Fed Coconut Oil Research Articles

The effect of coconut oil and palm oil on anthropometric parameters: a clinical trial

BackgroundDuring recent years several studies have investigated the impact of different dietary oils on body weight. They have shown differential positive and negative effects on anthropometry. We investigated the effects of palm and coconut oils on body weight and other anthropometric parameters, considering their importance as a primary source of saturated fat, controlling for other confounding variable such as total energy intake.MethodsThe study was conducted as a sequential feeding clinical trial with 40 healthy men and women divided into two feeding periods of initial palm oil (8 weeks) and subsequent coconut oil (8 weeks), with a 16-week washout period in between. Each participant received a pre-determined volume of each oil, which were integrated into their routine main meals and snacks during the respective study periods. Changes in body weight, body mass index (BMI), waist circumference (WC), hip circumference (HC), and waist-to-hip ratio (WHR) were evaluated. Physical activity levels and dietary intake were also evaluated as potential confounding factors.ResultsThirty-seven participants completed both oil treatment periods. The mean (± SD) age of the participants was 39 (± 13.1) years. There were no significant differences in any of the anthropometric parameters between the initial point of feeding coconut oil and the initial point of feeding palm oil. Following both oil treatment phases, no significant changes in the subjects’ body weight, BMI, or other anthropometric measurements (WC, HC, and WHR) were observed.ConclusionNeither coconut oil nor palm oil significantly changed anthropometry-related cardiovascular risk factors such as body weight, BMI, WC, HC, and WHR.Trial registrationSri Lankan Clinical Trial Registry: SLCTR/2019/034 on 4th October 2019 (https://slctr.lk/trials/slctr-2019-034).

Muscle Respiration in Rats Is Influenced by the Type and Level of Dietary Fat

Experiments were conducted to elucidate the role of muscle in the enhanced thermogenic response found in rats fed diets enriched with polyunsaturated fatty acids. Isolated soleus muscle respiration and plasma cholesterol and triglyceride concentrations were determined in rats (∼128 g wt, 5 wk age) fed diets (minimum 3 wk) containing coconut oil, beef tallow or safflower oil at 20, 40 or 60% of the total dietary energy in a 3 × 3 factorial design (5–6 rats per treatment). Diet type did not affect plasma cholesterol concentrations but plasma triglycerides were lower (P < 0.01) in rats fed safflower oil-based diets. Greater levels of fat in the diet resulted in higher (P < 0.01) plasma cholesterol concentrations and lower (P < 0.01) plasma triglyceride concentrations. Rats fed coconut oil had lower (P < 0.05) rates of soleus muscle respiration compared with rats fed the other two diets. This lower respiration rate was not related to changes in protein synthesis (cycloheximide-sensitive respiration). However, this change may partially be related to enhanced Na+,K+ transport (ouabain-sensitive respiration). The results indicate that muscle is partially responsible for the enhanced thermogenic response found in rats fed diets enriched with polyunsaturated fatty acids and that enhanced ion transport contributes to this response in muscle.

Diets Containing Corn Oil, Coconut Oil and Cholesterol Alter Ventricular Hypertrophy, Dilatation and Function in Hearts of Rats Fed Copper-Deficient Diets

