Effects of the level of polyunsaturated fatty acids of the diet on the functioning and depletion of energy substrates in the rat heart during perfusion by left atrial route

The effects of semi-liquid diets containing 6.6% in weight of refined sunflower seed oil (SSO) or hydrogenated coconut oil (HCO) on cardiac endogenous substrates and functional parameters of rats hearts were compared to a standard laboratory chow during seven days. No difference appeared for cardiac glycogen and lipid constituents. Cardiac performance, measured through left atrial perfusion was enhanced by SSO diet and HCO one altered it. A significative phospholipid depletion appeared during the 45 minutes perfusion only in the HCO group.     

Effects of diet on catabolism and excretion of (26-14C)cholesterol in rats.

The catabolism and excretion of [26-14C]cholesterol was studied in rats on semisynthetic and commercial diets low in fat or containing 15% butter or corn oil. Rats on the low fat commercial diet oxidized the labeled cholesterol to 14CO2 at more than twice the rate of those on the semisynthetic diet. Fecal excretion of labeled lipid was also somewhat higher with the commercial diet. The added fats had little effect on rate of oxidation of cholesterol but dietary corn oil stimulated fecal excretion of labeled lipid. The rate of loss of labeled cholesterol through oxidation and excretion showed a positive correlation with cholesterol biosynthesis, as measured previously by acetate incorporation into cholesterol in rats on the same kinds of diet. A simple method for efficient trapping and counting of 14CO2 was developed, which facilitated measurement of low levels of 14CO2 in expired air. Estimation of bile acid production from the rate of oxidation of [26-14C]cholesterol to expired 14CO2 and the specific activity of plasma cholesterol gave somewhat higher values than those obtained by other methods. Possible reasons for this difference are discussed.     

Corn fiber oil lowers plasma cholesterol levels and increases cholesterol excretion greater than corn oil and similar to diets containing soy sterols and soy stanols in hamsters

The aims of this study were to compare the cholesterol-lowering properties of corn fiber oil (CFO) to corn oil (CO), whether the addition of soy stanols or soy sterols to CO at similar levels in CFO would increase CO's cholesterol-lowering properties, and the mechanism(s) of action of these dietary ingredients. Fifty male Golden Syrian hamsters were divided into 5 groups of 10 hamsters each, based on similar plasma total cholesterol (TC) levels. The first group of hamsters was fed a chow-based hypercholesterolemic diet containing either 5% coconut oil + 0.24% cholesterol (coconut oil), 5% CO, 5% CFO, 5% CO + 0.6% soy sterols (sterol), or 5% CO + 0.6% soy stanols (stanol) in place of the coconut oil for 4 weeks. The stanol diet significantly inhibited the elevation of plasma TC compared to all other dietary treatments. Also, the CFO and sterol diets significantly inhibited the elevation of plasma TC compared to the CO and coconut oil diets. The CFO, sterol, and stanol diets significantly inhibited the elevation of plasma non-high density lipoprotein cholesterol compared to the CO and coconut oil diets. The stanol diet significantly inhibited the elevation of plasma high density lipoprotein cholesterol (HDL-C) compared to all other dietary treatments. The sterol diet significantly inhibited the elevation of plasma HDL-C compared to the CO and coconut oil diets, whereas the CFO diet significantly inhibited the elevation of plasma HDL-C compared to the coconut oil diet only. No differences were observed between the CFO and CO for plasma HDL-C. There were no differences observed between groups for plasma triglycerides. The CO and CFO diets had significantly less hepatic TC compared to the coconut oil, sterol, and stanol diets. The CO and CFO diets had significantly less hepatic free cholesterol compared to the sterol and stanol diets but not compared to the coconut oil diet; whereas the coconut oil and sterol diets had significantly less hepatic free cholesterol compared to the stanol diet. The CFO, sterol, and stanol diets excreted significantly more fecal cholesterol compared to the coconut oil and CO diets. In summary, CFO reduces plasma and hepatic cholesterol concentrations and increases fecal cholesterol excretion greater than CO through some other mechanism(s) in addition to increase dietary sterols and stanols-possibly oryzanols.     

