Hybrid Extraction Method; Innovative Method to Produce Non Oxidative Tuna Oil

Summary: The function of Polyunsaturated Fatty Acid such as DHA, EPA are now well known world widely through strong scientific evidences and the importance of nutritional value and popularity are increasing every day all over the world with the name of omega 3 fatty acids.^1,2,3^ However, the fish oil, the source of omega 3 fatty acid had been considered as very vulnerable to oxidation. Many papers say the reason why is because its very easy to oxidize fish oil. The greater the Polyunsaturated Fatty Acid contents in the fish oil is, the faster oxidation takes place.^4,5^ Here I show that tuna oil extracted from Albacore Tuna Head in closed circuit under low temperature, at first decompressing then pressurizing and heating in a container, is very stable against the oxidation and conserved natural contents of Vitamins richly. The oil ware kept in a transparent bottle under natural light and some time under the sun light, with room temperature and opened every day for the sensual odor test during three months. This oil showed a stability of Fatty Acid Composition, Acid Value and Peroxide Value. That mean omega 3 fatty acids are more easy to handle and ample use as food ingredient to put it in many foods such as in a ketchup, mayonnaise, bread and noodle, rather than use in the capsules only

Metabolomics of dietary fatty acid restriction in patients with phenylketonuria

Patients with phenylketonuria (PKU) have to follow a lifelong phenylalanine restricted diet. This type of diet markedly reduces the intake of saturated and unsaturated fatty acids especially long chain polyunsaturated fatty acids (LC-PUFA). Long-chain saturated fatty acids are substrates of mitochondrial fatty acid oxidation for acetyl-CoA production. LC-PUFA are discussed to affect inflammatory and haemostaseological processes in health and disease. The influence of the long term PKU diet on fatty acid metabolism with a special focus on platelet eicosanoid metabolism has been investigated in the study presented here. 12 children with PKU under good metabolic control and 8 healthy controls were included. Activated fatty acids (acylcarnitines C6-C18) in dried blood and the cholesterol metabolism in serum were analyzed by liquid chromatographic tandem mass spectrometry (LC-MS/MS). Fatty acid composition of plasma glycerophospholipids was determined by gas chromatography. LC-PUFA metabolites were analyzed in supernatants by LC-MS/MS before and after platelet activation and aggregation using a standardized protocol. Patients with PKU had significantly lower free carnitine and lower activated fatty acids in dried blood compared to controls. Phytosterols as marker of cholesterol (re-) absorption were not influenced by the dietary fatty acid restriction. Fatty acid composition in glycerophospholipids was comparable to that of healthy controls. However, patients with PKU showed significantly increased concentrations of y-linolenic acid (C18:3n-6) a precursor of arachidonic acid. In the PKU patients significantly higher platelet counts were observed. After activation with collagen platelet aggregation and thromboxane B(2) and thromboxane B(3) release did not differ from that of healthy controls. Long-term dietary fatty acid restriction influenced the intermediates of mitochondrial beta-oxidation. No functional influence on unsaturated fatty acid metabolism and platelet aggregation in patients with PKU was detected

