Do leafy green vegetables and their ready-to-eat [RTE] salads carry a risk of foodborne pathogens?

Over the past 10 years, there is an increasing demand for leafy green vegetables and their ready-to-eat (RTE) salads since people changed their eating habits because of healthier lifestyle interest. Nevertheless fresh leafy green vegetables and their RTE salads are recognized as a source of food poisoning outbreaks in many parts of the world. However, this increased proportion of outbreaks cannot be completely explained by increased consumption and enhanced surveillance of them. Both in Europe and in the USA, recent foodborne illness outbreaks have revealed links between some pathogens and some leafy green vegetables such as mostly lettuces and spinaches and their RTE salads since fresh leafy green vegetables carry the potential risk of microbiological contamination due to the usage of untreated irrigation water, inappropriate organic fertilizers, wildlife or other sources that can occur anywhere from the farm to the fork such as failure during harvesting, handling, processing and packaging. Among a wide range of pathogens causing foodborne illnesses, Escherichia coli O157:H7, Salmonella spp., and Listeria monocytogenes are the most common pathogens that contaminate leafy green vegetables. Children, the elderly, pregnant women and immunocompromised people are the most at risk for developing complications from foodborne illness as a result of eating contaminated leafy greens or their RTE salads. These outbreaks are mostly restaurant associated or they sometimes spread across several countries by international trade routes. This review summarizes current observations concerning the contaminated leafy green vegetables and their RTE salads as important vehicles for the transmission of some foodborne pathogens to humans.     

The ddY mouse: a model of postprandial hypertriglyceridemia in response to dietary fat

Postprandial hyperlipidemia (lipemia) is a risk factor for atherosclerosis. However, mouse models of postprandial hyperlipidemia have not been reported. Here, we report that ddY mice display marked postprandial hypertriglyceridemia in response to dietary fat. In ddY mice, the fasting serum total triacylglyceride (TG) concentration was 134 mg/dl, which increased to 571 mg/dl after an intragastric safflower oil load (0.4 ml/mouse). In C57BL/6J mice, these concentrations were 57 and 106 mg/dl, respectively. By lipoprotein analysis, ddY mice showed increases in chylomicron- and VLDL-sized TG fractions (remnants and VLDL) after fat load. In C57BL/6J mice, post-heparin plasma LPL activity after fat load was increased 4.8-fold relative to fasting. However, in ddY mice, the increase of LPL activity after fat load was very small (1.2-fold) and not significant. High fat feeding for 10 weeks led to obesity in ddY mice. A difference in LPL amino acid composition between C57BL/6J and ddY mice was detected but was deemed unlikely to cause hypertriglyceridemia because hypertriglyceridemia was not evident in other strains harboring the ddY-type LPL sequence. These findings indicate that postprandial hypertriglyceridemia in ddY mice is induced by decreased LPL activity after fat load and is associated with obesity induced by a high-fat diet.     

Emulsified lipids increase endotoxemia: possible role in early postprandial low-grade inflammation

Low-grade inflammation is a risk factor for the onset of atherosclerosis. Little is known about the involvement of endotoxin absorption from the gut during the digestion of lipids. In the present study, we first investigated in humans the impact of a mixed meal containing dispersed lipids on postprandial endotoxemia and inflammation. We then investigated the effect of (i) oil emulsification in vivo in rats and (ii) fatty acid amounts in vitro using Caco-2 cells on postprandial endotoxemia. In humans, postprandial endotoxemia increased early after the meal. Moreover, we evidenced that the endotoxin receptor sCD14 increased during digestion and that chylomicrons could contribute to absorbed endotoxin transport. This could explain the significant peak of inflammatory cytokine IL-6 that we observed 2 h after the mixed meal. Interestingly, in rats, the emulsion led to both higher endotoxemia and hypertriglyceridemia than oil and compared to a control saline load. In vitro, incubation of Caco-2 cells with increasing fatty acid concentrations enhanced epithelial absorption of endotoxin. To our knowledge, this is the first study evidencing in healthy humans that, following a mixed meal containing lipids, increased endotoxemia is associated with raised sCD14 and a peak of IL-6. On a repeated basis, this may thus be a triggering cascade for the onset of atherosclerosis. In this respect, optimizing both dietary fat amount and structure could be a possible strategy to limit such low-grade endotoxemia and inflammation by the control of postprandial lipemia.     