Attenuation of mammary duct development by menhaden oil in BALB/c mice

The predominant polyunsaturated fatty acids of the n-6 family found in corn oil (CO) are crucial for normal mammary duct formation when fed to animals. However, as shown here, not all polyunsaturated fatty acids are equally effective in stimulating mammary gland development. The n-3 fatty acids in a 10% menhaden oil (MO) diet fed to mice effectively reduced both the diameter and the length of the growing mammary ducts. Previously, we demonstrated a similar reduction in duct growth by feeding a 10% fat diet high in those saturated fats found in hydrogenated cotton seed oil. The inhibited rate of duct maturation caused by hydrogenated cotton seed oil was reversed when the mice were allowed to mature on a diet containing n-6 fatty acids prior to feeding the saturated fat diet. The addition of 1% CO to a 9% hydrogenated cotton seed oil diet fed to immature mice was also sufficient to restore duct growth. Mice fed menhaden oil diets, on the other hand, continued to show impaired ductal growth well into adulthood. Examination of the ovaries from MO-fed mice as compared with CO-fed mice revealed significantly fewer corpora lutea. When exogenous progesterone was given to MO-fed mice, ductal growth was partially restored, but not to the extent seen in mice fed corn oil diets. Investigation of the fatty acid contents of livers of these mice revealed reduced amounts of arachidonate (20:4) in MO-fed mice when compared with CO-fed animals. The addition of 1% CO to the 9% MO diets did not alter the arachidonate content, indicating a block in the conversion of linoleate (18:2) to 20:4 by the n-3 fatty acids. Hence, dietary n-6 fatty acids are essential for normal mammary ductal development when fed prior to maturation. Although saturated rats are ineffective, n-3 fatty acids can partially substitute for the required n-6 fatty acids in both ductal and ovarian development.     

Differential effect of sunflower seed oil on hepatic and renal D-amino acid oxidase in the rat.

1. The specific activity of hepatic and renal peroxisomal D-amino acid oxidase (D-AAOX) was measured in rats fed diets containing various quantities of vegetable oil. 2. Increasing the amount of dietary sunflower seed oil (SSO) from 10 to 25% (w/w) reduced the specific activity of hepatic D-AAOX by up to 30% after 10 days. 3. In both tissues, the enzyme activity was moderately decreased during the first two-day period after administration of the 25% SSO diet was begun. Unlike hepatic D-AAOX, renal D-AAOX returned to its baseline level in the kidney after the third day. 4. In contrast to SSO, hydrogenated coconut oil (HCO) did not evoke alterations of D-AAOX activity. 5. The activity levels of another peroxisomal enzyme, L-2-hydroxy acid oxidase (L-HAOX), in the liver of rats fed the high-SSO diet vs those fed the control diet were similar. 6. The subcellular distribution of D-AAOX and L-HAOX was not altered in the liver of rats fed the 25% SSO diet during the 10-day period.     

Dietary fats affect macrophage-mediated cytotoxicity towards tumour cells

In the present study, the effects of feeding mice diets of different fatty acid compositions on the production of TNF-alpha and nitric oxide by lipopolysaccharide-stimulated peritoneal macrophages and on macrophage-mediated cytotoxicity towards L929 and P815 cells were investigated. C57Bl6 mice were fed on a low-fat (LF) diet or on high-fat diets (21% fat by weight), which included coconut oil (CO), olive oil (OO), safflower oil (SO) or fish oil (FO) as the principal fat source. The fatty acid composition of the macrophages was markedly influenced by that of the diet fed. Lipopolysaccharide (LPS)-stimulated macrophages from FO-fed mice showed significantly lower production (up to 80%) of PGE2 than those from mice fed on each of the other diets. There was a significant positive linear correlation between the proportion of arachidonic acid in macrophage lipids and the ability of macrophages, to produce PGE2. Lipopolysaccharide-stimulated TNF-alpha production by macrophages decreased with increasing unsaturated fatty acid content of the diet (i.e. FO < SO < OO < CO < LF). Macrophages from FO-fed mice showed significantly lower production of TNF-alpha than those from mice fed on each of the other diets. Nitrite production was highest for LPS-stimulated macrophages from mice fed on the LF diet. Macrophages from FO-fed mice showed significantly higher production of nitrite than those from mice fed on the OO and SO diets. Compared with feeding the LF diet, feeding the CO, OO or SO diets significantly decreased macrophage- mediated killing of P815 cells (killed by nitric oxide). Fish oil feeding did not alter killing of P815 cells by macrophages, compared with feeding the LF diet; killing of P815 cells was greater after FO feeding than after feeding the other high fat diets. Compared with feeding the LF diet, feeding the OO or SO diets significantly decreased macrophage-mediated killing of L929 cells (killed by TNF). Coconut oil or FO feeding did not alter killing of L929 cells by macrophages, compared with feeding the LF diet. It is concluded that the type of fat in the diet affects macrophage composition and alters the ability of macrophages to produce cytotoxic and immunoregulatory mediators and to kill target tumour cells.     

