核桃多肽的制备及核桃多肽酒的研制

采用中性蛋白酶对核桃蛋白进行水解,得到最适反应条件是:酶解4.0h,底物浓度3%,加酶量6500U/g底物,温度50℃、pH7.5,水解度达到11.6%。核桃多肽酒最佳发酵工艺条件为:温度24℃,接种量0.05%,pH4.0,时间6d。发酵结束后为了掩蔽轻微的苦味,加入0.6%β-环糊精和4%蔗糖,最终产品口感良好。

酶解蚕豆蛋白制备多肽酒及其抗氧化性研究

以蚕豆蛋白为原料,采用碱性蛋白酶酶解、酒精发酵制备蚕豆多肽酒,并对其抗氧化性进行了研究。结果表明:蚕豆蛋白酶解优化工艺为底物浓度32 g/L,水解温度43.2℃,酶用量9 821.12 U/g,pH 9.50,在此条件下酶解2 h,蚕豆蛋白的水解度达到19.64%。以蚕豆酶解液为原料制备多肽酒的发酵工艺为加糖量20%,酵母接种量0.22%,发酵温度28℃,发酵时间6 d,在此条件下制得的蚕豆多肽酒的酒精含量为9.6%,呈透明的棕黄色,口感醇正、鲜爽、具有发酵酒的醇香。本试验条件下制备的蚕豆多肽酒具有较强的抗氧化性。

小麦多肽酒酿造及其抗氧化性研究

以小麦蛋白粉为原料,用中性蛋白酶酶解、酒精发酵制得小麦多肽酒,并对其抗氧化性进行研究。结果表明:小麦多肽酒的最佳酿造工艺为:多肽含量0.5%、加糖量17%、酵母添加量0.9‰,25℃下发酵9d后采用3500r/min离心10min后得小麦多肽酒为淡黄色,有光泽,澄清透明,无明显沉淀和悬浮物,小麦多肽酒的透光率为95.45%,多肽含量为5.20mg/ml,羟自由基清除率为30.63%,DPPH·清除率为64.47%,总还原力为1.35,超氧阴离子自由基(O2·)清除率为42.13%,溶血抑制率为49.92%。

乳清多肽酒的开发

采用蛋白酶水解乳清粉,并对乳清多肽进行酵母菌发酵,对发酵所得乳清酒进行风味调配。乳清粉最佳的水解条件为:[E/S]=1%、T=60℃、pH=9.0、时间=120min,水解度为DH=21.22%。乳清多肽酒的最优发酵条件:接种量为5%、起始pH为7.5、温度为22℃、发酵60h,酒度可达到3.9。多肽乳清酒的最佳基本调配是:酸量(苹果酸∶柠檬酸=1∶1)为0.1%、蔗糖为7%、环状糊精为0.6%。

乳清多肽的制备及乳清多肽酒的研制

采用蛋白酶水解乳清粉,并对乳清多肽进行酵母菌发酵,并对发酵所得乳清酒进行风味调配。乳清粉最佳的水解条件为:[E/S]=1%、T=60℃、pH=9.0、时间=120min,水解度为DH=21.22%。乳清多肽酒的最优发酵条件:接种量为5%、起始pH为7.5、温度为22℃、发酵60h,酒度可达到3.9。多肽乳清酒的最佳基本调配是:酸量(苹果酸:柠檬酸=1:1)为0.1%、蔗糖为7%、环状糊精为0.6%。

乳清多肽的制备及乳清多肽酒的研制

采用蛋白酶水解乳清粉,对乳清多肽进行酵母菌发酵,并对发酵所得乳清酒进行风味调配。乳清粉最佳的水解条件为:酶浓度与底物浓度之比为1%、温度60℃、pH9.0、时间120min,水解度21.22%。乳清多肽酒的最优发酵条件:接种量5%、起始pH7.5、温度22℃、发酵60h,酒精度可达到3.9%。多肽乳清酒的最佳基本调配是总酸(苹果酸:柠檬酸=1:1)为0.1%、蔗糖为7%、环状糊精为0.6%。

