Fish Oil-rich Diet Research Articles

Protective effect of fish oil targeting hadhaa (3-ketoacyl-CoA thiolase, alpha subunit a and hadhb (3-ketoacyl-CoA thiolase, beta subunit) against high cholesterol diet (HCD) induced atherosclerosis on Zebrafish

Currently a high mortality rate is observed due to heart diseases such as atherosclerosis and myocardial infarction, which are mainly caused due to high cholesterol. More novel drugs are needed to replace the currently available drugs to reduce the side effects. Zebrafish are an effective model for lipid metabolism studies in vertebrates. Because it shares 80% of diseases related genes similarity with humans. Zebrafish (Male) were fed with high cholesterol diet to induce atherosclerosis and the cholesterol levels of the Zebrafish are measured. Further, the m RNA expression of hadhaa and hadhb genes in the liver, intestine, and skeletal muscle of Zebrafish are studied. Finally, the atherosclerotic protective effects of fish oil are studied using fluorescence imaging of EGPF Zebrafish larvae and using nail red staining. In this study, we evaluated the effect of a fish oil-rich diet, dietary lipids reported having anti-obesity effects in animals, or cholesterol build-up in Zebrafish. Zebrafish were fed a high cholesterol diet containing 20% (w/w) fish oil. Zebrafish in the fish oil-fed group has 40% less cholesterol build-up than in the regular diet group. The genes encoding beta oxidases such as hadhaa and hadhb are expressed 2 fold higher in the gut of the fish oil treated group. Thiolase/enoyl coenzyme A-hydrates were 20% higher in the test (fish oil) diet group than in the normal diet (pellets) group (p < 0.05). The expression of the fatty acid synthesis gene (fasn) in the liver was considerably reduced in the fish oil group compared to the normal diet group (p < 0.05). These results show that fish oil may reduce cholesterol accumulation and might be used as an effective tool for anti-atherosclerotic drug development and on functional foods with further research. • In this research article we have discussed the possible effect of fish oil over HCD fed Zebrafish. • We have observed a positive effect on fish oil fed Zebrafish. • We suggest that the fish oil may have ability to reduce cholesterol accumulation and blood cholesterol level reduction. • All fishes subjected to the study are male Zebrafish.

A fish oil-rich diet leads to lower adiposity and serum triglycerides but increases liver lipid peroxidation in fructose-fed rats

BackgroundConsumption of refined carbohydrates has risen in recent years alongside chronic diseases such as type 2 diabetes mellitus, dyslipidemia, obesity, and non-alcoholic fatty liver disease (NAFLD). Fructose is a monosaccharide made widely available in industrialized products, capable of inducing excessive weight gain and liver steatosis in animal models, while omega-3 fatty acids, present in foods such as fatty fish and fish oil, have shown to inhibit genes related to lipogenesis and decrease cardiovascular risk. Therefore, our objective was to evaluate the impact of a high-fructose diet on weight gain, biochemical and oxidative stress parameters, and liver histology and investigate fish oil’s potential protective role. Thirty male Wistar rats were divided into 3 groups: regular chow diet (CT), regular chow diet plus 20% fructose in drinking water (Fr), and a diet containing 10% fish oil plus 20% fructose in drinking water (FOFr). After 12 weeks, tissues of interest were collected for biochemical and histological analyses.ResultsAlthough fructose consumption did not lead to increased hepatic fat, it caused a significant increase in weight gain, white adipose tissue, and serum triglycerides in the Fr group, while fish oil promoted normalized serum triglycerides and even reduced adiposity in the FOFr group. Additionally, the inclusion of fish oil in the FOFr diet led to increased liver lipid peroxidation in the form of increased hepatic MDA.ConclusionsIt is concluded that fish oil can prevent important metabolic alterations caused by fructose consumption, but its dosage must be taken into account to prevent oxidative stress and potential liver damage.