Effects of dietary fat on mammary development relative to age and hormones in BALB/c mice

Earlier studies reported that mammary ducts grew faster if the 10% fat in the diet was composed of oils containing polyunsaturated fatty acids (corn oil: CO) compared to hydrogenated cottonseed oil (HCTO), which is devoid of such fatty acids. These experiments were primarily carried out in immature mice and left unanswered questions regarding the effects of dietary fats on more differentiated stages of mammary development. The use of transplanted ducts permitted the study of mammary growth rates in adult mice. If the diet was started when the animals were adults, there was no difference in the growth rate of those fed HCTO diet compared to those fed CO diet. However, when the diets were fed to immature mice, the mammary gland grew slower in mice fed the HCTO diet, confirming our earlier observations. The HCTO and CO diets caused no difference in the growth rate or morphology of fine ducts and alveoli that developed during pregnancy. Furthermore, no differences were seen in female mice following 6 weeks of progesterone administration begun at 3 weeks of age. Experiments that used male mice to examine the initial stages of mammary duct growth also showed that the effect of dietary fat was not observed when estrogen (E) or E and progesterone (P) were injected. In addition, there was no effect of dietary fat in ovariectomized 3-week-old females when any dose of E was administered from 0.01 to 1 microgram/day. Examination of the ovaries from mice fed either HCTO or CO diets from 3 to 9 weeks or 3 to 13 weeks of age showed that mice fed HCTO diet did not develop corpora lutea, while those fed CO diet had normal appearing ovaries. The HCTO diet inhibits normal maturation of the follicle and corpus luteum formation. We conclude that the effect of the dietary fat on the developing mouse is on the maturation of the ovary and subsequently on mammary growth.     

Dietary Stearic Acid Leads to a Reduction of Visceral Adipose Tissue in Athymic Nude Mice

Stearic acid (C18:0) is a long chain dietary saturated fatty acid that has been shown to reduce metastatic tumor burden. Based on preliminary observations and the growing evidence that visceral fat is related to metastasis and decreased survival, we hypothesized that dietary stearic acid may reduce visceral fat. Athymic nude mice, which are used in models of human breast cancer metastasis, were fed a stearic acid, linoleic acid (safflower oil), or oleic acid (corn oil) enriched diet or a low fat diet ad libitum. Total body weight did not differ significantly between dietary groups over the course of the experiment. However visceral fat was reduced by ∼70% in the stearic acid fed group compared to other diets. In contrast total body fat was only slightly reduced in the stearic acid diet fed mice when measured by dual-energy x-ray absorptiometry and quantitative magnetic resonance. Lean body mass was increased in the stearic acid fed group compared to all other groups by dual-energy x-ray absorptiometry. Dietary stearic acid significantly reduced serum glucose compared to all other diets and increased monocyte chemotactic protein-1 (MCP-1) compared to the low fat control. The low fat control diet had increased serum leptin compared to all other diets. To investigate possible mechanisms whereby stearic acid reduced visceral fat we used 3T3L1 fibroblasts/preadipocytes. Stearic acid had no direct effects on the process of differentiation or on the viability of mature adipocytes. However, unlike oleic acid and linoleic acid, stearic acid caused increased apoptosis (programmed cell death) and cytotoxicity in preadipocytes. The apoptosis was, at least in part, due to increased caspase-3 activity and was associated with decreased cellular inhibitor of apoptosis protein-2 (cIAP2) and increased Bax gene expression. In conclusion, dietary stearic acid leads to dramatically reduced visceral fat likely by causing the apoptosis of preadipocytes.     

