The effect of fructose rich diet on the expression of renin-angiostensin system components and inflamatory molecules in the rat heart: sex specific differences

Ishrana bogata fruktozom predstavlja bitan faktor u razvoju metaboličkog sindroma koji je povezan sa povećanim rizikom za nastanak kardiovaskularnih bolesti. Smatra se da hronična inflamacija ima bitnu ulogu u njegovoj patogenezi. Ženke su zaštićene od ishranom izazvanih metaboličkih poremećaja i hipertenzije u reproduktivnom periodu. Estrogen, koji utiče na normalno funkcionisanje kardiovaskularnog sistema, bi mogao doprinositi uočenim polno specifičnim razlikama u nastanku simptoma metaboličkog sindroma. Proteinske komponente renin-angiotenzin sistema (RAS) imaju bitnu ulogu u nastanku inflamacije, hipertenzije i insulinske rezistencije i na njihovu ekspresiju utiče estradiol. Ova doktorska disertacija je za cilj imala da ispita da li pol i estradiol doprinose promenama u ekspresiji komponenti RAS-a [angiotenzin konvertujućeg enzima (ACE), angiotenzin konvertujućeg enzima 2 (ACE2), angiotenzinskog receptora tipa 1 (AT1R), angiotenzinskog receptora tipa 2 (AT2R) i kolektrina] i medijatora inflamacije i remodelovanja tkiva srca [nuklearnog faktora κB (NFκB), matriks metaloproteinaze-9 (MMP-9) i liganda 16 iz familije hemokina CXC (CXCL16)] kod animalnog modela metaboličkog sindroma. Mužjaci i ženke pacova koji su pili 10% rastvor fruktoze umesto vode u trajanju od 9 nedelja predstavljali su animalni model metaboličkog sindroma korišćen u ovoj studiji. Radi ispitivanja efekata estradiola jedan deo ženki pacova je ovarijektomisan i podeljen u tri grupe pri čemi je jedna grupa pored standardne laboratorijske hrane pila vodu, druga grupa je pila 10% rastvor fruktoze, a treća grupa je pored rasvora fruktoze primala i supstitucionu terapiju estradiolom. Ishrana bogata fruktozom je uzrokovala povećanje krvnog pritiska samo kod mužjaka pacova. Ovaj tip ishrane nije doveo do promena u masi srca niti u odnosu masa srca/masa tela ni kod jednog pola, kao ni kod ovarijektomisanih životinja što ukazuje da se hipertrofija srca nije razvila...Fructose rich diet (FRD) represents an important factor in the development of metabolic syndrome. Metabolic syndrome is associated with increased risk for cardiovascular diseases occurrence and chronic inflammation has a major role in its pathogenesis. Females are protected from diet-induced metabolic disturbances and hypertension in their reproductive period. Estrogen, which influences the cardiovascular system, could contribute to the observed gender-specific differences in the onset of metabolic syndrome. Components of the renin-angiotensin system (RAS), the synthesis of which is mediated by estrogen, have an important role in the inflammatory processes, hypertension and insulin resistance. Almost all of the components of metabolic syndrome increase the activity of RAS, which finally results in increased oxidative stress and inflammation. The aim of this doctoral dissertation was to investigate sex specific changes and role of estradiol in the expression of RAS components [angiotensin converting enzyme (ACE), angiotensin converting enzyme 2 (ACE2), angiotensin receptor type 1 (AT1R), angiotensin receptor type 2 (AT2R) and collectrin], as well as mediators of inflammation and remodeling of heart tissue [nuclear faktor κB (NFκB), matrix metalloproteinse-9 (MMP-9) and CXCL16 chemokine] in the animal model of metabolic syndrome. Male and female rats, which consumed 10% fructose solution instead of water for 9 weeks, represent an animal model of metabolic syndrome that was used in this study. In order to examine the effects of estradiol in the context of FRD, female rats were ovariectomized and divided in three groups: fed normal diet, fed FRD, and fed FRD and subjected to estradiol replacement therapy. FRD increased blood pressure only in male rats. This diet regime didn't cause heart hypertrophy neither in intact males and females, nor in ovariectomized females..

