A Three-Month Consumption of Eggs Enriched with ω-3, ω-5 and ω-7 Polyunsaturated Fatty Acids Significantly Decreases the Waist Circumference of Subjects at Risk of Developing Metabolic Syndrome: A Double-Blind Randomized Controlled Trial.

Alpha-linolenic acid (ALA), docosahexaenoic acid (DHA), rumenic acid (RmA), and punicic acid (PunA) are claimed to influence several physiological functions including insulin sensitivity, lipid metabolism and inflammatory processes. In this double-blind randomized controlled trial, we investigated the combined effect of ALA, DHA, RmA and PunA on subjects at risk of developing metabolic syndrome. Twenty-four women and men were randomly assigned to two groups. Each day, they consumed two eggs enriched with oleic acid (control group) or enriched with ALA, DHA, RmA, and PunA (test group) for 3 months. The waist circumference decreased significantly (-3.17 cm; p < 0.001) in the test group. There were no major changes in plasma insulin and blood glucose in the two groups. The dietary treatments had no significant effect on endothelial function as measured by peripheral arterial tonometry, although erythrocyte nitrosylated hemoglobin concentrations tended to decrease. The high consumption of eggs induced significant elevations in plasma low-density lipoprotein (LDL)- and high-density lipoprotein (HDL)-cholesterol (p < 0.001), which did not result in any change in the LDL/HDL ratio in both groups. These results indicate that consumption of eggs enriched with ALA, DHA, RmA and PunA resulted in favorable changes in abdominal obesity without affecting other factors of the metabolic syndrome.

Acute effects of delayed-release hydrolyzed pine nut oil on glucose tolerance, incretins, ghrelin and appetite in healthy humans.

BACGROUND & AIM: Pinolenic acid, a major component (~20%) of pine nut oil, is a dual agonist of the free fatty acid receptors, FFA1 and FFA4, which may regulate release of incretins and ghrelin from the gut. Here, we investigated the acute effects of hydrolyzed pine nut oil (PNO-FFA), delivered to the small intestine by delayed-release capsules, on glucose tolerance, insulin, incretin and ghrelin secretion, and appetite. METHODS: In two cross-over studies, we evaluated 3 g unhydrolyzed pine nut oil (PNO-TG) or 3 g PNO-FFA versus no oil in eight healthy, non-obese subjects (study 1), and 3 g PNO-FFA or 6 g PNO-FFA versus no oil in ten healthy, overweight/obese subjects (study 2) in both studies given in delayed-release capsules 30 min prior to a 4-h-oral glucose tolerance test (OGTT). Outcomes were circulating levels of glucose, insulin, GLP-1, GIP, ghrelin, appetite and gastrointestinal tolerability during OGTT. RESULTS: Both 3 g PNO-FFA in study 1 and 6 g PNO-FFA in study 2 markedly increased GLP-1 levels (p < 0.001) and attenuated ghrelin levels (p < 0.001) during the last 2 h of the OGTT compared with no oil. In study 2, these effects of PNO-FFA were accompanied by an increased satiety and fullness (p < 0.03), and decreased prospective food consumption (p < 0.05). PNO-FFA caused only small reductions in glucose and insulin levels during the first 2 h of the OGTT. CONCLUSIONS: Our results provide evidence that PNO-FFA delivered to the small intestine by delayed-release capsules may reduce appetite by augmenting GLP-1 release and attenuating ghrelin secretion in the late postprandial state. CLINICAL TRIAL REGISTRY NUMBERS: NCT03062592 and NCT03305367.

Punica granatum L.-derived omega-5 nanoemulsion improves hepatic steatosis in mice fed a high fat diet by increasing fatty acid utilization in hepatocytes.

Pomegranate seed oil (PSO) is mainly composed of punicic acid (PA), a polyunsaturated fatty acid also known as omega-5 (ω-5), a potent antioxidant associated with a variety of metabolic and cellular beneficial effects. However, the potential benefits of a nanoemulsified version of ω-5 (PSOn) have not been evaluated in a pathological liver condition. Here, we examined whether PSOn had beneficial effects on C57BL/6N mice fed a high-fat diet (HFD), specifically on hepatic steatosis. We observed that PSOn supplementation decreased body weight and body fat mass in control mice, whereas glucose intolerance, insulin resistance, energy expenditure, and hepatic steatosis were improved in both control mice and in mice fed a HFD. Interestingly, PSOn increased fatty acid oxidation in primary hepatocytes and antioxidant gene expression. Altogether, our data indicate that PSOn effectively reduces some of the HFD-derived metabolic syndrome indicators by means of an increase in fatty acid oxidation within hepatocytes.

