Dietary Intake of Medium- and Long-chain Triacylglycerols Prevents the Progression of Hyperglycemia in Diabetic ob/ob Mice.

We examined the effects of the dietary intake of medium- and long-chain triacylglycerol (MLCT) on hyperglycemia in diabetic ob/ob mice. Six-week-old male ob/ob mice were fed a diet containing longchain triacylglycerol (LCT) or MLCT for 3 wks. During the dietary treatment, we determined the plasma glucose and insulin concentrations in the fed state once a week.

Medium-chain triacylglycerol suppresses the decrease of plasma albumin level through the insulin-Akt-mTOR pathway in the livers of malnourished rats.

Recent studies have shown that medium-chain triacylglycerol (MCT) improved serum albumin concentration in elderly people with protein-energy malnutrition (PEM) and in malnourished rats. However, the mechanism for this effect has not been clarified. Dietary MCT promotes insulin secretion from the pancreas, and insulin activates mammalian target of rapamycin (mTOR) complex 1 (mTORC1) via the activation of phosphoinositide 3-kinase (PI3K) and its downstream effecter, Akt.

Dietary intake of medium- and long-chain triacylglycerols ameliorates insulin resistance in rats fed a high-fat diet.

Objective: Excessive accumulation of visceral fat is strongly associated with insulin resistance. The present investigation examined the effects of dietary intake of medium- and long-chain triacylglycerols (MLCTs), which have been shown to induce significantly lower visceral fat accumulation in rats and humans, on high-fat diet-induced obesity and insulin resistance in rats. These effects were then compared with those observed in long-chain triacylglycerol (LCT)-fed rats.

Effect of life-long dietary n-6/n-3 fatty acid ratio on life span, serum lipids and serum glucose in Wistar rats.

Types of dietary lipid affect the life span of rats. In this study, we investigated the influence of the life-long dietary n-6/n-3 ratio on life span and serum lipid and glucose levels. A semi-purified diet adjusted to a constant saturated : monounsaturated : polyunsaturated fatty acid ratio and an n-6/n-3 ratio of 1 (R1), 4 (R4) or 16 (R16) was fed to rats (n=33) from 4 wk of age until death.

Compensatory expression of MRP3 in the livers of MRP2-deficient EHBRs is promoted by DHA intake.

We have hypothesized a suppressive mechanism against dietary docosahexaenoic acid (22:6n-3; DHA)-induced tissue lipid peroxidation, in which the degradation products, including their conjugates, are excreted into the urine by xenobiotic or organic anion transporters. In this study, we employed parent-strain Sprague-Dawley rats (SDRs), together with their mutant strain, Eisai hyperbilirubinuria rats (EHBRs). EHBRs are deficient in multidrug resistance-associated protein (MRP) 2, and show defective urinary excretion of numerous xenobiotics and organic anions.

Alpha-linolenic acid-rich flaxseed oil ingestion increases plasma adiponectin level in rats.

Adiponectin, an adipose-specific secretory protein, exhibits antidiabetic and antiatherogenic properties. The effect of alpha-linolenic acid (ALA) on adiponectin has not been revealed. ALA is included abundantly in vegetable oils such as flaxseed oil.

Effect of dietary n-6/n-3 ratio on liver n-6/n-3 ratio and peroxisomal beta-oxidation activity in rats.

The optimal dietary n-6/n-3 ratio has not been fully elucidated. To investigate the influence of the dietary n-6/n-3 ratio on this ratio in the body and on liver beta-oxidation peroxisomal activity, rats were fed diets containing fat at an n-6/n-3 ratio of 1 to 16 for 4 weeks. To investigate whether elevation of the liver peroxisomal beta-oxidation activity increases the n-6/n-3 ratio in the body, rats were fed a diet containing a peroxisome-activating agent, bezafibrate, for 2 weeks, and its influence on the liver n-6/n-3 ratio was examined.

The application of medium-chain fatty acids: edible oil with a suppressing effect on body fat accumulation.