Addition of aspirin to a fish oil-rich diet decreases inflammation and atherosclerosis in ApoE-null mice

Aspirin (ASA) is known to alter the production of potent inflammatory lipid mediators, but whether it interacts with omega-3 fatty acids (FAs) from fish oil to affect atherosclerosis has not been determined. The goal was to investigate the impact of a fish oil-enriched diet alone and in combination with ASA on the production of lipid mediators and atherosclerosis. ApoE−/− female mice were fed for 13weeks one of the four following diets: omega-3 FA deficient (OD), omega-3 FA rich (OR) (1.8g omega-3 FAs/kg·diet per day), omega-3 FA rich plus ASA (ORA) (0.1g ASA/kg·diet per day) or an omega-3 FA deficient plus ASA (ODA) with supplement levels equivalent to human doses. Plasma lipids, atherosclerosis, markers of inflammation, hepatic gene expression and aortic lipid mediators were determined. Hepatic omega-3 FAs were markedly higher in OR (9.9-fold) and ORA (7-fold) groups. Mice in both OR and ORA groups had 40% less plasma cholesterol in very low-density lipoprotein-cholesterol and low-density lipoprotein fractions, but aortic plaque area formation was only significantly lower in the ORA group (5.5%) compared to the OD group (2.5%). Plasma PCSK9 protein levels were approximately 70% lower in the OR and ORA groups. Proinflammatory aortic lipid mediators were 50%–70% lower in the ODA group than in the OD group and more than 50% lower in the ORA group. In summary, less aortic plaque lesions and aortic proinflammatory lipid mediators were observed in mice on the fish oil diet plus ASA vs. just the fish oil diet.

Protective effect of soybean oil- or fish oil-rich diets on allergic airway inflammation.

BackgroundThe increased prevalence of asthma and allergic diseases in westernized societies has been associated with increased intake of diets rich in n-6 fatty acids (FAs) and poor in n-3 FAs. This study aimed to analyze the prophylactic effects of treatment with a soybean oil-rich diet (rich in n-6) or fish oil (rich in n-3) in an allergic airway inflammation model on lung inflammation score, leukocyte migration, T-helper cell (Th)-2 (interleukin [IL]-4, IL-5) and Th1 (interferon [IFN]-γ, tumor necrosis factor-α) cytokines, lipoxin A4, nitric oxide, bradykinin, and corticosterone levels in bronchoalveolar lavage (BAL) or lungs.MethodsMale Wistar rats fed with soybean oil- or fish oil-rich diet or standard rat chow were sensitized twice with ovalbumin–alumen and challenged twice with ovalbumin aerosol. The BAL and lungs were examined 24 hours later.ResultsBoth diets, rich in n-6 or n-3 FAs, impaired the allergic lung inflammation and reduced leukocyte migration, eosinophil and neutrophil percentages, and IL-4/IL-5/bradykinin levels in BAL and/or lungs, as well as increased the nitric oxide levels in BAL. The soybean oil-rich diet additionally increased the levels of lipoxin A4 and corticosterone in the lungs.ConclusionData presented demonstrated that the n-6 FA-rich diet had protective effect upon allergic airway inflammation and was as anti-inflammatory as the n-3 FA-rich diet, although through different mechanisms, suggesting that both diets could be considered as complementary therapy or a prophylactic alternative for allergic airway inflammation.

Fish Oil-Rich Diet Promotes Hematopoiesis and Alters Hematopoietic Niche.

The self-renewal and differentiation of hematopoietic stem cells (HSCs) in bone marrow are essential to replenish all blood cell types, but how this process is influenced by diet remains largely unclear. Here we show that a diet rich in fish oils promotes self-renewal of HSCs and extramedullary hematopoiesis. Chronic intake of a fish oil-rich diet increases the abundance of HSCs, alters the hematopoietic microenvironment, and, intriguingly, induces the expression of matrix metalloproteinase 12 (MMP12) in the bone marrow. Pointing to a direct effect of fish oil on MMP12 expression, omega-3 polyunsaturated fatty acids induce the expression of MMP12 in a dose-dependent manner in bone marrow cells. Importantly, down-regulation of MMP12 activity using an MMP12-specific inhibitor attenuates diet-induced myelopoiesis in both bone marrow and spleen. Thus, a fish oil-rich diet promotes hematopoiesis in the bone marrow and spleen, in part via the activity of MMP12. Taken together, these data provide new insights into diet-mediated regulation of hematopoiesis.