Topically applied linoleic/linolenic acid for chronic migraine.

The topical application of linoleic and linolenic acids is a potential prophylactic approach to migraine via an anti-inflammatory mechanism. We present a 45-year-old woman with chronic migraine without aura. Previous use of abortive or prophylactic therapies including sumatriptan, amitriptyline and topiramate had failed due to lack of efficacy or side-effects, especially vomiting. In search of a topical agent she performed an n-of-1 trial comparing application of linoleic acid (safflower oil) versus oleic acid (olive oil) for migraine relief. She found safflower oil to be effective. Topically applied safflower oil rich in linoleic and linolenic acids may offer a safe, easily applied, well-tolerated, effective anti-inflammatory approach for the prophylactic treatment of chronic migraine.

Meat quality of lambs fed diets with peanut cake.

Replacement of soybean meal by peanut cake was evaluated on the meat quality of 45 Dorper × Santa Inês crossbred lambs. Animals were distributed in a completely randomized design, with five treatments and nine repetitions, and fed Tifton-85 hay and a concentrate mixed with 0.0%, 25.0%, 50.0%, 75.0% or 100.0% peanut cake based on the dry mass of the complete diet. The longissimus lumborum muscle was used to determine the proximate composition, physical-chemical characteristics and fatty acid profile. Significant differences (P<0.05) were found for the crude protein and ether extract levels, with average values of 23.38% and 2.15% in the sheep meat, respectively. The physical-chemical characteristics of the loin were not affected (P>0.05) by the diets. The fatty acid profile was affected by peanut cake supplementation for myristic, myristoleic, palmitoleic, linolenic and arachidonic fatty acids. Peanut cake can be added in the diet of lambs no effect on physical-chemical characteristics. However, the total replacement of the soybean meal altered the proximate composition and fatty acid profile of the meat.

Disparate metabolic effects of blackcurrant seed oil in rats fed a basal and obesogenic diet.

PURPOSE: It was hypothesised that blackcurrant seed oil beneficially modulates metabolic disorders related to obesity and its complications. The study also aimed to investigate the potentially adverse effects of an unbalanced diet on the distal intestine. METHODS: Male Wistar rats were randomly assigned to four groups of eight animals each and were fed a basal or obesogenic (high in fat and low in fibre) diet that contained either rapeseed oil (Canola) or blackcurrant seed oil. A two-way analysis of variance was then applied to assess the effects of diet and oil and the interaction between them. RESULTS: After 8 weeks, the obesogenic dietary regimen increased the body weight, altered the plasma lipid profile and increased the liver fat content and the plasma transaminase activities. In addition, the obesogenic diet decreased bacterial glycolytic activity and short-chain fatty acid formation in the distal intestine. Dietary blackcurrant seed oil improved the lipid metabolism by lowering liver fat accumulation and the plasma triglyceride concentration and atherogenicity as well by increasing the plasma HDL-cholesterol concentration. However, in rats fed an obesogenic diet containing blackcurrant seed oil, the plasma HDL-cholesterol concentration was comparable with both rapeseed oil-containing diets, and a significant elevation of the plasma transaminase activities was noted instead. CONCLUSIONS: The obesogenic dietary regimen causes a number of metabolic disorders, including alterations in the hindgut microbial metabolism. Dietary blackcurrant seed oil ameliorates the lipid metabolism; however, the beneficial effect is restricted when it is provided together with the obesogenic diet, and a risk of liver injury may occur.

An in vitro study reveals the nutraceutical potential of punicic acid relevant to diabetes via enhanced GLUT4 expression and adiponectin secretion.

