Kazunori Koba

5c, 11c, 14c-Eicosatrienoic acid and 5c, 11c, 14c, 17c-eicosatetraenoic acid ofBiota orientalis seed oil affect lipid metabolism in the rat

The effects of 5c, 11c, 14c-eicosatrienoic acid (20∶3BSO) and 5c, 11c, 14c, 17c-eicosatetraenoic acid (20∶4BSO), polyunsaturated fatty acids (PUFA) contained inBiota orientalis seed oil (BSO), on lipid metabolism in rats were compared to the effects of fats rich in linoleic acid (LA) or α-linolenic acid (ALA) under similar conditions. The potential effect of ethyl 20∶4BSO as an essential fatty acid also was examined in comparison with the ethyl esters of LA. ALA and γ-linolenic acid (GLA). BSO- and ALA-rich fat decreased the concentration of plasma total cholesterol, high density lipoprotein cholesterol, triglyceride and phospholipid as compared to LA-rich fat. BSO was more effective in reducing plasma cholesterol concentrations than was the ALA-rich fat. Dietary BSO markedly decreased the hepatic triglyceride concentration as compared to the LA-rich or ALA-rich fats. Aortic production of prostaglandin I2 tended to decrease in rats fed BSO or ALA-rich fat compared to those fed the LA-rich fat. Adenosine diphosphate-induced platelet aggregation was similar in the three groups. The proportion of arachidonic acid (AA) in liver phosphatidylcholine (PC) of rats fed BSO was lowest compared to that of rats fed ALA-rich or LA-rich fats. Administration of 20∶4BSO, ALA or GLA to essential fatty acid-deficient rats decreased the ratio of 20∶3n−9 to AA in liver PC to the same extent; administration of LA was more effective. The results indicate that the effects of specific PUFA contained in BSO on lipid metabolism are different from those of LA and ALA. It is also suggested that 20∶4BSO may exhibit some essential fatty acid effects.

Effects of dietary proteins on linoleic acid desaturation and membrane fluidity in rat liver microsomes

The effect of dietary protein, casein (CAS) and soybean protein (SOY), on linoleic acid desaturation in liver microsomes was studied in rats. The activity of Δ6 desaturase in total and rough endoplasmic reticula (ER and RER) was significantly higher in the CAS group than in the SOY group. In ER and smooth endoplasmic reticulum, the steady-state fluorescence anisotropy of 1,6-diphenyl-1,3,5-hexatriene, when incorporated into the membrane, was decreased in the SOY group and accompanied by a reduction in the cholesterol/phospholipid (CHOL/PL) ratio, consistent with an increase in membrane fluidity. In a separate study, the effect of varying dietary proteins, CAS, milk whey protein, egg albumin, SOY, potato protein and wheat gluten, on the relationship between the Δ6 desaturase activity and microsomal membrane fluidity was also examined. The results indicated that the dietary protein-dependent change in the liver microsomal CHOL/PL ratio affected membrane fluidity, and subsequently the activity of Δ6 desaturase in liver microsomes. However, since dietary protein influenced the Δ6 desaturase activity in RER without influencing membrane fluidity, it is possible that some regulation might have taken place at the level of enzyme synthesis.

Effects of dietary protein and cholesterol on phosphatidylcholine and phosphatidylethanolamine molecular species in mouse liver.

The present study examined the effects of two atherogenic factors, animal protein and cholesterol, on the distribution of fatty acids and the molecular species of major liver phospholipids in mice. Weanling mice were fed a semisynthetic diet supplemented with either casein or soy protein (20%, w/w) in the presence or absence of 0.5% cholesterol for 4 wk. Results from mouse liver showed that animal protein and, more so, dietary cholesterol modified the fatty acid profiles of the phospholipids. Animal protein had no significant effect on the concentration of lipids, but it altered the relative distribution and fatty acid profiles of the phospholipids, phosphatidylcholine and phosphatidylethanolamine. Dietary cholesterol, on the other hand, significantly increased the concentration of liver lipids, but it did not alter the relative distribution of phosphatidylcholine and phosphatidylethanolamine. In cholesterol-fed mice, the proportions of molecular species containing 18∶2n−6 were increased, whereas those containing 20∶4n−6 were decreased, indicating that dietary cholesterol suppressed linoleic acid metabolism. Since cholesterol feeding selectively decreased the ratio of 18∶0/20∶4n−6 in phosphatidylcholine, whereas it increased the 18∶0/18∶2n−6 ratio in phosphatidylethanolamine, this finding suggests that dietary cholesterol may affect the incorporation of fatty acids but not the rate of synthesis of phosphatidylcholine and phosphatidylethanolamine.