234: Maternal fish oil-rich diet significantly alters fetal brain and liver fatty acid profiles in mice

234: Maternal fish oil-rich diet significantly alters fetal brain and liver fatty acid profiles in mice

Dietary fatty acids modulate liver mitochondrial cardiolipin content and its fatty acid composition in rats with non alcoholic fatty liver disease

No data are reported on changes in mitochondrial membrane phospholipids in non-alcoholic fatty liver disease. We determined the content of mitochondrial membrane phospholipids from rats with non alcoholic liver steatosis, with a particular attention for cardiolipin (CL) content and its fatty acid composition, and their relation with the activity of the mitochondrial respiratory chain complexes. Different dietary fatty acid patterns leading to steatosis were explored. With high-fat diet, moderate macrosteatosis was observed and the liver mitochondrial phospholipid class distribution and CL fatty acids composition were modified. Indeed, both CL content and its C18:2n-6 content were increased with liver steatosis. Moreover, mitochondrial ATP synthase activity was positively correlated to the total CL content in liver phospholipid and to CL C18:2n-6 content while other complexes activity were negatively correlated to total CL content and/or CL C18:2n-6 content of liver mitochondria. The lard-rich diet increased liver CL synthase gene expression while the fish oil-rich diet increased the (n-3) polyunsaturated fatty acids content in CL. Thus, the diet may be a significant determinant of both the phospholipid class content and the fatty acid composition of liver mitochondrial membrane, and the activities of some of the respiratory chain complex enzymes may be influenced by dietary lipid amount in particular via modification of the CL content and fatty acid composition in phospholipid.

Fish oil consumption prevents glucose intolerance and hypercorticosteronemy in footshock-stressed rats

BackgroundEnvironmental stress plays an important role in the development of glucose intolerance influencing lipid and glucose metabolism through sympathetic nervous system, cytokines and hormones such as glucocorticoids, catecholamines and glucagon. Otherwise, fish oil prevents glucose intolerance and insulin resistance. Although the mechanisms involved are not fully understood, it is known that sympathetic and HPA responses are blunted and catecholamines and glucocorticoids concentrations can be modulated by fish consumption. The aim of the present study was to evaluate whether fish oil, on a normal lipidic diet: 1) could prevent the effect of footshock-stress on the development of glucose intolerance; 2) modified adiponectin receptor and serum concentration; and 3) also modified TNF-α, IL-6 and interleukin-10 (IL-10) levels in adipose tissue and liver. The study was performed in thirty day-old male Wistar randomly assigned into four groups: no stressed (C) and stressed (CS) rats fed with control diet, and no stressed (F) and stressed (FS) rats fed with a fish oil rich diet. The stress was performed as a three daily footshock stress sessions.ResultsBody weight, carcass fat and protein content were not different among groups. FS presented a reduction on the relative weight of RET. Basal serum glucose levels were higher in CS and FS but 15 min after glucose load just CS remained with higher levels than other groups. Serum corticosterone concentration was increased in CS, this effect was inhibited in FS. However, 15 min after footshock-stress, corticosterone levels were similar among groups. IL-6 was increased in EPI of CS but fish oil consumption prevented IL-6 increase in FS. Similar levels of TNF-α and IL-10 in RET, EPI, and liver were observed among groups. Adipo R1 protein concentration was not different among groups. Footshock-stress did not modify AdipoR2 concentration, but fish oil diet increases AdipoR2 protein concentration.ConclusionsFootshock-stress promotes glucose intolerance associated to corticosterone serum level and epididymal white adipose tissue IL-6 concentration increase. The fish oil consumption by stressed rats normalized the stress responses. These results suggested that fish oil intake could be useful to minimize or prevent the development of diseases associated to the stress.