Oestradiol Treatment Counteracts the Effect of Fructose-Rich Diet on Matrix Metalloproteinase 9 Expression and NF kappa B Activation

Fructose-rich diet induces metabolic changes similar to those observed in metabolic syndrome. Among other matrix metalloproteinases, MMP-9 has an important role in adverse cardiac remodelling and might have a role in the development of cardiovascular disorders associated with metabolic syndrome. The changes of MMP-9 expression could be mediated via the NF kappa B pathway. In this study we investigated the effect of fructose-rich diet on MMP-9 expression in the heart of male and female rats, along with the effect of fructose-rich diet and oestradiol on MMP-9 expression in ovariectomized females. We further assessed the effect of fructose-rich diet and oestradiol on NF kappa B activation, measured as the level of p65 phosphorylation at Ser 276. The results showed that the diet regime did not affect the heart mass. Higher MMP-9 gene expression was found in cardiac tissue of male rats fed the fructose-rich diet than in females on the same diet regime. In ovariectomized females, fructose-rich diet upregulated MMP-9 protein and mRNA expression in the heart, as well as phosphorylation of the p65 subunit of NF kappa B at Ser 276. Oestradiol replacement therapy reverted these changes in the heart of ovariectomized females. This study has shown that oestradiol could revert the early molecular changes in MMP-9 expression induced by fructose-rich diet that occurred before cardiac hypertrophy development by decreasing phosphorylation of the NF kappa B p65 subunit at Ser 276

Plasmolyzed Yeast Cells as a Potential Wall Material for Probiotic Bacteria

The beneficial effects of probiotics are severely limited due to their low stability during production and storage. Encapsulation of probiotic cells remains the main strategy to overcome this problem, and in this regard, the use of yeast cells may have potential. Viable, sonicated and thermally treated yeast cells as well as yeast cell wall polymers have been shown to promote the growth and survival of probiotic bacteria; however, the effects of plasmolyzed yeast have not yet been investigated. Therefore, the aim of this work was to evaluate the potential of plasmolyzed yeast cells for maintaining the viability of probiotic bacteria. Plasmolysis of Saccharomyces uvarum yeast cells was performed using a 10% NaCl solution (55 °C, 48 h). The cells were then washed, spray-dried and mixed with a previously prepared Lactiplantibacillus plantarum 299v culture (DSM 9843) in two ratios (1:1 and 2:1, w/w). Finally, the mixtures were freeze-dried. The viability of the probiotic cells was assessed after encapsulation and every two weeks during three months of storage under refrigerated conditions using the plate count method. In addition, water activity and morphology analyses were performed and the auto/coaggregation properties of the cells were investigated. After storage, the number of viable cells in both formulations remained above 7 log CFU/g, i.e. above the minimum required for probiotic benefits. The obtained powders showed satisfactory water activity, while optical microscopy and aggregation assays indicate that the protective effect of the yeast may be due to direct cell-to-cell contact. The results suggest that plasmolyzed yeast cells have the potential to serve as wall material for probiotic bacteria by maintaining their viability during freezing and storage. Further studies are needed to gain a better insight into the properties of the encapsulates under gastrointestinal conditions and in food matrices.Apstrakt je greškom izdavača izostavljen u samoj knjizi apstrakata pa se, budući da štampanje korigovane verzije knjige nije bilo izvodljivo, uz apstrakt prilaže potvrda o učešću na konferenciji u formi memoranduma

Fructose-rich diet induces gender-specific changes in expression of the renin-angiotensin system in rat heart and upregulates the ACE/AT1R axis in the male rat aorta

Introduction: The cardiovascular renin-angiotensin system (RAS) could be affected by gender and dietary regime. We hypothesized that male rats will be more susceptible to activation of RAS in the heart and aorta, as a response to a fructose-rich diet (FRD). Materials and methods: Both male and female Wistar rats were given a 10% (w/v) fructose solution for 9 weeks. We measured the biochemical parameters, blood pressure (BP) and heart rate. We used Western blot and real-time polymerase chain reaction (PCR) to quantify protein and gene expression. Results: In the male rats, the FRD elevated BP and expression of cardiac angiotensin-converting enzyme (ACE), while the expression of angiotensin-converting enzyme 2 (ACE2) and angiotensin II Type 2 receptor (AT(2)R) were significantly decreased. In female rats, there were no changes in cardiac RAS expression due to FRD. Furthermore, the ACE/AT(1)R axis was overexpressed in the FRD male rats aortae, while only AT(1)R was upregulated in the FRD female rats aortae. ACE2 expression remained unchanged in the aortae of both genders receiving the FRD. Conclusions: The FRD induced gender-specific changes in the expression of the RAS in the heart and aortae of male rats. Further investigations are required in order to get a comprehensive understanding of the underlying mechanisms of gender-specific fructose-induced cardiovascular pathologies

