblast specialization, differentiation and fusion require the activity of myogenic regulatory factors, which include MyoD, myogenin, Myf5 and MRF4. MyoD and Myf5 play a role in muscle cell specialization, myogenin controls the differentiation process, whereas MRF4 is involved in myotube maturation. The deregulation of the cell cycle leads to uncontrolled proliferation, which antagonizes the functions of myogenic factors and it explains the lack of differentiation-specific gene expression in dividing cells. Conversely, the myogenic factor MyoD seems to cooperate with cell cycle inhibitors leading to inhibition of cell cycle progress and commitment to the differentiation process. The hypophosphorylated form of Rb and cdk inhibitors play an important role in permanent arrest of the cell cycle in differentiated myotubes. Furthermore, cyclin/cdk complexes not only regulate cell division by phosphorylation of several substrates, but may also control other cellular processes such as signal transduction, differentiation and apoptosis. Beyond regulating the cell cycle, Cip/Kip proteins play an important role in cell death, transcription regulation, cell fate determination, cell migration and cytoskeletal dynamics. The article summarizes current knowledge concerning the interactions of intracellular signaling pathways controlling crucial stages of fetal and regenerative myogenesis. Copyright © Postepy Higieny i Medycyny Dos̈wiadczalnej 2015.


Zielniok K.,Katedra Nauk Fizjologicznych | Gajewska M.,Katedra Nauk Fizjologicznych | Motyl T.,Katedra Nauk Fizjologicznych
Postepy Higieny i Medycyny Doswiadczalnej | Year: 2014

Sex steroids: 17β-estradiol and progesterone play a major role in modulation of reproductive functions of the organism and participate in regulation of a broad spectrum of cellular processes in target cells via their specific receptors. Our understanding of molecular mechanisms of sex steroid action has significantly developed over the last years. Apart from the well-established effect of sex steroids on regulation of gene expression, some rapid nongenomic mechanisms have been identified, which are involved in modulation of the activity of several cellular, membrane-bound and cytoplasmic regulatory proteins. 17β-estradiol and progesterone regulate several signal transduction pathways, which involve activation of enzymes such as mitogen-activated protein kinases (MAPK), phosphatidylinositol 3-kinase and tyrosine kinases. Biological effects of sex steroids action constitute a complex interplay of genomic and nongenomic mechanisms, and depend on the physiological and genetic context of the target cell. Understanding the molecular mechanisms of sex steroids action is therefore important and may broaden our knowledge about their role in both physiological and pathological processes. This review provides a comprehensive insight into the molecular actions of 17β-estradiol and progesterone, aiming to present the role of these sex steroids in regulation of cellular signaling pathways. Copyright © Postepy Higieny i Medycyny Dos̈wiadczalnej 2015.


Grabiec K.,Katedra Nauk Fizjologicznych | Milewska M.,Katedra Nauk Fizjologicznych | Grzelkowska-Kowalczyk K.,Katedra Nauk Fizjologicznych
Postepy Higieny i Medycyny Doswiadczalnej | Year: 2012

Suboptimal fetal environments due to inadequate maternal nutrition, obesity, inflammation or gestational diabetes expose the fetus to humoral cues that alter metabolism and growth parameters leading to metabolic disturbances later in life. The fetal stage is crucial for the development of skeletal muscle, a tissue playing an important role in metabolism. Maternal obesity induces inflammation in the fetus causing modifications in the development of fetal skeletal muscle. Changes in the normal course of myogenesis may arise through several mechanisms: changes in WNT/β-catenin signaling pathway, decreased AMPK activity evoked by TNF-α, increased activity of NF-κB in response to inflammation, which leads to a decrease in myogenic factor MyoD, and increased expression of TGF β1. Modification in fetal development associated with maternal obesity is attributed to epigenetic changes. Polyunsaturated fatty acids supplied in the diet did affect the development of insulin-sensitive tissues during both the fetal and postnatal period. The specific phenotype of skeletal muscle fibers may play a role in the development of obesity, i.e. fiber phenotype I (slow, oxidative) may protect against obesity and insulin resistance. Exploring the mechanisms of direct impact of maternal obesity on the development of tissues in the offspring may help to reduce the occurrence of metabolic diseases in later life.


Piotrowska I.,Katedra Nauk Fizjologicznych | Zgodka P.,Katedra Nauk Fizjologicznych | Milewska M.,Katedra Nauk Fizjologicznych | Blaszczyk M.,Katedra Nauk Fizjologicznych | Grzelkowska-Kowalczyk K.,Katedra Nauk Fizjologicznych
Postepy Higieny i Medycyny Doswiadczalnej | Year: 2014

Growth and development in utero is a complex and dynamic process that requires interaction between the mother organism and the fetus. The delivery of macro - and micronutrients, oxygen and endocrine signals has crucial importance for providing a high level of proliferation, growth and differentiation of cells, and a disruption in food intake not only has an influence on the growth of the fetus, but also has negative consequences for the offspring's health in the future. Diseases that traditionally are linked to inappropriate life style of adults, such as type 2 diabetes, obesity, and arterial hypertension, can be "programmed" in the early stage of life and the disturbed growth of the fetus leads to the symptoms of the metabolic syndrome. The structural changes of some organs, such as the brain, pancreas and kidney, modifications of the signaling and metabolic pathways in skeletal muscles and in fatty tissue, epigenetic mechanisms and mitochondrial dysfunction are the basis of the metabolic disruptions. The programming of the metabolic disturbances is connected with the disruption in the intrauterine environment experienced in the early and late gestation period. It causes the changes in deposition of triglycerides, activation of the hormonal "stress axis" and disturbances in the offspring's glucose tolerance. The present review summarizes experimental results that led to the identification of the above-mentioned links and it underlines the role of animal models in the studies of this important concept. Copyright © Postepy Higieny i Medycyny Dos̈wiadczalnej 2015.