Effect of lard and corn oil intake on serum lipids in young men

An experimental diet with lard (30 g/day for 7 days) and corn oil (30 g/day for 7 days) on high carbohydrate (basal diet) was given to four healthy Japanese young men and the effect of diets containing different fat on serum lipids was examined. Serum total cholesterol was increased significantly from a basal diet of 106 +/- 23 to 141 +/- 26 mg/dl on lard diet, and then decreased significantly (p less than 0.05) to 111 +/- 22 mg/dl on corn oil diet. Serum triglycerides increased significantly (p less than 0.01) from 66 +/- 38 to 173 +/- 32 mg/dl on basal diet. Serum HDL-cholesterol was decreased significantly (p less than 0.01) from 41.9 +/- 1.6 to 31.2 +/- 3.8 mg/dl on lard diet and increased significantly (p less than 0.05) to 41.9 +/- 4.6 mg/dl on corn oil diet. Serum HDL-cholesterol fraction was decreased significantly (p less than 0.01) from 41.6 +/- 4.9 to 28.1 +/- 3.2% on basal diets, but increased significantly (p less than 0.05) to 44.3 +/- 3.1% on lard diet, and then decreased to 36.3 +/- 2.5% on corn oil diet. Serum HDL phospholipid fraction decreased significantly (p less than 0.05) from 62.5 +/- 6.7 to 50.7 +/- 1.8% on basal diet and increased significantly (p less than 0.05) to 60.4 +/- 1.0% on lard and corn oil diet. Serum phospholipids did not change by experimental diets. It is concluded that lard and corn oil have different and specific roles in lipid metabolism.     

Sucrose counteracts the anti-inflammatory effect of fish oil in adipose tissue and increases obesity development in mice

Background

Polyunsaturated n-3 fatty acids (n-3 PUFAs) are reported to protect against high fat diet-induced obesity and inflammation in adipose tissue. Here we aimed to investigate if the amount of sucrose in the background diet influences the ability of n-3 PUFAs to protect against diet-induced obesity, adipose tissue inflammation and glucose intolerance.

Methodology/Principal Findings

We fed C57BL/6J mice a protein- (casein) or sucrose-based high fat diet supplemented with fish oil or corn oil for 9 weeks. Irrespective of the fatty acid source, mice fed diets rich in sucrose became obese whereas mice fed high protein diets remained lean. Inclusion of sucrose in the diet also counteracted the well-known anti-inflammatory effect of fish oil in adipose tissue, but did not impair the ability of fish oil to prevent accumulation of fat in the liver. Calculation of HOMA-IR indicated that mice fed high levels of proteins remained insulin sensitive, whereas insulin sensitivity was reduced in the obese mice fed sucrose irrespectively of the fat source. We show that a high fat diet decreased glucose tolerance in the mice independently of both obesity and dietary levels of n-3 PUFAs and sucrose. Of note, increasing the protein∶sucrose ratio in high fat diets decreased energy efficiency irrespective of fat source. This was accompanied by increased expression of Ppargc1a (peroxisome proliferator-activated receptor, gamma, coactivator 1 alpha) and increased gluconeogenesis in the fed state.

Conclusions/Significance

The background diet influence the ability of n-3 PUFAs to protect against development of obesity, glucose intolerance and adipose tissue inflammation. High levels of dietary sucrose counteract the anti-inflammatory effect of fish oil in adipose tissue and increases obesity development in mice.     