Evolutionary aspects of omega-3 fatty acids in the food supply

Information from archaeological findings and studies from modern day hunter-gatherers suggest that the Paleolithic diet is the diet we evolved on and for which our genetic profile was programmed. The Paleolithic diet is characterized by lower fat and lower saturated fat intake than Western diets; a balanced intake of omega-6 and omega-3 essential fatty acids; small amounts of trans fatty acids, contributing less than 2% of dietary energy; more green leafy vegetables and fruits providing higher levels of vitamin E and vitamin C and other antioxidants than today's diet and higher amounts of calcium and potassium but lower sodium intake. Studies on the traditional Greek diet (diet of Crete) indicate an omega-6/omega-3 ratio of about 1/1. The importance of a balanced ratio of omega-6:omega-3, a lower saturated fatty acid and lower total fat intake (30-33%), along with higher intakes of fruits and vegetables leading to increases in vitamin E and C, was tested in the Lyon Heart study. The Lyon study, based on a modified diet of Crete, confirmed the importance of omega-3 fatty acids from marine and terrestrial sources, and vitamin E and vitamin C, in the secondary prevention of coronary heart disease, and cancer mortality.     

Fatty acid composition of the depot fats of the Polynesian rat,Rattus exulans,Tokelau Islands

The fatty acid composition of the stomach contents, adipose tissue, and perinephric fat of Polynesian rats (Rattus exulans Peale), from the Tokelau Is indicated that the dietary fat consisted mainly, if not exclusively, of coconut oil. Lower ratios of lauric : myristic acids were found in the depot fats of the Polynesian rats than in the dietary coconut oil. These results were consistent with chain elongation of lauric to myristic acid after ingestion, as previously reported in rats and other mammals.     

Effects of interactions between various fats and active/passive phases on postprandial inflammation in rats

The circadian clock controls number of behavioral and physiological processes during daily light/dark cycle including inflammation and vascular injury. However, how reciprocal interaction of dietary fats and light/dark cycle affects postprandial inflammation is currently unknown. To this end, effects of various dietary fats given to rats by gavaging either in light or dark phase on postprandial inflammation were compared. Sunflower oil load activated greater number of inflammatory CD markers in passive phase whereas the butter load in active phase compared to their counter phase. The inflammatory influence of fish oil load appeared to be mostly confined to passive phase. Differences found between the levels of some of the inflammatory markers in active and passive phases of normal fed rats were altered by fat/oil administrations. We conclude that influences of dietary fats/oils on postprandial inflammatory changes might depend not only on their fatty acid compositions but also on their ingestion times.     

Influence of time, type of diet and ursodeoxycholic acid on biliary secretion in rats with intestinal resection

The effects of time and the type of dietary fat on biliary physiology in rats with 50% resection of the distal small intestine was investigated. The effects of ursodeoxycholic acid as an exogenous source in bile acid added to the diet were also studied. The fat composition of all diets was the same in quantitative terms (4%), and differed only in the type of lipid supplied: olive oil (diet A) or 1/3 medium chain triglycerides, 1/3 sunflower seed oil and 1/3 olive oil (diet B). Three months after intestinal resection, neither group of resected rats showed significant changes in bile flow or bile acid output in comparison to controls, whereas the slope of the regression line was notably increased, indicating that enterohepatic circulation failed to adapt to the different dietary fats during recovery from intestinal resection. The addition of ursodeoxycholic acid to diet B significantly raised bile acid flow and output in comparison to controls, as a result of the recovery of enterohepatic circulation. This was reflected in the lower slope of the regression line, thus suggesting that de novo synthesis in resected animals was less intensely stimulated.     