Abstract 5571: Effects of fish oil and Tamoxifen on preneoplastic lesion development and biomarkers of oxidative stress in the early stages of N-methyl-N-nitrosourea-induced rat mammary carcinogenesis

Abstract Our laboratories are interested in testing the value of combining omega-3 fatty acids and antiestrogens as a safe and effective chemopreventive strategy for breast cancer. We have shown that a fish oil rich diet (FO) (17% FO + 3% corn oil [CO]) enhances the chemopreventive action of Tamoxifen (Tam) in a prepubertal model of N-methyl-N-nitrosourea (MNU)-induced rat mammary carcinogenesis (A. Manni, et al., Cancer Prev Res 3:322, 2010). To gain insight into mechanisms of prevention and the importance of different ratios of n-3:n-6 fatty acids in inhibiting carcinogenesis, we tested the effects of two FO rich diets (17% FO + 3% CO and 10% FO + 10% CO) individually and in combination with Tam on the histologic progression of preneoplastic lesions, indices of proliferation and apoptosis, as well as expression of multiple mammary gland specific and systemic biomarkers of oxidative stress in carcinogen treated rats. Following MNU administration at 21 days of age, separate groups of rats within each experimental arm were sacrificed 24 hours, 21 days, 28 days and 35 days prior to the development of palpable tumors. Increasing the amount of FO in the diet progressively increased the n-3:n-6 ratio in the plasma from 0.13 (20% CO) to 0.38 (10% FO) and 0.96 (17% FO). Although the FO rich diets significantly reduced Ki67 expression in hyperplastic lesions in a dose-dependent fashion (17% FO &amp;gt; 10% FO), neither the diets nor Tam decreased the development of preneoplastic lesions indicating that the inhibitory effect on carcinogenesis results from blocking the transition from hyperplasia to adenocarcinoma, consistent with our recent published study. Dietary FO and/or Tam did not have major effects on systemic oxidative stress biomarkers (plasma protein carbonyls and blood protein bound GSH) or mammary specific biomarkers of oxidative stress, based on oxidative damage to DNA measured as 8-hydroxy-2’-deoxyguanosine (8-OH-dG) and lipid peroxidation assessed as thiobarbituric-acid reactive substances (TBARS). On the other hand, tissue levels of 8-isoprostanes, prostaglandin-like compounds formed by non-enzymatic oxidation of arachidonic acid in the cell membrane, were markedly reduced by both FO rich diets at all time points (p&amp;lt;0.0001). In conclusion, these results, together with our previous findings, suggest that Tam, either alone or in combination with FO, exerts its protective effects on mammary carcinogenesis by blocking the transition from hyperplasia to carcinoma. The effects of FO may be due to changes in arachidonic acid specific pathways but do not involve early changes in levels of select oxidative stress markers examined in this experimental system. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5571. doi:10.1158/1538-7445.AM2011-5571

Fish oil rich diet in comparison to saturated fat rich diet offered protection against lipopolysaccharide-induced inflammation and insulin resistance in mice