Caffeine-stimulated fatty acid oxidation is blunted in CD36 null mice

Aim: The increase in skeletal muscle fatty acid metabolism during exercise has been associated with the release of calcium. We examined whether this increase in fatty acid oxidation was attributable to a calcium-induced translocation of the fatty acid transporter CD36 to the sarcolemma, thereby providing an enhanced influx of fatty acids to increase their oxidation.Methods: Calcium release was triggered by caffeine (3 mM) to examine fatty acid oxidation in intact soleus muscles of WT and CD36-KO mice, while fatty acid transport and mitochondrial fatty acid oxidation were examined in giant vesicles and isolated mitochondria, respectively, from caffeine-perfused hindlimb muscles of WT and CD36-KO mice. Western blotting was used to examine calcium-induced signalling.Results: In WT, caffeine stimulated muscle palmitate oxidation (+136%), but this was blunted in CD36-KO mice (-70%). Dantrolene inhibited (WT) or abolished (CD36-KO) caffeine-induced palmitate oxidation. In muscle, caffeine-stimulated palmitate oxidation was not attributable to altered mitochondrial palmitate oxidation. Instead, in WT, caffeine increased palmitate transport (+55%) and the translocation of fatty acid transporters CD36, FABPpm, FATP1 and FATP4 (26-70%) to the sarcolemma. In CD36-KO mice, caffeine-stimulated FABPpm, and FATP1 and 4 translocations were normal, but palmitate transport was blunted (-70%), comparable to the reductions in muscle palmitate oxidation. Caffeine did not alter the calcium-/calmodulin-dependent protein kinase II phosphorylation but did increase the phosphorylation of AMPK and acetyl-CoA carboxylase comparably in WT and CD36-KO.Conclusion: These studies indicate that sarcolemmal CD36-mediated fatty acid transport is a primary mediator of the calcium-induced increase in muscle fatty acid oxidation

Lipid Metabolism in Liver Cancer

Hepatocellular carcinoma (HCC) represents 90% cases of liver cancer that is the second leading cause of cancer death in the world. With the pandemic of obesity and other metabolic syndromes in both adults and children, the incidences of fatty liver diseases and the derived HCC are on their upward track. Emerging metabolomic studies have revealed the perturbation of lipid profiles and other metabolites in fatty liver diseases and HCC. Two common metabolic features including enforced fatty acid oxidation and glycolysis could distinguish HCC from healthy liver and chronic non-tumor liver diseases. The potential translational impacts of fatty acid oxidation are gaining great interests, because many recent investigations have demonstrated that tumor cells were dependent on fatty acid oxidation for cell survival and tumor growth. Blockage of fatty acid oxidation could sensitize to metabolic stress-induced cell death and tumor growth inhibition. Thus, lipid catabolism, in terms of fatty oxidation, is tuned for tumor maintenance but vulnerable to pharmacological disruption. The therapeutic potentials of blocking fatty acid oxidation are yet to be further carefully examined

Novel role of FATP1 in mitochondrial fatty acid oxidation in skeletal muscle cells

Carnitine palmitoyltransferase 1 (CPT1) catalyzes the first step in long-chain fatty acid import into mitochondria, and it is believed to be rate limiting for beta-oxidation of fatty acids. However, in muscle, other proteins may collaborate with CPT1. Fatty acid translocase/CD36 (FAT/CD36) may interact with CPT1 and contribute to fatty acid import into mitochondria in muscle. Here, we demonstrate that another membrane-bound fatty acid binding protein, fatty acid transport protein 1 (FATP1), collaborates with CPT1 for fatty acid import into mitochondria. Overexpression of FATP1 using adenovirus in L6E9 myotubes increased both fatty acid oxidation and palmitate esterification into triacylglycerides. Moreover, immunocytochemistry assays in transfected L6E9 myotubes showed that FATP1 was present in mitochondria and coimmunoprecipitated with CPT1 in L6E9 myotubes and rat skeletal muscle in vivo. The cooverexpression of FATP1 and CPT1 also enhanced mitochondrial fatty acid oxidation, similar to the cooverexpression of FAT/CD36 and CPT1. However, etomoxir, an irreversible inhibitor of CPT1, blocked all these effects. These data reveal that FATP1, like FAT/CD36, is associated with mitochondria and has a role in mitochondrial oxidation of fatty acids

Quality characteristics of edible linseed oil

In this review the quality properties of linseed oil for food uses are discussed as well as factors affecting this quality. Linseed oil has a favourable fatty acid composition with a high linolenic acid content. Linseed oil contains nearly 60% á-linolenic acid, compared with 25% for plant oils generally. The content of linolenic acid and omega-3 fatty acids is reported to be high in linseed grown in northern latitudes. The composition of fatty acids, especially unsaturated fatty acids, reported in different studies varies considerably for linseed oil. This variation depends mainly on differences in the examined varieties and industrial processing treatments. The fatty acid composition leads also to some problems, rancidity probably being the most challenging. Some information has been published concerning oxidation and taste, whereas only a few studies have focused on colour or microbiological quality. Rancidity negatively affects the taste and odour of the oil. There are available a few studies on effects of storage on composition of linseed oil. In general, storage and heat promote auto-oxidation of fats, as well as decrease the amounts of tocopherols and vitamin E in linseed oil. Several methods are available to promote the quality of the oil, including agronomic methods and methods of breeding as well as chemical, biotechnological and microbiological methods. Time of harvesting and weather conditions affect the quality and yield of the oil