The prevalence of diabetes and heart diseases is increasing in the world. Nutraceuticals of natural origin are gaining importance as an alternative to modern drugs for the management of metabolic syndrome. In the present study, punicic acid (PA), a major bioactive found in pomegranate seed, was subjected for biological characterization with respect to peroxisome proliferator-activated receptor gamma (PPARγ) agonist property in an in vitro system (3T3-L1 adipocytes). We evaluated the adipogenic potential of various concentrations (5, 10 and 30 µM) of PA by studying triglyceride accumulation and glycerol-3-phosphate dehydrogenase (GPDH) activity in adipocytes, which were found to be increased moderately compared with the positive control, i.e. rosiglitazone (RG). Glucose uptake activity (↑225.93% ± 2.55% for 30 µM of PA), and the prevention of reactive oxygen species (ROS) generation (↓57 ± 1.83% for 30 µM of PA) in adipocytes with PA were also evaluated. We also found that PA increased adiponectin secretion and upregulated GLUT4 expression and translocation in adipocytes. Molecular modelling studies revealed a high binding affinity of PA to the PPARγ ligand binding domain. An in vitro ligand binding assay based on time-resolved fluorescence resonance energy transfer (TR-FRET) also proved PA as a PPARγ agonist. Finally, we conclude that PA is a potential nutraceutical and should be encouraged for use both as a prophylactic and therapeutic agent.

Protective effects of dietary PUFA against chronic disease: evidence from epidemiological studies and intervention trials.

This review considers evidence for a protective effect of PUFA on chronic disease. Estimates of PUFA intakes in prospective cohort studies are usually based on FFQ or biomarkers of intake. Cohort studies suggest that both linoleic and linolenic acid intake are associated with a lower risk of CHD. The intake of fish, the major source of long-chain n-3 PUFA is associated with a lower risk of both stroke and CHD, particularly sudden cardiac death. No relationship with common sites of cancer (breast and colon) and PUFA has been found. However, some recent studies suggest an association of high intakes of n-3 PUFA with risk of prostate cancer. An updated Cochrane review of dietary fat modification (replacing SFA with PUFA) randomised controlled trials to prevent CHD found a 14% lower incidence and a non-significant 7% lower mortality from CHD. The effects of an increased intake of n-3 PUFA on CHD incidence mortality have been tested in patients with pre-existing CHD in randomised controlled trials. Meta-analysis of these trials showed no overall benefit on total mortality or CVD incidence but a trend for lower risk of cardiac death was 0·91 (95% CI 0·85, 0·98). At present, there is little evidence from other trials demonstrating the clear benefits or harm from increased intakes of PUFA. In conclusion, present evidence intakes benefit from partial replacement of SFA with a balanced mixture of n-6 and n-3 PUFA which may contribute to CVD prevention.

Effect of fatty acid profile in vegetable oils and antioxidant supplementation on dairy cattle performance and milk fat depression.

This study was conducted to evaluate the effect of dietary supplementation of unprotected vegetable oils differing in fatty acid profiles with or without a commercial antioxidant (Agrado Plus, Novus International, St. Charles, MO) on dairy cattle performance, milk fatty acid profiles, and milk fat depression. Twenty-four multiparous Holstein cows were blocked by production (high and low) and assigned to Agrado Plus or no Agrado Plus diets as the main plot in this experiment. The 6 cows in each of the fixed effect groups (high with and without Agrado, low with and without Agrado) were then assigned to a 6 × 6 Latin square as a split plot with 21-d periods. The 6 dietary treatments in the split-plot Latin square were no added oil (control), or 5% DM as oil from palm (PO), high-oleic safflower (OSAF), high-linoleic safflower (LSAF), linseed (LNSD), or corn (CO). Added oil replaced corn starch in the total mixed ration. Diets were formulated to have similar crude protein and neutral detergent fiber, and consisted of 41.2% alfalfa silage, 18.3% corn silage, and 40.5% concentrate mix (dry matter basis). Feeding Agrado Plus did not affect milk, milk fat, or milk protein production or milk fatty acid composition in this study. No significant differences were found between oil feeding versus control for dry matter intake, milk yield, and milk protein yield, but oils other than PO significantly decreased milk fat concentration and proportion and yield of milk short- and medium-chain fatty acids (C(<16)). Feeding PO effectively maintained milk fat yield (1.18 kg/d) and concentration (3.44%), whereas the oils rich in linoleic acid (CO and LSAF) significantly decreased milk fat yield (0.98 and 0.86 vs. 1.14 kg/d) and concentration (3.05 and 2.83 vs. 3.41%) compared with control. Similar lactation performance between OSAF and LNSD suggests that oleic and linolenic acids are roughly equal in potency of milk fat depression.