Background and ObjectiveSystemic chronic inflammation is linked to metabolic syndrome, type-2 diabetes, and heart disease. Lipopolysaccharide (LPS), a Gram negative microbial product, triggers inflammation through toll-like-receptor-4 (TLR-4) signaling. It has been reported that dietary fatty acids also modulate inflammation through TLR-4. We investigated whether fish oil (FO) rich diet in comparison to saturated fat (SF) rich diet would confer protection from pathologies induced by LPS.MethodsTwenty C57BL/6 mice were divided into two groups. One group received FO-diet and other received SF-diet ad libitum for 60 days. Diets were isocaloric containing 45% energy from fat. After 60-days of feeding, blood was collected after overnight fast. Mice were allowed to recover for 4-days, fasted for 5-hours, challenged with 100 ng/mL of LPS intraperitonially, and bled after 2-hours. After 7-days of recuperation, mice were challenged with 500 ng/mL of LPS intraperitonially and observed for physical health.ResultsFood intake was similar in FO- and SF-fed mice. FO-fed mice compared to SF-fed mice had significantly less body weight gain (P = 0.005), epididymal fat weight (P = 0.005), fasting blood glucose (70.8 vs 83.3 ng/dL; P < 0.05), HOMA-IR (5.0 vs 13.6; P < 0.019), and serum cholesterol (167 vs 94 mg/dL; P < 0.05). When challenged with LPS, FO-fed mice had significantly lower serum IL-1β compared to SF-fed mice (2.0 vs 30.0 pg/mL; P < 0.001). After LPS-challenge, SF-fed mice had higher mortality, lost more body weight, and had greater decrease in blood glucose compared to FO-fed mice.ConclusionOverall, FO-diet compared to SF-diet offered protection against deleterious effects of LPS in mice.

Acute Pancreatitis in Obesity: Adipokines and Dietary Fish Oil

Acute pancreatitis is a substantial clinical problem accounting for 240,000 hospital admissions yearly in the United States. Obesity is epidemic and is clearly an independent risk factor for increased severity of acute pancreatitis (AP). Adipose tissue is an endocrine organ that secretes a variety of metabolically active substances termed adipokines. However, the role of adipokines in modulating acute pancreatitis severity remains incompletely understood. Dietary fish oil is rich in omega-3 free fatty acids and attenuates adipose tissue-induced inflammation. Therefore, we hypothesized that feeding obese mice diets rich in fish oil would alter the adipokine milieu and attenuate the severity of pancreatitis. Lean (C57BL/6 J) and obese (LepDb) mice were fed either a soybean oil- or fish oil-rich diet for 4 weeks. AP was induced by six hourly intraperitoneal injections of cerulein (50 μg/kg). Serum adipokine levels were measured, and pancreatitis severity was assessed histologically and by measuring pancreatic concentrations of interleukin-1 beta (IL-1β), interleukin-6 (IL-6), myleoperoxidase (MPO), and monocyte chemoattractant protein-1 (MCP-1). Obese mice developed more severe pancreatitis than lean mice. Fish oil significantly decreased serum leptin (lean and obese) and increased serum adiponectin (lean only). Fish oil did not alter the baseline pancreatic inflammatory milieu, nor did it change histologic or biochemical pancreatitis severity. These data demonstrate that a diet rich in fish oil altered the adipokine milieu in lean and congenitally obese mice; however, fish oil did not improve pancreatitis severity induced with cerulein hyperstimulation.

Fish oil supplementation reverses the effect of cholesterol on apoptotic gene expression in smooth muscle cells

BackgroundNutritional control of gene regulation guides the transformation of smooth muscle cells (SMC) into foam cells in atherosclerosis. Oxidative stress has been reported in areas of lipid accumulation, activating proliferation genes. Suppression of oxidative stress by antioxidant administration reduces this activation and the progression of lesions. We hypothesized that fish oil consumption may protect against atherosclerotic vascular disease. The study objective was to determine the effects of dietary cholesterol and fish-oil intake on the apoptotic pathways induced by 25-hydroxycholesterol (25-HC) in SMC cultures.MethodsAn in vivo/in vitro cell model was used, culturing SMC isolated from chicks exposed to an atherogenic cholesterol-rich diet with 5% of cholesterol (SMC-Ch) alone or followed by an anti-atherogenic fish oil-rich diet with 10% of menhaden oil (SMC-Ch-FO) and from chicks on standard diet (SMC-C). Cells were exposed to 25-HC, studying apoptosis levels by flow cytometry (Annexin V) and expressions of caspase-3, c-myc, and p53 genes by quantitative real-time reverse transcriptase-polymerase chain reaction. Results: Exposure to 25-HC produced apoptosis in all three SMC cultures, which was mediated by increases in caspase-3, c-myc, and p53 gene expression. Changes were more marked in SMC-Ch than in SMC-C, indicating that dietary cholesterol makes SMC more susceptible to 25-HC-mediated apoptosis. Expression of p53 gene was elevated in SMC-Ch-FO. This supports the proposition that endogenous levels of p53 protect SMC against apoptosis and possibly against the development of atherosclerosis. Fish oil attenuated the increase in c-myc levels observed in SMC-C and SMC-Ch, possibly through its influence on the expression of antioxidant genes.ConclusionReplacement of a cholesterol-rich diet with a fish oil-rich diet produces some reversal of the cholesterol-induced changes, increasing the resistance of SMC to apoptosis.