The bulk of fatty acids found in our diets consists of long-chain fatty acids (LCFA), which are molecules containing 12 or more carbon atoms. In contrast, medium-chain fatty acids (MCFA) are composed of 8-10 carbon atoms, and are found in palm kernel oil, among other types of foods. MCFA have attracted attention as being part of a healthy diet, because they are absorbed directly into the portal vein, transported rapidly to the liver for beta-oxidation, and thus increase diet-induced thermogenesis.

Effect of Docosahexaenoic Acid Ingestion on Temporal Change in Urinary Excretion of Mercapturic Acid in ODS Rats.

We hypothesized a suppressive mechanism for docosahexaenoic acid (22:6n-3; DHA)-induced tissue lipid peroxidation in which the degradation products, especially aldehydic compounds, are conjugated with glutathione through catalysis by glutathione S-transferases, and then excreted into urine as mercapturic acids. In the present study, ascorbic acid-requiring ODS rats were fed a diet containing DHA (3.6% of total energy) for 31 days.

Effect of dietary lard containing higher alpha-linolenic acid on plasma triacylglycerol in rats.

It is well known that the consumption of n-3 polyunsaturated fatty acid (PUFA) decreases the plasma triacylglycerol (TAG) level. The technology of elevating the content of n-3 PUFAs in pig meat has already reached a practical level. In this study, the effects of dietary lard containing higher alpha-linolenic acid (LNA) on plasma TAG were compared with those of normal lard in rats.

Antihypertensive effect and safety of dietary alpha-linolenic acid in subjects with high-normal blood pressure and mild hypertension.

We investigated the antihypertensive effect and safety of alpha-linolenic acid (ALA) in human subjects. In Experiment 1, subjects with high-normal blood pressure and mild hypertension ingested bread containing 14 g of common blended oil (control oil) or ALA-enriched oil for 12 weeks. The test oil contained 2.

Lowering systolic blood pressure and increases in vasodilator levels in SHR with oral alpha-linolenic acid administration.

The present study attempted to clarify the antihypertensive effect and its mechanism when alpha-linolenic acid (ALA) is administered orally. For this purpose, 1 mL of flaxseed oil, which is rich in ALA, and high oleic safflower oil was administered orally to spontaneously hypertensive rats (SHR) of a control and an ALA group on days 1 and 5. Systolic blood pressure was measured on day 1, and blood and liver were collected on day 5.

Lower weight gain and higher expression and blood levels of adiponectin in rats fed medium-chain TAG compared with long-chain TAG.

Previous studies demonstrated that, compared with long-chain TAG (LCT), dietary medium-chain TAG (MCT) could improve glucose tolerance in rats and humans. It has been well established that adiponectin acts to increase insulin sensitivity. The effects of dietary MCT on adiponectin serum concentration and mRNA levels in adipose tissue were studied in rats.

Induction of multidrug resistance-associated protein MRP3 in the liver of rats fed with docosahexaenoic acid.

To clarify the alternative mechanisms to vitamin E (VE) regulating lipid peroxide accumulation in the liver after docosahexaenoic acid (DHA) ingestion, we examined the relationship between the DHA-induced lipid peroxide formation and induction of the xenobiotic transporters, Ral-binding GTPase-activating protein (RalBP1) and multidrug resistance-associated proteins 1, 2 and 3 (MRP1-3), in the liver of rats fed with DHA. The test diets contained DHA and linoleic acid (LA) (8.7% and 2.

Dietary docosahexaenoic acid-induced generation of liver lipid peroxides is not suppressed further by elevated levels of glutathione in ODS rats.

Objectives: We examined the effects of ascorbic acid (AsA) and glutathione (GSH; experiment 1) and of GSH in acetaminophen-fed rats (experiment 2) on dietary docosahexaenoic acid (DHA)-induced tissue lipid peroxidation.

Methods: In experiment 1, AsA-requiring Osteogenic Disorder Shionogi/Shi-od/od (ODS) rats were fed soybean protein diets containing DHA (10.0% total energy) and AsA at 50 (low) or 300 (normal) mg/kg without (low) or with (normal) methionine at 2 g/kg for 32 d.