The influence of estrogen on hepatic cholesterol metabolism and biliary lipid secretion in rats fed fish oil

Both estrogen and dietary n-3 polyunsaturated fatty acids are known to be hypocholesterolemic, but appear to exert their effects by different mechanisms. In this study, the interaction between dietary fish oil (rich in n-3 polyunsaturated fatty acids) and estrogen in the regulation of hepatic cholesterol metabolism and biliary lipid secretion in rats was studied. Rats fed a low fat or a fish oil-supplemented diet for 21 days were injected with 17alpha-ethinyl estradiol (5 mg/kg body weight) or the vehicle only (control rats) once per day for 3 consecutive days. Estrogen-treatment led to a marked reduction in plasma cholesterol levels in fish oil-fed rats, which was greater than that observed with either estrogen or dietary fish oil alone. The expression of mRNA for cholesterol 7alpha-hydroxylase was decreased by estrogen in rats fed a low fat or a fish oil-supplemented diet, while the output of cholesterol (micromol/h/kg b.wt.) in the bile was unchanged in both groups. Cholesterol levels in the liver were increased by estrogen in rats given either diet, but there was a significant shift from cholesterol esterification to cholesteryl ester hydrolysis only in the fish oil-fed animals. Estrogen increased the concentration of cholesterol (micromol/ml) in the bile in rats fed the fish oil, but not the low fat diet. However, the cholesterol saturation index was unaffected. The output and concentration of total bile acid was also unaffected, but changes in the distribution of the individual bile acids were observed with estrogen treatment in both low fat and fish oil-fed groups. These results show that interaction between estrogen-treatment and dietary n-3 polyunsaturated fatty acids causes changes in hepatic cholesterol metabolism and biliary lipid secretion in rats, but does not increase the excretion of cholesterol from the body.     

Angelica keiskei Extract Improves Insulin Resistance and Hypertriglyceridemia in Rats Fed a High-Fructose Drink

Angelica keiskei is a traditional herb peculiar to Japan and abundantly contains vitamins, dietary fiber and such polyphenols as chalcone. We investigated in the present study the effect of A. keiskei on insulin resistance and hypertriglyceridemia in fructose-drinking rats as a model for the metabolic syndrome. Male Wistar rats were given a 15% fructose solution as drinking water for 11 weeks. Fructose significantly increased the levels of serum insulin and triglyceride (TG) compared with the control level. Treatment with an ethanol extract of A. keiskei (AE) significantly reduced the levels of blood glucose (?16.5%), serum insulin (?47.3%), HOMA-R (?56.4%) and TG (?24.2%). A hepatic gene analysis showed that fructose reduced the expression of the genes related to fatty acid β-oxidation and high-density lipoprotein (HDL) production. Treatment with AE enhanced the expression of the acyl-CoA oxidase 1 (ACO1), medium-chain acyl-CoA dehydrogenase (MCAD), ATP-binding membrane cassette transporter A1 (ABCA1) and apolipoprotein A1 (Apo-A1) genes. These results suggest that AE improved the insulin resistance and hypertriglyceridemia of the fructose-drinking rats.     