Omega-3 Fatty Acids for the Prevention of Myocardial Infarction and Arrhythmias

In1978,areportfromtheChiefMedicalOfficerinGreen-land documented that coronary heart disease (CHD) wasresponsible for only 3.5% of all deaths in GreenlandEskimos [1], a strikingly small number compared to thetypical figures found in the Western countries. Seekingpotential explanations for such low frequency of cardiacevents, investigators at the University of Aalborg, in Den-mark, noted that the serum lipids of Eskimos was en-riched in omega-3 fatty acids, that is, polyunsaturatedfatty acids with the first double bond found in position3 when the molecule is scanned from its methyl (-CH3)end (n-3 PUFA) [2,3]. They then identified fish oil as theprimary source of n-3 PUFA in Eskimos’ diet [4], in par-ticular eicosapentaenoic acid (EPA) and docosahexaenoicacid(DHA),whoseabundanceinplasmaandplateletshasantihemostatic, hence antithrombotic effects [5]. Thesemolecules consequently became the target of a wealthof studies aimed at explaining their preventive effectsagainst cardiovascular diseases.In 1985, Kromhout et al. evaluated the long-term im-pact of dietary n-3 PUFA on a cohort of 852 healthymen in the town of Zutphen, in the Netherlands. After20 years of follow-up they found a 50% reduction inCHD-related deaths in subjects consuming at least 30 gof fish per day, as compared to the rest of the population[6].Spurred by these findings in humans, later studies insmall and large animal models sought to determine themechanisms responsible for the beneficial impact of n-3 PUFA consumption on cardiovascular mortality. Reineretal.reportedareductionofaorticatherosclerosisinmicewith saturated fat diet supplemented with n-3 PUFA, andattributed it to the modulation of the expression andsecretion of several macrophage effector molecules [7].Other studies confirmed the reduction of atherogenesis inrodents and dog models of hypercholesterolemia or vas-cular injury subjected to fish oil rich diet, and highlightedthe positive modulation of platelet function as a possiblemechanism of action of n-3 PUFA [8–11].

Defective Phagocytosis of Apoptotic Cells by Macrophages in Atherosclerotic Lesions of ob/ob Mice and Reversal by a Fish Oil Diet

The complications of atherosclerosis are a major cause of death and disability in type 2 diabetes. Defective clearance of apoptotic cells by macrophages (efferocytosis) is thought to lead to increased necrotic core formation and inflammation in atherosclerotic lesions. To determine whether there is defective efferocytosis in a mouse model of obesity and atherosclerosis. We quantified efferocytosis in peritoneal macrophages and in atherosclerotic lesions of obese ob/ob or ob/ob;Ldlr(-/-) mice and littermate controls. Peritoneal macrophages from ob/ob and ob/ob;Ldlr(-/-) mice showed impaired efferocytosis, reflecting defective phosphatidylinositol 3-kinase activation during uptake of apoptotic cells. Membrane lipid composition of ob/ob and ob/ob;Ldlr(-/-) macrophages showed an increased content of saturated fatty acids (FAs) and decreased omega-3 FAs (eicosapentaenoic acid and docosahexaenoic acid) compared to controls. A similar defect in efferocytosis was induced by treating control macrophages with saturated free FA/BSA complexes, whereas the defect in ob/ob macrophages was reversed by treatment with eicosapentaenoic acid/BSA or by feeding ob/ob mice a fish oil diet rich in omega-3 FAs. There was also defective macrophage efferocytosis in atherosclerotic lesions of ob/ob;Ldlr(-/-) mice and this was reversed by a fish oil-rich diet. The findings suggest that in obesity and type 2 diabetes elevated levels of saturated FAs and/or decreased levels of omega-3 FAs contribute to decreased macrophage efferocytosis. Beneficial effects of fish oil diets in atherosclerotic cardiovascular disease may involve improvements in macrophage function related to reversal of defective efferocytosis and could be particularly important in type 2 diabetes and obesity.

