Effect of chloride on the formation of 3-monochloro-1,2-propanediol fatty acid diesters and glycidol fatty acid esters in fish,meats and acylglycerols during heating

The effects of the presence of chloride on the formation of 3-monochloro-1,2-propanediol fatty acid esters (3-MCPDEs) and glycidol fatty acid esters (GEs) in saltwater fish, meats and acylglycerols (diacylglycerol and triacylglycerol) during heating were investigated in this study. Five saltwater fish species (salmon, saury, yellowtail, mackerel and Spanish mackerel) were grilled with a fish griller. 3-MCPDEs and GEs were detected in all of the grilled fish samples. The total amount of GEs was higher than 3-MCPDEs. Beef and pork patties with or without sodium chloride (1.5%) were cooked using gaseous fuel. The formation of 3-MCPDEs was significantly increased by the addition of sodium chloride to the meat patties, whereas the concentration of GEs in the cooked meat patties was not changed by the content of sodium chloride. Hexadecane solutions of diacylglycerol or triacylglycerol containing FeCl₃ were heated at 240°C. The formation of 3-MCPDEs was greatly increased by adding FeCl₃ to the solutions of triacylglycerol. The amounts of 3-MCPDEs decreased with the extension of the heating time. From these results, it is suggested that 3-MCPDEs and GEs are formed in saltwater fish and meats by cooking, and that the formation of 3-MCPDEs was affected by chloride in foodstuffs.     

原子吸收测定甘油脂中钠的含量

通过对溶样时间、酸度的选择,以及工作曲线法与标准加入法的比较,介绍了甘油脂中钠含量的测定方法。样品经硝酸加热溶解、稀释、过滤,原子吸收分光光度计测定,实验数据表明:分析方法结果准确,其相对标准偏差为2.3%～2.8%,回收率为97%～101%,可用于甘油脂产品中钠的分析检测工作。     

Triolein and Trilinolein Ameliorate Oxidized Low-Density Lipoprotein-Induced Oxidative Stress in Endothelial Cells

Uptake of oxidized low-density lipoprotein by endothelial cells is a critical step for the initiation of atherosclerosis. Triacylglycerol uptake in these cells is understood to be a part of the process. The present investigation, comparison among the effects of simple acylglycerol, including tristearin, triolein, and trilinolein, upon oxidized low-density lipoprotein -induced oxidative stress was undertaken. Results indicated that trilinolein (78 % ± 0.02) and triolein (90 % ± 0.01) increased cell viability of endothelial cells exposed to oxidized low-density lipoprotein, whereas tristearin decreased the cell viability (55 % ± 0.03) (P < 0.05). Oxidized low-density lipoprotein treatment significantly increased apoptosis (23 %), compared to cells simultaneously exposed to trilinolein (19 %) or triolein (16 %), where apoptosis was reduced (P < 0.05). On the other hand, exposure to tristearin further increased oxidized low-density lipoprotein -induced cell apoptosis (34 %). Treatment with trilinolein or triolein on oxidized low-density lipoprotein -stimulated endothelial cells inhibited the expression of ICAM-1 and E-selectin mRNA. Moreover, both trilinolein and triolein demonstrated a strong antioxidant response to oxidative stress caused by oxidized low-density lipoprotein. Taken together, the results indicate trilinolein and triolein possess anti-inflammatory properties, which are mediated via the antioxidant defense system.     

Lipase‐catalyzed synthesis of partial acylglycerols of acetoacetate

Immobilized Rhizomucor miehei lipase (Lipozyme RMIM) was employed in the synthesis of partial acylglycerols of acetoacetate (C₄H₆O₃, 3‐oxobutanoic acid). Both 1(3)‐sn‐monoacetoacetyl glycerol (MAcG) and 1,3‐sn‐diacetoacetyl glycerol (DAcG) resulting from esterification of glycerol with ethylacetoacetate were isolated and identified by ¹H and ¹³C NMR. An HPLC method for the separation and quantitation of these species was developed. The effects on product yield of coordinate variations in the amounts of enzyme, water, ethyl acetoacetate, and the ratio of immobilizing silica to glycerol were explored. This allowed creation of predictive equations relating these variables to product yield. Reaction conditions were thereby identified and validated under which maximum yields of MAcG and/or DAcG or total ester were predicted. The production of both MAcG and DAcG was markedly sensitive to water, with optimal yields obtained within a narrow range of added water contents. Substantial excesses of ethylacetoacetate ameliorated the inhibitory effect of water. MAcG was effectively produced with the lowest amount of RMIM investigated. It was necessary to use larger amounts of lipase to achieve high yields of DAcG, and even then actual yields were only 30% of theoretical maximum. In the absence of silica only MAcG was produced. Practical applications: Aceotacetyl esters of glycerol are potential prochiral building blocks for further chemical synthesis and exhibit the chemical reactivity of both the acetoacetyl moiety and of glycerol. They are thus of potential use in, for example, the production of biopolymers exhibiting any of a variety of features and functionalities. The use of enzymatic catalysis rather than chemical synthesis for their production offers advantages of reduced degradation and contamination due to the gentler reaction conditions characteristic of enzymatic catalysis, as well as a potential reduction in the costs to procure and dispose of catalyst.     