Primary aminophospholipids in the external layer of liposomes protect their component polyunsaturated fatty acids from 2,2'-azobis(2-amidinopropane)- dihydrochloride-mediated lipid peroxidation.

We showed in our previous study that docosahexaenoic acid-rich phosphatidylethanolamine in the external layer of small-size liposomes, as a model for biomembranes, protected its docosahexaenoic acid from 2,2'-azobis(2-amidinopropane)dihydrochloride- (AAPH-) mediated lipid peroxidation in vitro. Besides phosphatidylethanolamine, both phosphatidylserine and an alkenyl-acyl analogue of phosphatidylethanolamine, phosphatidylethanolamine plasmalogen, are reported to possess characteristic antioxidant activities. However, there are few reports about the relationship between the protective activity of phosphatidylethanolamine plasmalogen and/or phosphatidylserine against lipid peroxidation and their distribution in a phospholipid bilayer.

Transbilayer distribution of aminophospholipids and the oxidative stability of their component polyunsaturated fatty acids.

We examined the relationship between the transbilayer distribution of aminophospholipids, such as phosphatidylethanolamine (PE), PE plasmalogen and phosphatidylserine, and the oxidative stability of polyunsaturated fatty acids (PUFAs) in the aminophospholipids. To modulate the transbilayer distribution of aminophospholipid in liposomes, we used phosphatidylcholine (PC) with two types of acyl chain region: dipalmitoyl (PC16:0) or dioleoyl (PC18:1). In the smaller-sized liposomes, the proportions of aminophospholipid in the liposomal external layer were significantly higher in liposomes containing PC18:1 than in those containing PC16:0.

Effect of dietary DHA on DHA levels in retinal rod outer segments in young versus mature rats.

We compared the effect of direct supplementation with docosahexaenoic acid (DHA) on the fatty acid composition of the liver and the rod outer segment (ROS) membranes of the retina in young (five-week-old) and mature (one-year-old) rats. In young rats, a high content of DHA in the diet (9.7% of total energy) effectively increased the proportion of DHA in ROS membranes (41.

Dietary docosahexaenoic acid-induced production of tissue lipid peroxides is not suppressed by higher intake of ascorbic acid in genetically scorbutic Osteogenic Disorder Shionogi/Shi-od/od rats.

In previous studies, we showed that docosahexaenoic acid (DHA) ingestion enhanced the susceptibility of rat liver and kidney to lipid peroxidation, but did not increase lipid peroxide formation to the level expected from the relative peroxidizability index (P-index) of the total tissue lipids. The results suggested the existence of some suppressive mechanisms against DHA-induced tissue lipid peroxide formation, as increased tissue ascorbic acid (AsA) and glutathione levels were observed. Therefore, we focused initially on the role of AsA for the suppressive mechanisms.

Effect of docosahexaenoic acid and ascorbate on peroxidation of retinal membranes of ODS rats.

Mutant male osteogenic disorder Shionogi (ODS) rats, unable to synthesize ascorbic acid, were fed diets containing a high content of docosahexaenoic acid (DHA) and different amounts of ascorbic acid, to study the effect of DHA on peroxidative susceptibility of the retina and possible antioxidant action of ascorbic acid. ODS rats were fed from 7 weeks of age with diets containing high DHA (6.4% of total energy).

Docosahexaenoic acid-containing phosphatidylethanolamine in the external layer of liposomes protects docosahexaenoic acid from 2,2'-azobis(2-aminopropane)dihydrochloride-mediated lipid peroxidation.

We have proposed that incorporation of docosahexaenoic acid (DHA) into phosphatidylethanolamine (PE) might enhance resistance to lipid peroxidation in vivo. In this study, we examined the relationship between the transbilayer distribution of PE and the oxidative stability of DHA in PE. Liposomes composed of a phospholipid mixture were used as models for biological membranes.