Circadian PER1 controls daily fat absorption with the regulation of PER1-PKA on phosphorylation of bile acid synthetase

Several epidemiological studies suggest a correlation between eating time and obesity. Night eating syndrome characterized by a time-delayed eating pattern is positively associated with obesity in humans as well as in experimental animals. Here, we show that oil intake at night significantly makes more fat than that at day in wild-type mice, and circadian Period 1 (Per1) contributes to this day–night difference. Per1-knockout mice are protected from high-fat diet–induced obesity, which is accompanied by a reduction in the size of the bile acid pool, and the oral administration of bile acids restores fat absorption and accumulation. We identify that PER1 directly binds to the major hepatic enzymes involved in bile acid synthesis such as cholesterol 7alpha-hydroxylase and sterol 12alpha-hydroxylase. A biosynthesis rhythm of bile acids is accompanied by the activity and instability of bile acid synthases with PER1/PKA-mediated phosphorylation pathways. Both fasting and high fat stress enhance Per1 expression, increasing the fat absorption and accumulation. Our findings reveal that Per1 is an energy regulator and controls daily fat absorption and accumulation. Circadian Per1 controls daily fat absorption and accumulation, suggesting Per1 is a potential candidate of a key regulator in stress response and the relevant obesity risk.     

Characterization of a model of dietary-induced hypertriglyceridemia in young, nonobese rats.

Healthy, nonobese, young rats developed hypertriglyceridemia (mean triglyceride levels of 250 mg/dl) following consumption of a sucrose-lard diet. The hypertriglyceridemia was apparent three days after start of the diet and persisted throughout the 4-week experimental period. Body weight, liver weight, and serum glucose levels were similar in animals eating either the sucrose-lard diet or standard rat chow. On the other hand, serum free fatty acid levels were slightly increased and serum insulin levels were substantially increased in animals eating the sucrose-lard diet. Determination of very low density lipoprotein turnover revealed that total triglyceride secretion in rats eating the sucrose-lard diet was significantly (P < 0.01) increased over that of rats eating standard chow. Direct measurement of hepatic and intestinal very low density lipoprotein secretion indicated that the observed rise in total triglyceride secretion was secondary to increased secretion of very low density lipoproteins by the liver. Finally, lipoprotein lipase activity of adipose tissue from rats eating the sucrose-lard diet was equal to, or greater than (depending upon sampling time), the activity of the enzyme from adipose tissue of rats eating the control diet. These data indicate that young, nonobese, rats develop hypertriglyceridemia when they ingest a sucrose-lard diet, and that the rise in plasma triglyceride levels results from an increase in hepatic very low density lipoprotein secretion. The dietary-induced hypertriglyceridemia is associated with elevated serum insulin levels, and, as such, may provide a useful animal model to use in studies aimed at defining the pathogenesis of endogenous hypertriglyceridemia in man.-Reaven, G. M., T. R. Risser, Y-D. I. Chen, and E. P. Reaven. Characterization of a model of dietary-induced hypertriglyceridemia in young, nonobese rats.     

Effects of Triterpenes on the Mutagenicities of Various Mutagens toward Salmonella

The effects of different dietary levels of gamma-linolenic acid (GLA) on lipid metabolism was studied in rats using a combination of evening primrose oil (EPO) and palm oil (PLO). EPO compared to PLO significantly reduced liver cholesterol and triglyceride after 4 weeks of feeding, and the effect remained even when EPO was mixed with PLO at the same weight basis. The serum triglyceride level also tended to be low on feeding EPO. Neither liver Δ6-desaturase and phospholipase A₂ activities nor aortic production of prostacyclin and thromboxane A₂ production by platelets were influenced significantly by the fat type, suggesting a peculiar effect of PLO. The percentage of arachidonic acid in liver, serum, and aortic phosphatidylcholine depended on the dietary level of GLA. A more distinct increase in arachidonic acid was observed in tissue triglycerides of rats fed EPO. GLA appears to exert favorable effects on lipid metabolism even when the P/S ratio was lowered from 13.7 of EPO to 1.8 of the 1:1 mixture of EPO and PLO.     