Impact of Dietary Protein on Polyunsaturated Fatty Acid Desaturation in Rats Fed Diets Rich in α-Linolenic Acid.

Delta 6-desaturase activity and fatty acid composition of liver microsomes were measured periodically in rats fed diets high in α-Iinolenic acid (perilla oil) containing either casein (CAS) or soybean protein (SOY) as a protein source. Delta 6-desaturase activity measured by using linoleic· acid as a substrate (18: 2n-6→18: 3n-6) and the linoleic acid desaturation index as estimated by the (20: 3+20: 4)/18: 2 ratio in microsomal phospholipids were significantly higher in rats fed the CAS diet than in those fed the SOY diet at days 4 and thereafter. The proportion of eicosapentaenoic acid (20: 5n-3) was also significantly higher in the CAS group than in the SOY group. These results confirmed a differential impact of the dietary protein type on the metabolism of polyunsaturated fatty acids even when rats were fed fat rich in α-Iinolenic acid.

Effect of dietary linoleic acid content on the distribution of phosphatidylcholine molecular species in rat plasma

Abstract The effect of dietary linoleic acid on the profiles of phosphatidylcholine molecular species in rat plasma was investigated. On changing from an essential fatty acid-deficient state to an essential fatty acid sufficient state, the levels of molecular species containing 18:1 and 20:3n−9 were decreased, whereas those containing 18:2n−6 and 20:4n−6 were increased. However, the decrease was greater in the molecular species containing 20:3n−9 than in those containing 18:1, and the increase was greater in the molecular species containing 20:4n−6 than in those containing 18:2n−6. In rats fed the essential fatty acid deficient diet (containing 0.001 g/kg diet of linoleic acid), the major molecular species in plasma phosphatidylcholine was 16:0–8:1 and most of the molecular species have the total carbon chain length around 34. In rats fed the essential sufficient diet (containing 2.4 g/kg diet of linoleic acid), the major phosphatidylcholine molecular species was 18:0–20:4n−6, and most species had the total carbon chain length around 38. The changes of the molecular species profiles indicated that the metabolism of 18:1 to 20:3n−9 which was active in the essential fatty acid deficient rats was replaced with that of 18:2n−6 to 20:4n−6 in the essential fatty acid sufficient state.

Nutrition of Tocotrienols and Lipid Metabolism

Lymphatic absorption of α-tocotrienols (α-Toc3) given as a mixture of Toc 3 and α-tocopherol (α-Toc) was significantly higher than in γ-Toc 3, δ-Toc 3 and α-Toc in rats. This was confirmed when the rate of absorption of individual Toc 3 was measured. Approximately 50 to 60% of the absorbed Toc 3 and α-Toc was transported as chylomicrons in lymph. More α-Toc was excreted into feces than α-Toc 3 when these were given to rats, but the content in the liver markedly higher in the former than in the latter. Either α-Toc or Toc 3 concentrate contain α-, γ-, and δ-Toc 3 and α-Toc (dietary level; 0.13% α-Toc or 0.07% Toc 3 and 0.06% α-Toc) did not reduce systolic blood pressure of SHR when 0.5% salt solution was given as drinking water, whereas they suppressed an increase in blood pressure with age when the dietary was increased to 0.2% and no saline was given. The effect of Toc 3 concentrate and α-Toc, in particular the former, on aortic production of PGI2 was diverse depending on their dietary level whereas no effect was observed on the degree of maximum platelet aggregation induced by ADP. Although the activity of liver microsomal Δ5- and Δ6- desaturates was not influenced by Toc3 concentrate and α-Toc, they repressed conversion of the linoleic acid to arachidonic acid. These results suggest that Toc 3 have diverse nutritional and physiological impacts on various parameters, and their effects are not necessary the same as those of α-Toc.