Changes of hen eggs and their components caused by non-thermal pasteurizing treatments II. Some non-microbiological effects of gamma irradiation or hydrostatic pressure processing on liquid egg white and egg yolk

Experiments were performed to study changes caused by irradiation or high hydrostatic pressure pasteurization of liquid egg white by differential scanning calorimetry, spectrofluorimetry, electronic nose measurements and NIR-spectrometry. The non-thermal pasteurization treatments were also assessed in relation to loss of carotenoid content, and lipid- and cholesterol oxidation of liquid egg yolk. Unlike radiation pasteurization, high pressure processing caused protein denaturation in egg white, which manifested in changes of its DSC-thermogram and intrinsic tryptophan fluorescence. Electronic nose testing showed changes of the head-space volatile composition of egg albumen, particularly as a function of radiation treatment. Both treatments caused changes in the NIR-spectrometric “fingerprint” of the liquid egg white. Various chemometric analyses of the results of the latter instrumental methods, particularly statistical techniques developed by the group of one of the co-authors of this article, demonstrated the potential for detection and characterization of the applied non-thermal processing techniques on liquid egg white. Irradiation induced more carotenoid degradation and lipid oxidation in liquid egg yolk than pressure processing

Dietary manipulation of meat fatty acid composition in Hungarian Mangalica and an industrial genotype pig

Fat content and fatty acid composition were investigated in Musculus gluteus medius of pigs from two different breeds: traditional Hungarian Mangalica and a crossbreed of Hungarian Large White and Dutch Landrace. Animals of both varieties were divided into two groups and were kept individually on control or experimental mixtures of feeds. Experimental feed contained significantly higher amount of linoleic and linolenic acid than the control one. Significantly higher fat content was detected in meat of Mangalica pigs kept on both feed mixtures than in those of crossbred. The proportion of saturated fatty acids was nearly the same in the meat of both genotypes. More monounsaturated fatty acids were detected in Mangalica meat than in crossbred ones expressed in percent of total fatty acids and absolute amount, as well. As a result of experimental diet, percentage and absolute amount of oleic acid decreased significantly in both genotypes. Less polyunsaturated fatty acids expressed as percent of total acids were observed in the muscle of Mangalica than in those of crossbred ones. Absolute amount and the proportion of total polyunsaturated fatty acids (especially linoleic and linolenic acids) increased significantly as a result experimental diets. The ratio of n-6 and n-3 fatty acids changed beneficially in both genotypes consuming a diet containing 20% full-fat soy from 13.6:1 to 10.0:1 in Mangalica and from 15.4:1 to 10.3:1 in crossbred genotype. According to present results, it has became clear that the fatty acid composition of the meat of the traditional Hungarian Mangalica can be successfully modified by the diet, and this manipulation can make the meat healthier in spite of its high fat content

Fructose Mediated Non-Alcoholic Fatty Liver Is Attenuated by HO-1-SIRT1 Module in Murine Hepatocytes and Mice Fed a High Fructose Diet