Pomegranate seed oil, a rich source of punicic acid, prevents diet-induced obesity and insulin resistance in mice.

BACKGROUND: Pomegranate seed oil has been shown to protect against diet induced obesity and insulin resistance. OBJECTIVE: To characterize the metabolic effects of punicic acid on high fat diet induced obesity and insulin resistance. DESIGN: High-fat diet or high-fat diet with 1% Pomegranate seed oil (PUA) was fed for 12 weeks to induce obesity and insulin resistance. We assessed body weight and composition (pSABRE DEXA-scan), energy expenditure (Columbus Instruments) and insulin sensitivity at the end of the 12 weeks. RESULTS: PSO intake resulted in a lower body weight, 30.5±2.9 vs 33.8±3.2 g PSO vs HFD respectively, p=0.02, without affecting food intake or energy expenditure. The lower body weight was fully explained by a decreased body fat mass, 3.3±2.3 vs 6.7±2.7 g for PSO and HFD fed mice, respectively, p=0.02. Insulin clamps showed that PSO did not affect liver insulin sensitivity but clearly improved peripheral insulin sensitivity, 164±52% vs 92±24% for PSO and HFD fed mice respectively, p=0.01. CONCLUSIONS: We conclude that dietary PSO ameliorates high-fat diet induced obesity and insulin resistance in mice, independent of changes in food intake or energy expenditure.

Incorporation and metabolism of punicic acid in healthy young humans.

The objective of this study was to investigate the incorporation and metabolism of punicic acid (PA, cis9,trans11,cis13-18:3) in healthy young humans. The study was a randomized controlled trial. After 7 days adaptation with sunflower seed kernels supplementation, 30 subjects were then divided into the control and test group (n = 15). The test group was supplemented with Trichosanthes kirilowii (TK) seed kernels containing 3 g of PA per day in the form of triacylglycerols for 28 days. The control group was provided with sunflower seed kernels. After consumption of TK seeds containing 3 g PA per day for 28 days, the proportion of PA was increased from 0.00 to 0.47% in plasma and 0.00 to 0.37% in red blood cell membranes (RBCM), respectively. The proportion of cis9,trans11-18:2 was increased from 0.05 to 0.23% in plasma and 0.03 to 0.17% in RBCM after 28 days of intervention, respectively. Our results suggest that PA can be effectively incorporated into human plasma and RBCM, and is also associated with the increasing proportion of cis9,trans11-18:2 in humans, presumably as a result of metabolism by a saturation reaction. Edible TK seeds could be a potential dietary source of conjugated linoleic acids.

Punicic acid from Trichosanthes kirilowii seed oil is rapidly metabolized to conjugated linoleic acid in rats.

The incorporation and metabolism of orally administered punicic acid (PA), one isomer of conjugated linolenic acid (CLNA), in rat tissues and plasma were studied over a 24-hour period. The punic acid was derived from Trichosanthes kirilowii Maxim seed oil, a unique PA-containing material, and identified and analyzed by high-performance liquid chromatography and gas chromatography-mass spectrometry. The results show that PA was incorporated and metabolized to 9c,11t-conjugated linoleic acid (CLA) in rat plasma, liver, kidney, heart, brain, and adipose tissue. The level of PA and CLA in liver and plasma was higher than in brain, heart, kidney, and adipose tissue, and the lowest accumulation occurred in the brain. The observation that PA can be converted into 9c,11t-CLA has gained increased importance since it has been demonstrated that 9c,11t-CLA exerts many biological activities. Therefore natural resources containing CLNA, especially edible T. kirilowii seed, could be a potential dietary source of CLA, following PA metabolism. PA is expected to be used as a functional food and nutraceutical.

Differential incorporation of dietary conjugated linolenic and linoleic acids into milk lipids and liver phospholipids in lactating and suckling rats.