The effect of fructose rich diet on the expression of renin-angiostensin system components and inflamatory molecules in the rat heart: sex specific differences

Ishrana bogata fruktozom predstavlja bitan faktor u razvoju metaboličkog sindroma koji je povezan sa povećanim rizikom za nastanak kardiovaskularnih bolesti. Smatra se da hronična inflamacija ima bitnu ulogu u njegovoj patogenezi. Ženke su zaštićene od ishranom izazvanih metaboličkih poremećaja i hipertenzije u reproduktivnom periodu. Estrogen, koji utiče na normalno funkcionisanje kardiovaskularnog sistema, bi mogao doprinositi uočenim polno specifičnim razlikama u nastanku simptoma metaboličkog sindroma. Proteinske komponente renin-angiotenzin sistema (RAS) imaju bitnu ulogu u nastanku inflamacije, hipertenzije i insulinske rezistencije i na njihovu ekspresiju utiče estradiol. Ova doktorska disertacija je za cilj imala da ispita da li pol i estradiol doprinose promenama u ekspresiji komponenti RAS-a [angiotenzin konvertujućeg enzima (ACE), angiotenzin konvertujućeg enzima 2 (ACE2), angiotenzinskog receptora tipa 1 (AT1R), angiotenzinskog receptora tipa 2 (AT2R) i kolektrina] i medijatora inflamacije i remodelovanja tkiva srca [nuklearnog faktora κB (NFκB), matriks metaloproteinaze-9 (MMP-9) i liganda 16 iz familije hemokina CXC (CXCL16)] kod animalnog modela metaboličkog sindroma. Mužjaci i ženke pacova koji su pili 10% rastvor fruktoze umesto vode u trajanju od 9 nedelja predstavljali su animalni model metaboličkog sindroma korišćen u ovoj studiji. Radi ispitivanja efekata estradiola jedan deo ženki pacova je ovarijektomisan i podeljen u tri grupe pri čemi je jedna grupa pored standardne laboratorijske hrane pila vodu, druga grupa je pila 10% rastvor fruktoze, a treća grupa je pored rasvora fruktoze primala i supstitucionu terapiju estradiolom. Ishrana bogata fruktozom je uzrokovala povećanje krvnog pritiska samo kod mužjaka pacova. Ovaj tip ishrane nije doveo do promena u masi srca niti u odnosu masa srca/masa tela ni kod jednog pola, kao ni kod ovarijektomisanih životinja što ukazuje da se hipertrofija srca nije razvila...Fructose rich diet (FRD) represents an important factor in the development of metabolic syndrome. Metabolic syndrome is associated with increased risk for cardiovascular diseases occurrence and chronic inflammation has a major role in its pathogenesis. Females are protected from diet-induced metabolic disturbances and hypertension in their reproductive period. Estrogen, which influences the cardiovascular system, could contribute to the observed gender-specific differences in the onset of metabolic syndrome. Components of the renin-angiotensin system (RAS), the synthesis of which is mediated by estrogen, have an important role in the inflammatory processes, hypertension and insulin resistance. Almost all of the components of metabolic syndrome increase the activity of RAS, which finally results in increased oxidative stress and inflammation. The aim of this doctoral dissertation was to investigate sex specific changes and role of estradiol in the expression of RAS components [angiotensin converting enzyme (ACE), angiotensin converting enzyme 2 (ACE2), angiotensin receptor type 1 (AT1R), angiotensin receptor type 2 (AT2R) and collectrin], as well as mediators of inflammation and remodeling of heart tissue [nuclear faktor κB (NFκB), matrix metalloproteinse-9 (MMP-9) and CXCL16 chemokine] in the animal model of metabolic syndrome. Male and female rats, which consumed 10% fructose solution instead of water for 9 weeks, represent an animal model of metabolic syndrome that was used in this study. In order to examine the effects of estradiol in the context of FRD, female rats were ovariectomized and divided in three groups: fed normal diet, fed FRD, and fed FRD and subjected to estradiol replacement therapy. FRD increased blood pressure only in male rats. This diet regime didn't cause heart hypertrophy neither in intact males and females, nor in ovariectomized females..