Effect of fish oil diet on immune response and proteinuria in mice

In this study, we examined the immune response and proteinuria caused by dietary polyunsaturated fatty acids in normal NZW/N and autoimmune NZB/NZW mice. Mice were maintained more than one year on five dietary groups: normal (5% corn oil), calorie-restricted, high fat (20% corn oil), high fat (20% fish oil), and Purina laboratory rodent chow. Normal mice fed with the fish oil diet had a more reduced anti-sheep red blood cells (SRBC) plaque-forming cell (PFC) response and less interleukin-2 (IL-2) enhancement of PFC than did the group with the restricted diet and the young control group. The corn oil (5 and 20%) diet animals also showed reduced PFC response and IL-2 utilization. NZB/NZW mice fed with the fish oil diet showed similar reduced PFC response but had a significantly lower response to IL-2 than did those on the corn oil diets and the restricted diet. The IL-2 production by macrophages from NZW/N mice was reduced in both the fish oil and corn oil diet groups. However, mice fed with the fish oil diet had less proteinuria and good survival rates, similar to the group with the restricted diet. These results suggest that the beneficial effect of the fish oil diet in these animals may be attributed in part to the immunosuppression mechanism.     

Dietary extra-virgin olive oil rich in phenolic antioxidants and the aging process: long-term effects in the rat

The aim of the present work was to verify whether extra-virgin olive oil, a food naturally containing phenolic antioxidants, has the potential to protect from the pro-aging effects of a high-calorie diet. Male rats were fed from age 12 months to senescence a high-calorie diet containing either corn oil (CO), or extra-virgin olive oil with high (H-EVOO) or low (L-EVOO) amounts of phenols. The prolonged high fat intake led to obesity, liver lipid degeneration and insulin resistance, which were not counteracted by high phenol intake. No difference in overall survival was found at the end of the experiment in the animals treated with H-EVOO compared to the other groups. However, we did detect a protective effect of olive oil on some age-related pathologies and on blood pressure, of which the former was associated with the antioxidant content. Concomitantly, a decrease in DNA oxidative damage in blood cells and plasma TBARS and an increase in liver superoxide dismutase were detected following H-EVOO consumption. Thus, although olive oil phenols cannot reverse the detrimental effects of a prolonged intake of high amounts of fat, improving the quality of olive oil in terms of antioxidant content can be beneficial.     

Modulation of phorbol ester-elicited events in mouse epidermis by dietary n-3 and n-6 fatty acids

Because arachidonic acid-derived eicosanoids are potent modulators of hyperproliferation and inflammation during skin tumor promotion with the phorbol ester, 12-0-tetradecanoylphorbol-13-acetate (TPA) (17, 18), it was hypothesized that dietary modification of epidermal fatty acids might modulate TPA-induced biochemical events in mouse skin. Semipurified diets containing 10% total fat composed of corn oil (CO) or a combination of CO and menhaden oil (MO) or coconut oil (CT) were fed to SENCAR mice for 4 weeks. Fatty acid composition of epidermal phospholipids generally reflected fatty acid composition of dietary oils fed to the mice. Since fatty acid-derived eicosanoids are thought to be essential in tumorigenesis, we compared the effects of dietary fats on prostaglandin E (PGE) production in epidermis treated with a single dose of TPA. TPA-induced PGE production in mouse epidermis from mice fed the MO diet was significantly reduced compared to PGE production in epidermal homogenates from mice fed the CO or CT diets. Type of dietary fats did not appear to modulate TPA-induced vascular permeability, however hyperplasia was slightly elevated in skins of mice fed MO. The subcellular distribution of protein kinase C, the plasma membrane receptor for TPA predominantly located in the cytosol (80%), was altered in epidermis from mice fed the MO diet compared to preparations from mice fed CO or CT diets which exhibited normal protein kinase C distribution. Our results suggest that n-3 rich dietary lipids modulate TPA-elicited events in mouse skin to a greater extent than diets containing higher proportions of saturated or n-6 fatty acids.     