Interest in health benefits of conjugated fatty acids is growing. The present study compared the incorporation pattern of dietary conjugated linolenic acids (CLnA) into milk with that of conjugated linoleic acids (CLA). Lactating Sprague-Dawley rats (Day 1) were divided into five groups fed the control diet (n=4) or one of four experimental diets supplemented with 1-2% CLA or CLnA mixture (n=8 each). Supplementation of 1% and 2% CLA led to enrichment of 4.17% and 8.57% CLA, respectively, while supplementation of 1% and 2% CLnA resulted in enrichment of only 0.98% and 1.71% CLnA in the milk lipids, demonstrating the transfer of CLnA from maternal diet to milk was discriminated. When the lactating rats were given a diet containing a CLnA mixture of 9t,11t,13t-, 9c,11t,13t- and 9c,11t,13c-CLnA isomers, two CLA isomers, namely, 9t,11t (0.59-0.90%) and 9c,11t (1.21-1.96%), were found in the milk, suggesting that three CLnA isomers were Delta-13 saturated. Dietary CLnA at 1-2% had no effect on liver phospholipid (PL) fatty acid composition of both maternal and suckling rats, whereas dietary CLA increased docosahexaenoic acid (4c,7c,10c,13c,16c,19c-22:6) and palmitic acid (16:0) proportionally in the PL of maternal rats, but it suppressed 16:0 in the PL of suckling rats. It is concluded that maternal rats incorporate CLnA isomers into milk differently from that of CLA isomers. Most interesting is that maternal rats can metabolically convert CLnA to CLA.

Genetically modified rapeseed oil containing cis-9,trans-11,cis-13-octadecatrienoic acid affects body fat mass and lipid metabolism in mice.

Punicic acid, one of the conjugated linolenic acid (CLN) isomers, exerts a body-fat reducing effect. Although punicic acid is found in pomegranate and Tricosanthes kirilowii seeds, the amount of this fatty acid is very low in nature. The goal of this study was to produce a transgenic oil containing punicic acid. A cDNA encoding conjugase that converts linoleic acid to punicic acid was isolated from T. kirilowii, and the plant expression vector, pKN-TkFac, was generated. The pKN-TkFac was introduced into Brassica napus by Agrobacterium-mediated transformation. As a result, a genetically modified rapeseed oil (GMRO) containing punicic acid was obtained, although its proportion to the total fatty acids was very low (approximately 2.5%). The effects of feeding GMRO in ICR CD-1 male mice were then examined. Wild-type rapeseed (B. napus) oil (RSO) containing no CLN was used as a control oil. For reference oils, RSO-based blended oils were prepared by mixing with different levels of pomegranate oil (PO), either 2.5% (RSO + PO) or 5.0% (RSO + 2PO) punicic acid. Mice were fed purified diets containing 10% of either RSO, RSO + PO, RSO + 2PO, or GMRO for 4 weeks, and dietary PO dose-dependently reduced perirenal adipose tissue weight with a significant difference between the RSO group and the RSO + 2PO group. GMRO, as compared to RSO, lowered the adipose tissue weight to the levels observed with RSO + 2PO. The liver triglyceride level of the RSO + 2PO and GMRO groups but not that of the RSO + PO group was lower than that of the RSO group. The RSO + 2PO and GMRO groups, but not the RSO + PO group, had increased carnitine-palmitoyltransferase activity in the liver and brown adipose tissue. These results showed that dietary GMRO, even at a dietary punicic acid level as low as 0.25 wt % of diet, reduced body fat mass and altered liver lipid metabolism in mice and was more effective than an equal amount of punicic acid from PO.

Effectiveness of oils rich in linoleic and linolenic acids to enhance conjugated linoleic acid in milk from dairy cows.

Forty Holstein dairy cows were used to determine the effectiveness of linoleic or linolenic-rich oils to enhance C18:2 cis-9, trans-11 conjugated linoleic acid (CLA) and C18:1 trans-11 (vaccenic acid; VA) in milk. The experimental design was a complete randomized design for 9 wk with measurements made during the last 6 wk. Cows were fed a basal diet containing 59% forage (control) or a basal diet supplemented with either 4% soybean oil (SO), 4% flaxseed oil (FO), or 2% soybean oil plus 2% flaxseed oil (SFO) on a dry matter basis. Total fatty acids in the diet were 3.27, 7.47, 7.61, and 7.50 g/100 g in control, SO, FO, and SFO diets, respectively. Feed intake, energy-corrected milk (ECM) yield, and ECM produced/kg of feed intake were similar among treatments. The proportions of VA were increased by 318, 105, and 206% in milk fat from cows in the SO, FO, and SFO groups compared with cows in the control group. Similar increases in C18:2 cis-9, trans-11 CLA were 273, 150, and 183% in SO, FO, and SFO treatments, respectively. Under similar feeding conditions, oils rich in linoleic acid (soybean oil) were more effective in enhancing VA and C18:2 cis-9, trans-11 CLA in milk fat than oils containing linolenic acid (flaxseed oil) in dairy cows fed high-forage diets (59% forage). The effects of mixing linoleic and linolenic acids (50:50) on enhancing VA and C18:2 cis-9, trans-11 CLA were additive, but not greater than when fed separately. Increasing the proportion of healthy fatty acids (VA and CLA) by feeding soybean or flaxseed oil would result in milk with higher nutritive and therapeutic value.