<div><p>Background</p><p>Oxidative stress underlies the etiopathogenesis of nonalcoholic fatty liver disease (NAFLD), obesity and cardiovascular disease (CVD). Heme Oxygenase-1 (HO-1) is a potent endogenous antioxidant gene that plays a key role in decreasing oxidative stress. Sirtuin1 (SIRT1) belongs to the family of NAD-dependent de-acyetylases and is modulated by cellular redox.</p><p>Hypothesis</p><p>We hypothesize that fructose-induced obesity creates an inflammatory and oxidative environment conducive to the development of NAFLD and metabolic syndrome. The aim of this study is to determine whether HO-1 acts through SIRT1 to form a functional module within hepatocytes to attenuate steatohepatitis, hepatic fibrosis and cardiovascular dysfunction.</p><p>Methods and Results</p><p>We examined the effect of fructose, on hepatocyte lipid accumulation and fibrosis in murine hepatocytes and in mice fed a high fructose diet in the presence and absence of CoPP, an inducer of HO-1, and SnMP, an inhibitor of HO activity. Fructose increased oxidative stress markers and decreased HO-1 and SIRT1 levels in hepatocytes (p<0.05). Further fructose supplementation increased FAS, PPARα, pAMPK and triglycerides levels; CoPP negated this increase. Concurrent treatment with CoPP and SIRT1 siRNA in hepatocytes increased FAS, PPARα, pAMPK and triglycerides levels suggesting that HO-1 is upstream of SIRT1 and suppression of SIRT1 attenuates the beneficial effects of HO-1. A high fructose diet increased insulin resistance, blood pressure, markers of oxidative stress and lipogenesis along with fibrotic markers in mice (p<0.05). Increased levels of HO-1 increased SIRT1 levels and ameliorated fructose-mediated lipid accumulation and fibrosis in liver along with decreasing vascular dysfunction (p<0.05 vs. fructose). These beneficial effects of CoPP were reversed by SnMP.</p><p>Conclusion</p><p>Taken together, our study demonstrates, for the first time, that HO-1 induction attenuates fructose-induced hepatic lipid deposition, prevents the development of hepatic fibrosis and abates NAFLD-associated vascular dysfunction; effects that are mediated by activation of SIRT1 gene expression.</p></div

Effect of induction of HO-1 (CoPP) and inhibition of HO (SnMP) on metabolic profile and hepatic lipid content in mice fed a high fructose diet for 8 weeks.

<p>(A) Blood pressure. (B) Fasting blood glucose levels. (C) HOMA-IR (D) Plasma ALT levels. (E) Triglycerides levels in hepatic tissue. (F) Cholesterol levels in hepatic tissue. Results are mean±SE, n = 6/group. * <i>p</i><0.05 vs CTR; # <i>p</i><0.05 vs HFr, + <i>p</i><0.05 vs HFr+CoPP.</p

Effect of high-fructose (HFr) supplementation (500 μM) on markers of oxidative stress and HO-1 and SIRT1 gene expressions in hepatocytes treated with and without CoPP (5 μM) and SnMP (5 μM).

<p>(A) Isoprostanes level in condition media of hepatocytes (B) heme content measurement in hepatocytes (C) superoxide measurement in hepatocytes. (D) HO-1 mRNA levels (E) SIRT-1 protein levels. (F) Effect of Biliverdin and Tempol on SIRT1 expression in fructose (Fr)-treated hepatocytes. Hepatocytes were treated with biliverdin (10 μM) and with Tempol (100 μM) in presence of fructose (500 μM) for 24 hours. Results are mean±SE, n = 6/group. * <i>p</i><0.05 vs CTR; # <i>p</i><0.05 vs HFr, + <i>p</i><0.05 vs HFr+CoPP.</p

Effect of induction of HO-1 (CoPP) and inhibition of HO (SnMP) on hepatic fibrosis, markers of hepatic fibrosis in mice fed high-fructose diet for 20 weeks.

<p>(A) Masson’s trichrome staining in liver and quantitative analysis of WT, high fructose, high fructose treated with CoPP, and high fructose treated with CoPP and SnMP, magnifications: 40× (n = 4) (* Indicates fibrosis). A representative section for each group is shown. (B) Plasma TNFα levels. (C) MMP2 protein expression and (D) TGFβ protein expression on western blot analysis. Data are shown as mean band density normalized to β-actin. Results are mean±SE, n = 4/group. * <i>p</i><0.05 vs CTR; # <i>p</i><0.05 vs HFr, + <i>p</i><0.05 vs HFr+CoPP.</p

Schematic demonstrating HO-1 induction attenuates fructose-induced hepatic lipid deposition, prevent the development of hepatic fibrosis and abate NAFLD-associated vascular dysfunction; effects that are mediated by activation of the SIRT1 gene expression.

<p>Schematic demonstrating HO-1 induction attenuates fructose-induced hepatic lipid deposition, prevent the development of hepatic fibrosis and abate NAFLD-associated vascular dysfunction; effects that are mediated by activation of the SIRT1 gene expression.</p