Effect of the ingestion of thermically treated fat on blood lipids and blood lipoproteins in the rat

The effect on rats fed on a diet with 15% solid frying fat (diet B) is compared to the effect of a diet with 15% of the same fat but in the raw state (diet A). After 10 weeks being fed on these diets serum triglycerides, phospholipids, total cholesterol, free cholesterol, esterified cholesterol, high density lipoprotein-cholesterol and free fatty acid levels were checked. Percentage of very low density lipoproteins (VLDL), low density lipoproteins (LDL) and high density lipoproteins as well as the composition of these lipoproteins was determined in parallel. Rats fed on diet B showed a significant increase in phospholipids and a significant decrease in VLDL when compared to those fed on diet A. Phospholipids on LDL decreased significantly in diet B fed rats. The data obtained seem to indicate that the hypercholesterolemic tendency induced by frying fat is neutralized by a decrease in VLDL levels.     

Lipid composition of liver microsomes in rats fed a high monounsaturated fatty acid diet

The fatty acid and cholesterol contents of tissue membranes are the determinants of membrane stability and functionality. This study was designed to evaluate the influence of a high monounsaturated fatty acid diet on the fatty acid composition of rat liver microsomes and on their cholesterol and lipid phosphorus content. Weanling animals were fed for 5 weeks with high fat diets containing olive oil or corn oil. Saturated fatty acids were increased and oleic acid decreased in microsomal total phospholipids and in the three major phosphoglycerides, phosphatidylcholine (PC), phosphatidylethanolamine (PE) and phosphatidylinositol (PI), of rats fed corn oil as compared to the olive oil group. The percentage of linoleic acid was higher in the corn oil group, but only for total phospholipids and PC. Linoleic and alpha-linolenic metabolites were significantly increased in total phospholipids of olive oil-fed animals with respect to those fed corn oil. These changes were responsible for the low unsaturation index found in microsomal phospholipids of the corn oil group. The diet did not affect the microsome cholesterol or the lipid phosphorus content. These results show that, in olive oil-fed rats, the cholesterol content and the degree of unsaturation of liver microsomes was similar to that observed in weanling animals; this probably suggests an adequate maintenance of functionality of membranes in olive oil-fed animals.     

Influence of amount and type of dietary fat on plasma cholesterol concentrations in goats

Adult, non-pregnant, dry goats were fed diets differing in the amount and type of fat. To modulate the type of dietary fat, rations containing either palm oil or olive oil were used, the amount of fat being 86 g/kg dry matter (DM). To modulate the amount of dietary fat, the oils were replaced by an isoenergetic amount of native corn starch so that the dietary fat concentration dropped to 26 g/kg DM. The high fat diets, when compared with the low fat diet, significantly raised plasma total cholesterol by 91%, high-density lipoprotein (HDL) cholesterol by 100%, triglycerides by 47% and phospholipids by 57%. On an average, dietary palm oil versus olive oil significantly increased plasma total cholesterol by 6%, HDL cholesterol by 9% and phospholipids by 4%, but left plasma triglycerides unchanged. This study shows that plasma lipid concentrations in goats respond to the amount and type of fat in the diet.     

Tissue fatty acid composition of pigs fed different fat sources

Dietary fat influences the physico-chemical properties of meat, and fatty acid (FA) composition may have implications on human health. The objectives of the experiment were to study tissue FA partitioning and the effect of dietary fat source on tissue FA composition. Seventy crossbred gilts (61.8 ± 5.2 kg BW average) were fed one of seven treatments: a diet containing a very low level of fat (no fat (NF)) and six fat-supplemented diets (10%: tallow (T), high-oleic sunflower oil (HOSF), sunflower oil (SFO), linseed oil (LO), fat blend (FB: 55% tallow, 35% SFO, 10% LO) and fish oil blend (FO: 40% fish oil, 60% LO). Differential tissue FA depositions were observed, with flare fat being the most saturated, followed by intermuscular, and subcutaneous being the least saturated. Monounsaturated fatty acid (MUFA) deposition showed an opposite tissue pattern. Subcutaneous fat showed the highest MUFAs, intermuscular fat showed intermediate values and flare fat showed the lowest MUFAs. Intramuscular polyunsaturated fatty acid (PUFA) content was less susceptible to dietary treatment modifications compared with other depots. Significant tissue FA modifications were observed due to dietary treatments, mainly in diets rich in PUFA. The saturated fatty acids (SFA) were high in NF-fed and low in HOSF-fed animals, MUFA were high in HOSF-fed and low in SFO-, LO- and FO-fed animals, while PUFA were high in SFO- and LO-fed and low in HOSF-, T- and NF-fed animals. Pigs fed LO and FB showed detectable levels of EPA, which depended on the linolenic content of the diet. The only effective way to increase tissue DHA contents was to add DHA in the diet through FO feeding. Araquidonic acid was high in SFO diets and low in LO and FB diets, and also high in intramuscular fat compared with other tissues. EPA and DHA were also high in intramuscular fat compared with other fat depots. The deposition of oleic and linoleic acids depended on the composition of dietary fat, as their deposition varied between diets, even at similar levels of intake of each FA. The NF diet resulted in the greatest proportion of SFAs (palmitic and stearic) of all treatments tested. SFAs were less susceptible to modification than MUFA in response to the different PUFA levels supplemented in the diet. T resulted in less fat deposition in some of the fat depots and more in others, suggesting that T could partition fat differently among fat depots.     