Activities of liver microsomal fatty acid desaturases in zinc-deficient rats force-fed diets with a coconut oil/safflower oil mixture of linseed oil

The present study was conducted to investigate the effect of zinc deficiency on fatty acid desaturation in rats fed two different types of dietary fat, a mixture of coconut oil and safflower oil (7∶1, w/w, “coconut oil diet”) or linseed oil (“linseed oil diet”). In order to ensure an adequate food intake, all rats were force-fed by gastric tube. Zinc deficiency caused statistical significant reducion of Δ9-desaturase activity in liver microsomes of rats fed coconut oil diet and tendencial reduction (p<0.15) in rats fed linseed oil diet compared with control rats fed diets with the same type of fat. In agreement with this effect, zinc deficiency in the rats fed both types of dietary fat increased the ratio between total saturated and total monounsaturated fatty in liver phospholipids and liver microsomes. Zinc deficient rats on the coconut oil diet had unchanged Δ6-desaturase activity with linoleic acid as substrate and lowered activity with α-linolenic acid as substrate. In contrast, zinc deficient rats on the linseed oil diet had increased Δ6-desaturase activity with linoleic acid as substrate and unchanged activity with α-linolenic acid. Because linoleic acid is the main substrate for Δ6-desaturase in the rats fed coconut oil diet, and α-linolenic acid is the main substrate in the rats fed linseed oil diet, it is concluded that in vivo Δ6-desaturation was not changed by zinc deficiency in the rats fed both types of dietary fat. Activity of Δ5-desaturase was also not changed by zinc deficiency in the rats fed both dietary fats. Levels of fatty acids in liver phospholipids and microsomes derived by Δ4-, Δ5-, and Δ6-desaturation were not consistently changed by zinc deficiency in the rats fed both types of dietary fat. Thus, the enzyme studies and also fatty acid composition data of liver phospholipids and microsomes indicate that zinc deficiency does not considerably disturb desaturation of linoleic and α-linolenic acid. Therefore, it is suggested that similarities between deficiencies of zinc and essential fatty acids described in literature are not due to disturbed desaturation of linoleic acid in zinc deficiency. The present study also indicates that zinc deficiency enhances incorporation of eicosapentaenoic acid into phosphatidylcholine of rats fed diets with large amounts ofn-3 polyunsaturated fatty acids.     

Suppression of postprandial hypertriglyceridemia in rats and mice by oolong tea polymerized polyphenols

Oolong tea-polymerized polyphenols (OTPP) are characterized polyphenols produced from semi-fermented tea (oolong tea). In the present study, we evaluated the suppressive effects of oolong tea extract and OTPP on postprandial hypertriglyceridemia in rats and mice. Lymphatic recovery of triglycerides in rats cannulated in the thoracic duct was delayed by the administration of oolong tea extract at 100 and 200 mg per head, and more effectively than with green tea extract. OTPP delayed lymphatic triglyceride absorption at 20 mg/head, though (-)-epigallocatechin gallate (EGCG) did not do so at the same dose. OTPP also suppressed postprandial hypertriglyceridemia after administration of olive oil in mice. The area under the curve (AUC) of plasma triglycerides was significantly decreased, by 53% and 76%, in the 500 and 1,000 mg/kg OTPP groups respectively, as compared with the control group. These results suggest that OTPP is responsible for the suppression of hypertriglyceridemia by ingestion of oolong tea.     

Reduction of postprandial triglyceridemia in humans by dietary n-3 fatty acids

Long chain n-3 fatty acids present in fish oils have been shown to reduce fasting plasma triglyceride and very low density lipoprotein levels in normal and hyperlipidemic human subjects. The present studies were designed to examine whether dietary n-3 fatty acids influence chylomicron formation and metabolism in healthy volunteers. In the first study seven subjects were fed either saturated fat, vegetable oil, or fish oil-based diets for 4 weeks each, and test meals containing 50 g of the background fat were administered after the second week of each diet. The postprandial rise in triglyceride levels was significantly lower following the fish oil test meal as compared to the saturated fat or vegetable oil test meals. In the second study, six subjects eating their usual home diets were given two fat tolerance tests. The first contained saturated fat and the second, given 1 week later, contained fish oil. There was no difference in the postprandial triglyceride response between the fish oil and the saturated fat meals. A third study was then conducted with eight volunteers in which saturated fat and fish oil test meals were administered during saturated fat and fish oil background diets in a crossover design. The presence of fish oil in the background diet reduced postprandial lipemia regardless of the type of fat in the test meal. Although there was no effect of the fish oil diet on the lipoprotein lipase and hepatic lipase activity of postheparin plasma measured in vitro, stimulation of in vivo lipolysis was not ruled out. Our results suggest that chronic (but not acute) intake of fish oil may inhibit the synthesis or secretion of chylomicrons from the gut. However, accelerated clearance due to decreased VLDL competition cannot be excluded.     