薏仁多肽的制备及薏仁多肽酒的研制

以薏仁为原料,采用碱性蛋白酶解、酒精发酵制得薏仁多肽酒。最佳水解条件为:底物浓度为20%、酶添加为1300u/g、温度为45℃、时间为6h、p H为9.0,多肽得率为60.1%。薏仁多肽酒的最优发酵条件为:薏仁米曲添加量15%、发酵温度26℃、发酵时间为7d,在此条件下制得的薏仁多肽酒的酒精含量为11.3%vol,产品颜色微黄、清亮透明、口感醇和。

酶解蚕豆蛋白制备多肽的工艺优化及多肽酒的发酵

以蚕豆蛋白为原料,采用碱性蛋白酶酶解、酒精发酵制备蚕豆多肽酒,对其加工工艺进行了研究。结果表明:1)蚕豆蛋白酶解的优化工艺为:蚕豆蛋白质量浓度32g/L,水解温度43.2℃,酶用量9 821.12U/g,pH9.5,在此条件下酶解2h,蚕豆蛋白的水解度达到19.64%;2)以蚕豆酶解液为原料制备多肽酒的发酵工艺为:加糖量200g/L,酵母接种量0.22%,发酵温度28℃,发酵时间6d,在此条件下制得的蚕豆多肽酒的酒精体积分数为9.6%;发酵结束后添加柠檬酸1.5g/L,白砂糖70g/L,环糊精6g/L时,产品风味较好,显著降低了产品的苦味。

甲鱼多肽酒发酵工艺及抗氧化性分析

以甲鱼为原料研究甲鱼多肽酒的发酵工艺,并对其抗氧化性进行分析。通过单因素试验和正交试验获得甲鱼多肽酒的最佳发酵条件:蔗糖添加量20%,酵母添加量0.2%,发酵温度24℃,发酵时间6 d。在此条件下发酵得到的甲鱼多肽酒的酒精度达到10.5%vol,多肽含量为9.79 mg/mL,并且具有一定的抗氧化能力。

Is iron overload in alcohol-related cirrhosis mediated by hepcidin?

In this case report we describe the relationship between ferritin levels and hepcidin in a patient with alcohol-related spur cell anemia who underwent liver transplantation.We demonstrate a reciprocal relation-ship between serum or urinary hepcidin and serum ferritin,which indicates that inadequate hepcidin production by the diseased liver is associated with elevated serum ferritin.The ferritin level falls with increasing hepcidin production after transplantation.Neither inflammatory indices(IL6)nor erythropoietin appear to be related to hepcidin expression in this case.We suggest that inappropriately low hepcidin production by the cirrhotic liver may contribute substantially to elevated tissue iron stores in cirrhosis and speculate that hepcidin replacement in these patients may be of therapeutic benefi t in the future.

Is the iron regulatory hormone hepcidin a risk factor for alcoholic liver disease?

Despite heavy consumption over a long period of time, only a small number of alcoholics develop alcoholic liver disease. This alludes to the possibility that other factors, besides alcohol, may be involved in the progression of the disease. Over the years, many such factors have indeed been identified, including iron. Despite being crucial for various important biological processes, iron can also be harmful due to its ability to catalyze Fenton chemistry. Alcohol and iron have been shown to interact synergistically to cause liver injury. Iron-mediated cell signaling has been reported to be involved in the pathogenesis of experimental alcoholic liver disease. Hepcidin is an iron-regulatory hormone synthesized by the liver, which plays a pivotal role in iron homeostasis. Both acute and chronic alcohol exposure suppress hepcidin expression in the liver. The sera of patients with alcoholic liver disease, particularly those exhibiting higher serum iron indices, have also been reported to display reduced prohepcidin levels. Alcohol-mediated oxidative stress is involved in the inhibition of hepcidin promoter activity and transcription in the liver. This in turn leads to an increase in intestinal iron transport and liver iron storage. Hepcidin is expressed primarily in hepatocytes. It is noteworthy that both hepatocytes and Kupffer cells are involved in the progression of alcoholic liver disease. However, the activation of Kupffer cells and TNF-α signaling has been reported not to be involved in the down-regulation of hepcidin expression by alcohol in the liver. Alcohol acts within the parenchymal cells of the liver to suppress the synthesis of hepcidin. Due to its crucial role in the regulation of body iron stores, hepcidin may act as a secondary risk factor in the progression of alcoholic liver disease. The clarification of the mechanisms by which alcohol disrupts iron homeostasis will allow for further understanding of the pathogenesis of alcoholic liver disease.