Effect of fatty acid composition of dietary fat on energy balance and expenditure in hamsters

The comparative effects of feeding diets containing corn, olive, coconut, or menhaden fish oil on efficiency of energy deposition and on short term energy expenditure were examined in growing hamsters. Diets comprising oils mixed with laboratory diets at 10% oil w/w were fed ad libitum for 3 weeks. Animals fed laboratory diets were used as controls. Body composition was determined before and after the feeding period using 3H2O distribution space. Oxygen consumption was measured in each animal during the final week. Weight gains of groups fed corn and olive oil diets exceeded those of the group fed laboratory diet alone (p less than 0.05), although metabolizable energy intakes were similar across groups. Corn oil fed animals demonstrated higher carcass energy gains as fat compared with laboratory diet fed or menhaden oil fed groups. This was reflected in an increased fractional deposition of metabolizable energy intake in the group fed corn oil diet compared with the latter two groups. Fecal energy losses were lower in the group fed corn oil diet, and higher in the group fed laboratory diet alone, compared with other groups. Oxygen consumption did not differ between groups. These findings indicate that feeding dietary fish oil, compared with corn oil, favours energy substrate oxidation reducing the fraction of metabolizable energy partitioned for storage.     

Activation state alters the effect of dietary fatty acids on pro-inflammatory mediator production by murine macrophages

Studies investigating the effect of dietary fats on pro-inflammatory cytokine production by macrophages (M phis) have yielded conflicting results. We hypothesised that this may be due to the different capacities of the M phis studied commonly (resident, thioglycollate-elicited) to produce prostaglandin E(2)(PGE(2)) and leukotriene B(4)(LTB(4)) which inhibit and stimulate, respectively, tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) production. To investigate this, male C57Bl6 mice were fed for 6 weeks on a low fat (LF) diet or on high fat diets which contained coconut oil (CO), olive oil (OO), safflower oil (SO) or fish oil (FO) as the main fat source. Production of TNF-alpha, IL-1 beta, PGE(2)and LTB(4)by lipopolysaccharide-stimulated resident and thioglycollate-elicited (i.e. inflammatory) peritoneal M phis was measured. PGE(2)production by both inflammatory and resident M phis was significantly decreased by FO feeding. FO also decreased LTB(4)production by resident M phis compared with LF feeding. Production of both cytokines by inflammatory M phis decreased with increasing unsaturation of the high fat diets, such that cells from FO-fed mice showed significantly decreased production of TNF-alpha and IL-1 beta compared to those from mice fed on each of the other diets. In contrast, resident M phis from mice fed FO showed increased TNF-alpha production compared to those from CO-fed mice. Thus, FO feeding decreases production of TNF-alpha and IL-1 beta by inflammatory M phis and increases production of TNF-alpha by resident M phis, at least in comparison to some other dietary fats. These results indicate the mechanisms by which dietary fats exert their effects upon pro-inflammatory cytokine production are most likely different for resident and inflammatory M phis.