Endotoxin increase after fat overload is related to postprandial hypertriglyceridemia in morbidly obese patients

The low-grade inflammation observed in obesity has been associated with a high-fat diet, though this relation is not fully understood. Bacterial endotoxin, produced by gut microbiota, may be the linking factor. However, this has not been confirmed in obese patients. To study the relationship between a high-fat diet and bacterial endotoxin, we analyzed postprandial endotoxemia in morbidly obese patients after a fat overload. The endotoxin levels were determined in serum and the chylomicron fraction at baseline and 3 h after a fat overload in 40 morbidly obese patients and their levels related with the degree of insulin resistance and postprandial hypertriglyceridemia. The morbidly obese patients with the highest postprandial hypertriglyceridemia showed a significant increase in lipopolysaccharide (LPS) levels in serum and the chylomicron fraction after the fat overload. Postprandial chylomicron LPS levels correlated positively with the difference between postprandial triglycerides and baseline triglycerides. There were no significant correlations between C-reactive protein (CRP) and LPS levels. The main variables contributing to serum LPS levels after fat overload were baseline and postprandial triglyceride levels but not glucose or insulin resistance. Additionally, superoxide dismutase activity decreased significantly after the fat overload. Postprandial LPS increase after a fat overload is related to postprandial hypertriglyceridemia but not to degree of insulin resistance in morbidly obese patients.     

Stimulation of acyl-CoA oxidase by alpha-linolenic acid-rich perilla oil lowers plasma triacylglycerol level in rats

The effect of dietary polyunsaturated fatty acids (PUFA) on hepatic peroxisomal oxidation was investigated with respect to the postprandial triacylglycerol levels. Male Sprague--Dawley rats were fed semipurified diets containing either 1% (w/w) corn oil, or 10% each of beef tallow, corn oil, perilla oil, and fish oil for 4 weeks and 4 days. Hepatic and plasma triacylglycerol levels were reduced in rats fed fish and perilla oil diets compared with corn oil and beef tallow diets. The peroxisomal beta-oxidation, catalase activity, and acyl-CoA oxidase (AOX) activity were markedly increased by fish oil feeding. To a lesser extent, perilla oil elevated AOX activity in a 4-day feeding although the effect gradually decreased in a 4-week feeding. Similarly, the mRNA levels were increased in rats fed fish and perilla oils. AOX activity was negatively correlated with postprandial triacylglycerol levels. In addition, the stimulation of AOX was highly associated with the content of long chain n-3 PUFA such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in hepatic microsome. These effects were evident within 4 days of initiating feeding. Therefore, alpha-linolenic perilla oil exerts a similar effect to fish oil in stimulating hepatic activity and gene expression of AOX by enriching long chain n-3 PUFA in hepatic membrane fraction, which can partly account for the reduction of postprandial triglyceridemia.     