Disorders of Fatty Acid Oxidation in the Era of Tandem Mass Spectrometry in Newborn Screening

With recent advances in laboratory technology with tandem mass spectrometry (MS/MS), the number of infants identified with a fatty acid oxidation disorder has increased dramatically. Disorders of fatty acid oxidation comprise one of the most rapidly growing groups within the field of errors of metabolism. This review will explore the recent developments in newborn screening related to the use of tandem mass spectrometry and disorders of fatty acid oxidation

The Effects of Dietary Food Fortified with Vitamin B4 on Lipid Profiles in Serum and Liver Tissue

The effects of dietary food fortified with vitamin B4 on lipid profiles in serum and liver tissue were studied. Rats were paired-fed a 0.25% vitamin B4 diet or a diet without vitamin B4 for 10 days. Serum lipid levels were measured using enzyme assay kits. Lipids of liver tissues were extracted and the lipid contents were determined. A piece of liver was prepared to determine the activities of fatty acid synthase (FAS) and fatty acid β-oxidation. The results showed that animals fed a food fortified with vitamin B4 had higher level of serum TG, PL, total cholesterol, and high density lipoprotein. Their increases were approximately by 74%, 20%, 27%, and 27%, respectively. The significant changes in liver lipid were only found in PL component. This treatment promoted FAS activity, but impaired the fatty acid β-oxidation. In conclusion: Dietary food fortified with vitamin B4 induces hypertriglyceridemia and liver PL level

PPAR/RXR Regulation of Fatty Acid Metabolism and Fatty Acid ω-Hydroxylase (CYP4) Isozymes: Implications for Prevention of Lipotoxicity in Fatty Liver Disease

Fatty liver disease is a common lipid metabolism disorder influenced by the combination of individual genetic makeup, drug exposure, and life-style choices that are frequently associated with metabolic syndrome, which encompasses obesity, dyslipidemia, hypertension, hypertriglyceridemia, and insulin resistant diabetes. Common to obesity related dyslipidemia is the excessive storage of hepatic fatty acids (steatosis), due to a decrease in mitochondria β-oxidation with an increase in both peroxisomal β-oxidation, and microsomal ω-oxidation of fatty acids through peroxisome proliferator activated receptors (PPARs). How steatosis increases PPARα activated gene expression of fatty acid transport proteins, peroxisomal and mitochondrial fatty acid β-oxidation and ω-oxidation of fatty acids genes regardless of whether dietary fatty acids are polyunsaturated (PUFA), monounsaturated (MUFA), or saturated (SFA) may be determined by the interplay of PPARs and HNF4α with the fatty acid transport proteins L-FABP and ACBP. In hepatic steatosis and steatohepatitis, the ω-oxidation cytochrome P450 CYP4A gene expression is increased even with reduced hepatic levels of PPARα. Although numerous studies have suggested the role ethanol-inducible CYP2E1 in contributing to increased oxidative stress, Cyp2e1-null mice still develop steatohepatitis with a dramatic increase in CYP4A gene expression. This strongly implies that CYP4A fatty acid ω-hydroxylase P450s may play an important role in the development of steatohepatitis. In this review and tutorial, we briefly describe how fatty acids are partitioned by fatty acid transport proteins to either anabolic or catabolic pathways regulated by PPARs, and we explore how medium-chain fatty acid (MCFA) CYP4A and long-chain fatty acid (LCFA) CYP4Fω-hydroxylase genes are regulated in fatty liver. We finally propose a hypothesis that increased CYP4A expression with a decrease in CYP4F genes may promote the progression of steatosis to steatohepatitis