Effect of Different Vegetable Oils on Growth and Fatty Acid Profile of Rohu (Labeo rohita, Hamilton); Evaluation of a Return Fish Oil Diet to Restore Human Cardio-protective Fatty Acids

Two experiments in the sequential order were conducted to determine the effects of different dietary lipid sources on the growth and fatty acid composition of rohu (Labeo rohita) and to examine the viability of a return fish oil finisher diet in restoring the human cardio-protective fatty acid profile. In the first experiment, fish were fed either with coconut oil (Dl), olive oil (D2), sunflower oil (D3), linseed oil (D4) and fish oil (D5) as the main lipid source in the isonitrogenous diet for 90 days. No significant differences in growth were observed. Among the experimental diets moisture content of fish varied significantly (p<0.05) between the groups. Dietary lipid sources had a profound influence on the fatty acid profile of the muscle and liver as tissue fatty acid profile reflected the dietary fatty acid composition. Increased amounts of eicosapentaenoic acid and docosahexaenoic acid were observed in tissue of fish fed D4 and arachidonic acid was observed in the tissue of fish fed D3. We have also detected the metabolites of n-3 and n-6 pathway in D4 and D3 groups respectively, which prompted us to conclude that rohu, can desaturate and elongate C 18 essential fatty acids to C 20 and C 22 HUFA. A second feeding trial was conducted using the animals from the five different treatment groups for the duration of 30 days with fish oil rich diet (D5). Feeding with fish-oil rich washout diet resulted in the near equalization of all the other treatment groups tissue fatty acid profiles to that of fish oil (D5) fed group. These results indicate that a finishing fish oil diet can be effectively used to restore the human cardioprotective fatty acid profile in rohu fed with vegetable oils as lipid source.

N-3 Polyunsaturated fatty acids are still underappreciated and underused post myocardial infarction

Interest in the possible cardio-protective effects of n-3 polyunsaturated fatty acids (n-3 PUFA) has existed since the late 1970s. Early observations in Greenland Eskimos and the Japanese population linked a...

Effect of Oxysterol‐Induced Apoptosis of Vascular Smooth Muscle Cells on Experimental Hypercholesterolemia

Smooth muscle cells (SMCs) undergo changes related to proliferation and apoptosis in the physiological remodeling of vessels and in diseases such as atherosclerosis and restenosis. Recent studies also have demonstrated the vascular cell proliferation and programmed cell death contribute to changes in vascular architecture in normal development and in disease. The present study was designed to investigate the apoptotic pathways induced by 25-hydroxycholesterol in SMCs cultures, using an in vivo/in vitro cell model in which SMCs were isolated and culture from chicken exposed to an atherogenic cholesterol-rich diet (SMC-Ch) and/or an antiatherogenic fish oil-rich diet (SMC-Ch-FO). Cells were exposed in vitro to 25-hydroxycholesterol to study levels of apoptosis and apoptotic proteins Bcl-2, Bcl-XL and Bax and the expression of bcl-2 and bcl-xL, genes. The quantitative real-time reverse transcriptase-polymerase chain reaction and the Immunoblotting western blot analysis showed that 25-hydroxycholesterol produces apoptosis in SMCs, mediated by a high increase in Bax protein and Bax gene expression. These changes were more marked in SMC-Ch than in SMC-Ch-FO, indicating that dietary cholesterol produces changes in SMCs that make them more susceptible to 25-hydroxycholesterol-mediated apoptosis. Our results suggest that the replacement of a cholesterol-rich diet with a fish oil-rich diet produces some reversal of cholesterol-induced changes in the apoptotic pathways induced by 25-hydroxycholesterol in SMCs cultures, making SMCs more resistant to apoptosis.