Pomegranate seed oil rich in conjugated linolenic acid suppresses chemically induced colon carcinogenesis in rats.

Pomegranate (Punica granatum L.) seed oil (PGO) contains more than 70% cis(c)9,trans(t)11,c13-18:3 as conjugated linolenic acids (CLN). Our previous short-term experiment demonstrated that seed oil from bitter melon (Momordica charantia) (BMO), which is rich in c9,t11,t13-CLN, inhibited the occurrence of colonic aberrant crypt foci (ACF) induced by azoxymethane (AOM). In this study, we investigated the effect of dietary PGO on the development of AOM-induced colonic malignancies and compared it with that of conjugated linoleic acid (CLA). To induce colonic tumors, 6-week old male F344 rats were given subcutaneous injections of AOM (20 mg/kg body weight) once a week for 2 weeks. One week before the AOM treatment they were started on diet containing 0.01%, 0.1%, or 1% PGO or 1% CLA for 32 weeks. Upon termination of the bioassay (32 weeks) colon tumors were evaluated histopathologically. AOM exposure produced colonic adenocarcinoma with an incidence of 81% and multiplicity of 1.88 +/- 1.54 at week 32. Administration of PGO in the diet significantly inhibited the incidence (AOM + 0.01% PGO, 44%, P < 0.05; AOM + 0.1% PGO, 38%, P < 0.01; AOM + 1% PGO, 56%) and the multiplicity (AOM + 0.01% PGO, 0.56 +/- 0.73, P < 0.01; AOM + 0.1% PGO, 0.50 +/- 0.73, P < 0.005; AOM + 1% PGO, 0.88 +/- 0.96, P < 0.05) of colonic adenocarcinomas, although a clear dose-response relationship was not observed at these dose levels. CLA feeding also slightly, but not significantly, reduced the incidence and multiplicity of colonic adenocarcinomas. The inhibition of colonic tumors by PGO was associated with an increased content of CLA (c9,t11-18:2) in the lipid fraction of colonic mucosa and liver. Also, administration of PGO in the diet elevated expression of peroxisome proliferator-activated receptor (PPAR) gamma protein in the non-tumor mucosa. These results suggest that PGO rich in c9,t11,c13-CLN can suppress AOM-induced colon carcinogenesis, and the inhibition is associated in part with the increased content of CLA in the colon and liver and/or increased expression of PPARgamma protein in the colon mucosa.

The metabolic conversion of 9,11,13-eleostearic acid (18:3) to 9,11-conjugated linoleic acid (18:2) in the rat.

The presence of a significant amount of 9,11-conjugated linoleic acid (CLA, 9,11-18:2) was confirmed in the liver and plasma lipids of rats fed a 1% (w/w % of diet) eleostearic acid (ESA, 9,11,13-18:3) diet for 4 wk. The chemical structure of the 9,11-CLA apparent in the tissue lipids was identified by gas chromatography-electron impact mass spectrometry after its conversion to a 4,4-dimethyloxazoline derivative. The concentration of CLA in the total fatty acids of the liver and plasma lipids reached to about 1%, for each in the CLA-supplemented rats, while reaching 3.2% and 2.5%, respectively, in the ESA-supplemented rats. The results suggest that alpha-ESA is metabolized partially to CLA via a delta 13-saturation reaction in the rat. Some biological activities observed in alpha-ESA-fed animals may be ascribed also to CLA that is formed from ESA in the body.

Effect of dietary tung oil on the growth and lipid metabolism of laying hens.