PubMed | Katedra Nauk Fizjologicznych
Type: | Journal: Postepy higieny i medycyny doswiadczalnej (Online) | Year: 2012

Suboptimal fetal environments due to inadequate maternal nutrition, obesity, inflammation or gestational diabetes expose the fetus to humoral cues that alter metabolism and growth parameters leading to metabolic disturbances later in life. The fetal stage is crucial for the development of skeletal muscle, a tissue playing an important role in metabolism. Maternal obesity induces inflammation in the fetus causing modifications in the development of fetal skeletal muscle. Changes in the normal course of myogenesis may arise through several mechanisms: changes in WNT/-catenin signaling pathway, decreased AMPK activity evoked by TNF-, increased activity of NF-B in response to inflammation, which leads to a decrease in myogenic factor MyoD, and increased expression of TGF 1. Modification in fetal development associated with maternal obesity is attributed to epigenetic changes. Polyunsaturated fatty acids supplied in the diet did affect the development of insulin-sensitive tissues during both the fetal and postnatal period. The specific phenotype of skeletal muscle fibers may play a role in the development of obesity, i.e. fiber phenotype I (slow, oxidative) may protect against obesity and insulin resistance. Exploring the mechanisms of direct impact of maternal obesity on the development of tissues in the offspring may help to reduce the occurrence of metabolic diseases in later life.


PubMed | Katedra Nauk Fizjologicznych
Type: | Journal: Postepy higieny i medycyny doswiadczalnej (Online) | Year: 2014

Cachexia is a multifactorial syndrome of atrophy of skeletal muscle and adipose tissue, resulting in progressive loss of body weight associated with low quality of life and poor prognosis in cancer. Studies on experimental animal models and observations on patients have shown that the soluble factors secreted by tumor cells and tissues of the patient can participate in regulation of the wasting process. Cachexia is often accompanied by anorexia, which is caused by predominance of signals inhibiting appetite in the hypothalamus, such as release of proopiomelanocortin and anorexigenic action of proinflammatory cytokines (IL-1, IL-1, IL-6, TNF-). Cachexia is also accompanied by extensive metabolic changes consisting of increase of resting energy expenditure and disturbance of carbohydrate, protein and lipid metabolism. Increased expression of protein uncoupling phosphorylation leads to increased thermogenesis in skeletal muscle. Tumor tissue hypoxia caused by its growth beyond blood vessels activates the transcription factor HIF-1, which results in increase in glycolysis, and leads to lactic acid accumulation and activation of the energy inefficient Cori cycle. Loss of fat tissue is caused by increase of lipolysis induced by lipid-mobilizing factor (LMF) and proinflammatory cytokines. Skeletal muscle wasting in cachexia is caused by a reduction of protein synthesis at the stage of initiation and elongation of translation and the simultaneous increase of protein degradation via ubiquitin-dependent and lysosomal pathways. The main mediators of skeletal muscle wasting in cancer are proteolysis-inducing factor (PIF), proinflammatory cytokines, and angiotensin II acting through increased levels of reactive oxygen species (ROS) and nuclear factor NF-B activation, as well as glucocorticoid activated FOXO transcription factors and myostatin. Understanding of the complexity of the interaction of factors produced by the tumor and the patients body may form the basis for the development of effective treatments for cachexia in cancer and other pathological conditions.


PubMed | Katedra Nauk Fizjologicznych
Type: | Journal: Postepy higieny i medycyny doswiadczalnej (Online) | Year: 2014

SEX STEROIDS: 17-estradiol and progesterone play a major role in modulation of reproductive functions of the organism and participate in regulation of a broad spectrum of cellular processes in target cells via their specific receptors. Our understanding of molecular mechanisms of sex steroid action has significantly developed over the last years. Apart from the well-established effect of sex steroids on regulation of gene expression, some rapid nongenomic mechanisms have been identified, which are involved in modulation of the activity of several cellular, membrane-bound and cytoplasmic regulatory proteins. 17-estradiol and progesterone regulate several signal transduction pathways, which involve activation of enzymes such as mitogen-activated protein kinases (MAPK), phosphatidylinositol 3-kinase and tyrosine kinases. Biological effects of sex steroids action constitute a complex interplay of genomic and nongenomic mechanisms, and depend on the physiological and genetic context of the target cell. Understanding the molecular mechanisms of sex steroids action is therefore important and may broaden our knowledge about their role in both physiological and pathological processes. This review provides a comprehensive insight into the molecular actions of 17-estradiol and progesterone, aiming to present the role of these sex steroids in regulation of cellular signaling pathways.

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