An n-3 PUFA-rich microalgal oil diet protects to a similar extent as a fish oil-rich diet against AOM-induced colonic aberrant crypt foci in F344 rats

The chemopreventive effects of high fat microalgal oil diet on azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF) were studied in male Fischer 344 rats following 8 weeks of dietary treatment. These effects were compared to the effects of high fat fish oil and high fat corn oil diets to determine whether microalgal oil is a good alternative for fish oil regarding protection against colorectal cancer. Despite the difference in fatty acid composition and total amount of n-3 polyunsaturated fatty acids (PUFAs) between microalgal oil and fish oil, both these oils gave the same 50% reduction of AOM-induced ACF when compared to corn oil. To determine whether oxidative stress could play a role in the chemoprevention of colorectal cancer by n-3 PUFAs, feces and caecal content were examined using the TBA assay. The results showed that lipid peroxidation does occur in the gastrointestinal tract. As several lipid peroxidation products of n-3 PUFAs can induce phase II detoxifying enzymes by an EpRE-mediated pathway, the in vivo results suggest that this route may contribute to n-3 PUFA-mediated chemoprevention. All in all, n-3 PUFA-rich oil from microalgae is as good as fish oil regarding chemoprevention in the colon of the rat.

Dietary fish oil did not prevent sleep deprived rats from a reduction in adipose tissue adiponectin gene expression

Sleep deprivation in humans has been related to weight gain and consequently, increased risk for insulin resistance. In contrast, there is a significant loss of weight in sleep deprived rats suggesting a state of insulin resistance without obesity interference. Thus, we aimed to assess the effects of a rich fish oil dietetic intervention on glucose tolerance, serum insulin and adiponectin, and adipose tissue gene expression of adiponectin and TNF-α of paradoxically sleep deprived (PSD) rats. The study was performed in thirty day-old male Wistar randomly assigned into two groups: rats fed with control diet (soybean oil as source of fat) and rats fed with a fish oil rich diet. After 45 days of treatment, the animals were submitted to PSD or maintained as home cage control group for 96 h. Body weight and food intake were carefully monitored in all groups. At the end of PSD period, a glucose tolerance test was performed and the total blood and adipose tissues were collected. Serum insulin and adiponectin were analyzed. Adipose tissues were used for RT-PCR to estimate the gene expression of adiponectin and TNF-α. Results showed that although fish oil diet did not exert any effect upon these measurements, PSD induced a reduction in adiponectin gene expression of retroperitoneal adipose tissues, with no change in serum adiponectin concentration or in adiponectin and TNF-α gene expression of epididymal adipose tissue. Thus, the stress induced by sleep deprivation lead to a desbalance of adiponectin gene expression.

Deficiency and supplementation of PUFA in the diet have similar effects on the age-associated changes in rat-plasma cholesterol levels

Levels of plasma cholesterol, particularly LDL cholesterol, increase with increasing age in humans and rodents. Feeding a fish oil-rich diet may exert hypocholesterolemic effects. The aim of this work was to examine the effects of a life-long administration of a PUFA-enriched diet and of a PUFA-deficient diet in male Sprague–Dawley rats on the age-associated increases in plasma cholesterol and triglycerides. Diet had small effects on body-weight, and had dramatic effects on liver phospholipids-fatty acids. Surprisingly, both diets counteracted the age-associated changes in plasma cholesterol and triglycerides similarly and benefits were already visible in adult rats.