The influence of dietary tung oil, containing a high level of alpha-eleostearic acid (cis-9, trans-11, trans-13-octadecatrienoic acid, EA) on growth, egg production, and lipid and fatty acid compositions in tissues and egg yolks of laying hens was studied in White Leghorn hens. Forty-week-old hens were divided into three groups of eight birds each and fed diets containing 0, 0.5, or 1.0% tung oil for 6 wk. The average body weight, feed consumption, rate of egg production, and weights of eggs and yolks were not affected. The weight of adipose tissue was remarkably small in hens fed tung oil, whereas the yolk lipid content did not change. Triglyceride level in heart and adipose tissue decreased in hens fed tung oil, and the level of linolenic acid (C18:3) in all tissues was decreased. Alpha-EA was not almost deposited in the tissues and egg yolk of hens fed tung oil, but conjugated linoleic acid (CLA) was detected in all tissues and egg yolks. The level of CLA in the tissues was significantly higher with increased dietary tung oil. The order of CLA level in tissue lipids was adipose tissue>liver>heart>breast muscle. Especially, the level of CLA in the lipids of adipose tissue and egg yolks of hens fed 1.0% tung oil was 2.0% of the total fatty acid. These results supposed that dietary tung oil affected the lipid metabolism of laying hens and could modify the lipid and fatty acid composition in tissues and eggs.

Docosahexaenoic and arachidonic acid prevent a decrease in dopaminergic and serotoninergic neurotransmitters in frontal cortex caused by a linoleic and alpha-linolenic acid deficient diet in formula-fed piglets.

This study examined the effects of diets deficient (D) in linoleic [18:2(n-6)] and linolenic acid [18:3(n-3)] at 0.8 and 0.05% energy, respectively, or adequate (C) in 18:2(n-6) and 18:3(n-3) at 8.3 and 0.8% energy, respectively, without (-) or with (+) 0.2% energy arachidonic [20:4(n-6)] and 0.16% energy docosahexaenoic [22:6(n-3)] acid in piglets fed from birth to 18 d. Frontal cortex dopaminergic and serotoninergic neurotransmitters and phospholipid fatty acids were measured. Piglets fed the D- diet had significantly lower frontal cortex dopamine, 3,4-dihydroxyphenylacetic (DOPAC), homovanillic acid (HVA), serotonin and 5-hydroxyindoleacetic acid (5-HIAA) concentrations than did piglets fed the C- diets. Frontal cortex dopamine, norepinephrine, DOPAC, HVA, serotonin and 5-HIAA were higher in piglets fed the D+ compared to those fed the D- diet (P < 0.05) and not different between piglets fed the D+ and those fed the C- diets or the C- and C+ diets. Piglets fed the D- diet had lower frontal cortex phosphatidylcholine (PC) and phosphatidylinositol (PI) 20:4(n-6) and PC and phosphatidylethanolamine (PE) 22:6(n-3) than did piglets fed the C- diet (P < 0.05). Piglets fed the D+ diet had higher frontal cortex PC and PI 20:4(n-6) and PC, PE, PS and PI 22:6(n-3) than did piglets fed the D- diet. These studies show that dietary essential fatty acid deficiency fed for 18 d from birth affects frontal cortex neurotransmitters in rapidly growing piglets and that these changes are specifically due to 20:4(n-6) and/or 22:6(n-3).

Blackcurrant seed oil, zinc, and fetal alcohol syndrome.

The effects of dietary supplementation by blackcurrant seed oil (BSO) and zinc sulphate on PGI2 gastric release and on serum zinc levels were investigated in 50 pregnant Sprague-Dawley rats which received watery alcohol solutions from 5% to 30% (v/v) as well as in their newborns. Blood zinc was assayed by atomic absorption spectroscopy; PGI2 was evaluated by platelet aggregation PGI2-dependent test. Dietary supplementation by BSO increased gastric release of PGI2 both in the mothers and their newborns; blood zinc levels were significantly (p < 0.01) lower in both vs control. The content of PGI2 in the stomachs was significantly (p < 0.01) higher in the mothers treated by zinc sulphate vs their new-borns. Protection of gastric mucosa of the new-born rats from alcohol fetal exposure might depend on polyunsaturated fatty acids (PUFA) dietary supplementation, because of the capability of PUFA to cross placenta; the efficacy in the protection might be monitored by platelet aggregation PGI2-dependent test.