The effect of fructose rich diet on the expression of renin-angiostensin system components and inflamatory molecules in the rat heart: sex specific differences

Ishrana bogata fruktozom predstavlja bitan faktor u razvoju metaboličkog sindroma koji je povezan sa povećanim rizikom za nastanak kardiovaskularnih bolesti. Smatra se da hronična inflamacija ima bitnu ulogu u njegovoj patogenezi. Ženke su zaštićene od ishranom izazvanih metaboličkih poremećaja i hipertenzije u reproduktivnom periodu. Estrogen, koji utiče na normalno funkcionisanje kardiovaskularnog sistema, bi mogao doprinositi uočenim polno specifičnim razlikama u nastanku simptoma metaboličkog sindroma. Proteinske komponente renin-angiotenzin sistema (RAS) imaju bitnu ulogu u nastanku inflamacije, hipertenzije i insulinske rezistencije i na njihovu ekspresiju utiče estradiol. Ova doktorska disertacija je za cilj imala da ispita da li pol i estradiol doprinose promenama u ekspresiji komponenti RAS-a [angiotenzin konvertujućeg enzima (ACE), angiotenzin konvertujućeg enzima 2 (ACE2), angiotenzinskog receptora tipa 1 (AT1R), angiotenzinskog receptora tipa 2 (AT2R) i kolektrina] i medijatora inflamacije i remodelovanja tkiva srca [nuklearnog faktora κB (NFκB), matriks metaloproteinaze-9 (MMP-9) i liganda 16 iz familije hemokina CXC (CXCL16)] kod animalnog modela metaboličkog sindroma. Mužjaci i ženke pacova koji su pili 10% rastvor fruktoze umesto vode u trajanju od 9 nedelja predstavljali su animalni model metaboličkog sindroma korišćen u ovoj studiji. Radi ispitivanja efekata estradiola jedan deo ženki pacova je ovarijektomisan i podeljen u tri grupe pri čemi je jedna grupa pored standardne laboratorijske hrane pila vodu, druga grupa je pila 10% rastvor fruktoze, a treća grupa je pored rasvora fruktoze primala i supstitucionu terapiju estradiolom. Ishrana bogata fruktozom je uzrokovala povećanje krvnog pritiska samo kod mužjaka pacova. Ovaj tip ishrane nije doveo do promena u masi srca niti u odnosu masa srca/masa tela ni kod jednog pola, kao ni kod ovarijektomisanih životinja što ukazuje da se hipertrofija srca nije razvila...Fructose rich diet (FRD) represents an important factor in the development of metabolic syndrome. Metabolic syndrome is associated with increased risk for cardiovascular diseases occurrence and chronic inflammation has a major role in its pathogenesis. Females are protected from diet-induced metabolic disturbances and hypertension in their reproductive period. Estrogen, which influences the cardiovascular system, could contribute to the observed gender-specific differences in the onset of metabolic syndrome. Components of the renin-angiotensin system (RAS), the synthesis of which is mediated by estrogen, have an important role in the inflammatory processes, hypertension and insulin resistance. Almost all of the components of metabolic syndrome increase the activity of RAS, which finally results in increased oxidative stress and inflammation. The aim of this doctoral dissertation was to investigate sex specific changes and role of estradiol in the expression of RAS components [angiotensin converting enzyme (ACE), angiotensin converting enzyme 2 (ACE2), angiotensin receptor type 1 (AT1R), angiotensin receptor type 2 (AT2R) and collectrin], as well as mediators of inflammation and remodeling of heart tissue [nuclear faktor κB (NFκB), matrix metalloproteinse-9 (MMP-9) and CXCL16 chemokine] in the animal model of metabolic syndrome. Male and female rats, which consumed 10% fructose solution instead of water for 9 weeks, represent an animal model of metabolic syndrome that was used in this study. In order to examine the effects of estradiol in the context of FRD, female rats were ovariectomized and divided in three groups: fed normal diet, fed FRD, and fed FRD and subjected to estradiol replacement therapy. FRD increased blood pressure only in male rats. This diet regime didn't cause heart hypertrophy neither in intact males and females, nor in ovariectomized females..