Effects of a High-Fat Diet and Strain on Hypothalamic Gene Expression in Rats

Objective: This study was designed to investigate whether dietary fat and genetic background might differentially alter the expression of hypothalamic genes involved in food intake. Research Methods and Procedures: Three-month-old Osborne-Mendel (OM) and S5B/Pl rats were fed either a high-fat or a low-fat diet for 14 days. mRNA for neuropeptide Y (NPY), corticotrophin-releasing hormone, NPY Y-1 receptor and Y-5 receptor, and serotonin 2c (5-HT2c) receptors were measured using Northern blotting or ribonuclease protection assays. Results: OM rats showed an increased expression of NPY and corticotrophin-releasing hormone compared with S5B/Pl rats. The expression of NPY-Y1 and -Y5 receptor mRNA was significantly higher in the hypothalamus of OM rats compared with S5B/Pl rats. The expression of 5HT-2c receptor mRNA was significantly reduced in both strains of rats eating a high-fat diet when compared with the animals eating the low-fat diet. Discussion: These data suggest that over activity of the NPY system may contribute to the development of obesity in OM rats and that expression of the 5HT-2c receptor gene may be modulated by dietary fat.     

Fat Intake Affects Adiposity,Comorbidity Factors,and Energy Metabolism of Sprague‐Dawley Rats

Objective: Childhood obesity is an emerging health problem. This study assesses the effects of three levels of dietary fat (10%, 32%, and 45% measured by kilocalories) on weight gain, body composition, energy metabolism, and comorbidity factors in rats from weaning through maturation. Research Methods and Procedures: The role of dietary fat on the susceptibility to obesity was assessed by feeding diets containing three levels of dietary fat to rats from weaning through 7 months of age. Body composition was analyzed by DXA after 6 and 12 weeks of dietary treatment. Energy metabolism was measured by indirect calorimetry. Results: Energy intake, weight gain, fat mass, and plasma glucose, cholesterol, triglyceride, free fatty acid, leptin, and insulin levels increased dose‐dependently with increased dietary fat. No difference in absolute lean mass among the three groups was observed. Therefore, the differences in weight gain are accounted for primarily by increased fat accretion. Compared with rats that were relatively resistant to obesity when on a 45% fat diet, diet‐induced obesity‐prone rats were in positive energy balance and had an elevated respiratory quotient, indicating a switch in energy substrate use from fat to carbohydrate, which promotes body‐fat accretion. Discussion: Our data support the hypothesis that administration of increasing amount of dietary fat to very young rats enhances susceptibility to diet‐induced obesity and its comorbidities.     

Coordinate induction of peroxisomal acyl-CoA oxidase and UCP-3 by dietary fish oil: a mechanism for decreased body fat deposition

Rats fed dietary fats rich in 20- and 22-carbon polyenoic fatty acids deposit less fat and expend more energy at rest than rats fed other types of fats. We hypothesized that this decrease in energetic efficiency was the product of: (a) enhanced peroxisomal fatty acid oxidation and/or (b) the up-regulation of genes encoding proteins that were involved with enhanced heat production, i.e. mitochondrial uncoupling proteins (UCP-2, UCP-3) and peroxisomal fatty acid oxidation proteins. Two groups of male Fisher 344 rats 3-4 week old (n=5 per group) were pair fed for 6 weeks a diet containing 40% of its energy fat derived from either fish oil or corn oil. Epididymal fat pads from rats fed the fish oil diet weighed 25% (P < 0.05) less than those found in rats fed corn oil. The decrease in fat deposition associated with fish oil ingestion was accompanied by a significant increase in the abundance of skeletal muscle UCP-3 mRNA. The level of UCP-2 mRNA skeletal muscle was unaffected by the type of dietary oil, but the abundance of UCP-2 mRNA in the liver and heart were significantly lower (P < 0.05) in rats fed fish oil than in rats fed corn oil. In addition to inducing UCP-3 expression, dietary fish oil induced peroxisomal acyl-CoA oxidase gene expression 2-3 fold in liver, skeletal muscle and heart. These data support the hypothesis that dietary fish oil reduces fat deposition by increasing the expression of mitochondrial uncoupling proteins and increasing fatty acid oxidation by the less efficient peroxisomal pathway.