n‐3 PUFA Esterified to Glycerol or as Ethyl Esters Reduce Non‐Fasting Plasma Triacylglycerol in Subjects with Hypertriglyceridemia: A Randomized Trial

To date, treatment of hypertriglyceridemia with long‐chain n‐3 polyunsaturated fatty acids (n‐3 PUFA) has been investigated solely in fasting and postprandial subjects. However, non‐fasting triacylglycerols are more strongly associated with risk of cardiovascular disease. The objective of this study was to investigate the effect of long‐chain n‐3 PUFA on non‐fasting triacylglycerol levels and to compare the effects of n‐3 PUFA formulated as acylglycerol (AG‐PUFA) or ethyl esters (EE‐PUFA). The study was a double‐blinded randomized placebo‐controlled interventional trial, and included 120 subjects with non‐fasting plasma triacylglycerol levels of 1.7–5.65 mmol/L (150–500 mg/dL). The participants received approximately 3 g/day of AG‐PUFA, EE‐PUFA, or placebo for a period of eight weeks. The levels of non‐fasting plasma triacylglycerols decreased 28 % in the AG‐PUFA group and 22 % in the EE‐PUFA group (P < 0.001 vs. placebo), with no significant difference between the two groups. The triacylglycerol lowering effect was evident after four weeks, and was inversely correlated with the omega‐3 index (EPA + DHA content in erythrocyte membranes). The omega‐3 index increased 63.2 % in the AG‐PUFA group and 58.5 % in the EE‐PUFA group (P < 0.001). Overall, the heart rate in the AG‐PUFA group decreased by three beats per minute (P = 0.045). High‐density lipoprotein (HDL) cholesterol increased in the AG‐PUFA group (P < 0.001). Neither total nor non‐HDL cholesterol changed in any group. Lipoprotein‐associated phospholipase A2 (LpPLA2) decreased in the EE‐PUFA group (P = 0.001). No serious adverse events were observed. Supplementation with long‐chain n‐3 PUFA lowered non‐fasting triacylglycerol levels, suggestive of a reduction in cardiovascular risk. Regardless of the different effects on heart rate, HDL, and LpPLA2 that were observed, compared to placebo, AG‐PUFA, and EE‐PUFA are equally effective in reducing non‐fasting triacylglycerol levels.     

Characterization of a Novel Splicing Variant in Acylglycerol Kinase (AGK) Associated with Fatal Sengers Syndrome

Mitochondrial functional integrity depends on protein and lipid homeostasis in the mitochondrial membranes and disturbances in their accumulation can cause disease. AGK, a mitochondrial acylglycerol kinase, is not only involved in lipid signaling but is also a component of the TIM22 complex in the inner mitochondrial membrane, which mediates the import of a subset of membrane proteins. AGK mutations can alter both phospholipid metabolism and mitochondrial protein biogenesis, contributing to the pathogenesis of Sengers syndrome. We describe the case of an infant carrying a novel homozygous AGK variant, c.518+1G>A, who was born with congenital cataracts, pielic ectasia, critical congenital dilated myocardiopathy, and hyperlactacidemia and died 20 h after birth. Using the patient’s DNA, we performed targeted sequencing of 314 nuclear genes encoding respiratory chain complex subunits and proteins implicated in mitochondrial oxidative phosphorylation (OXPHOS). A decrease of 96-bp in the length of the AGK cDNA sequence was detected. Decreases in the oxygen consumption rate (OCR) and the OCR:ECAR (extracellular acidification rate) ratio in the patient’s fibroblasts indicated reduced electron flow through the respiratory chain, and spectrophotometry revealed decreased activity of OXPHOS complexes I and V. We demonstrate a clear defect in mitochondrial function in the patient’s fibroblasts and describe the possible molecular mechanism underlying the pathogenicity of this novel AGK variant. Experimental validation using in vitro analysis allowed an accurate characterization of the disease-causing variant.