Cardiac hypertrophy and function were evaluated in rats fed diets containing deficient, marginal or adequate levels of copper. The fat concentration of the diets was either 10 g/100 g corn oil, 10 g/100 g coconut oil or 10 g/100 g coconut oil + 1 g/100 g added cholesterol. Left ventricular (LV) wall thickening of hearts in rats fed copper-deficient diets was characterized by greater (P < 0.05) LV free wall width, regardless of dietary fat type, and greater intraventricular septum width in the rats fed corn oil. Rats fed the copper-deficient diet with coconut oil + cholesterol had LV chamber volumes that were twofold larger than those of rats fed the copper-deficient diet with coconut oil or corn oil. Copper deficiency reduced LV chamber volume only in rats fed coconut oil + cholesterol. Cardiac LV end diastolic pressure in rats fed copper-deficient diets was twofold larger than in copper-adequate and copper-marginal groups fed corn oil or coconut oil. Hearts from rats fed the copper-deficient diet with corn oil compared with those from rats fed the copper-deficient diet with coconut oil + cholesterol had greater right ventricular (RV) and LV end diastolic pressures, LV pressures and LV and RV maximal rates of positive pressure development. Our data suggest that cardiac adaptations in rats fed copper-deficient diets are influenced by dietary fat type: 1) hearts of rats fed the copper-deficient diet with corn oil were concentrically hypertrophied, whereas cardiac contractility was maintained in the presence of high preload; 2) preload and contractility in hearts of coconut oil-fed rats was greater than cardiac response to cholesterol addition to the coconut oil diet; 3) hearts in copper-deficient rats fed coconut oil + cholesterol exhibited eccentric hypertrophy and ventricular dysfunction.

Feeding Coconut Oil Reduces Fatty Acid Oxidation and Exacerbates Steatosis in the Liver of Neonatal Pigs

Coconut oil is commonly used to enhance the energy content of infant formulas due to its high medium‐chain fatty acid (MCFA) content. Using neonatal pigs as model for the human infant, we previously reported that feeding a formula rich in MCFA led to hepatic fat accumulation compared to an isocaloric long‐chain fatty acid formula (LCFA). In addition, isolated hepatocytes from MCFA fed pigs oxidized more glutamate than LCFA fed pigs, suggesting a shift in liver metabolism. Thus, the objectives of this study were to investigate whether MCFA and LCFA feeding affect hepatic laurate (C12:0), and palmitate (C16:0) oxidation, and determine whether fat type influences the expression of genes related to fatty acid metabolism in the liver. Twenty‐six, 3‐day‐old pigs were allotted one of three sow milk replacer formulas: a control (CONT) formula that provided 80% of caloric requirements, and two isocaloric formulas that provided 120% of caloric requirements with fat either as LCFA or MCFA. Pigs were fed 250 ml∙kg‐1∙day‐1 for 22 days, weights were determined every other day, and formula allowance adjusted accordingly. Body composition was determined using DXA at day ‐1 and 21. On day 22, pigs were euthanized. Muscle and organs were excised, weighed, and sampled. Liver samples were homogenized and incubated with [2‐C14]palmitate or [2‐C14]laurate. Following a 60 min incubation, radio‐labelled enrichment of CO2 and acid‐soluble metabolites were determined. Fat was extracted from liver samples using a modified Bligh and Dyer method, fatty acids were methylated to fatty acid methyl esters, and their concentrations determined by gas chromatography/mass spectrometry. Expression of genes related to fatty acid metabolism was determined using Real‐Time PCR. In addition, citrate synthase (CS) activity was measured in liver homogenates using spectrophotometry. Body weight of pigs fed the LCFA formula was greater (8.3%) than those fed the MCFA and CONT formulas (P&lt; 0.05). In addition, LCFA lean tissue mass was greater (29%) when compared with CONT while MCFA was intermediate (P&lt; 0.05). Liver weight of MCFA pigs was 25 and 77% greater than LCFA and CONT groups (P&lt; 0.05). Liver fat was greater (142%) for MCFA pigs compared with LCFA and CONT counterparts (P&lt; 0.05). Palmitate and laurate oxidation to CO2 was greater (49%) for pigs fed the LCFA and CONT formulas compared with those fed MCFA (P&lt; 0.05). In addition, complete oxidation of palmitate and laurate was greater (112%) for LCFA and CONT pigs (P&lt; 0.05). MCFA fed pigs had greater proportions of laurate, myristate and palmitate in their livers compared with LCFA and CONT groups (P&lt; 0.05). Expression of fatty acid synthase 3 (FASN‐3), fatty acid binding protein 1(FABP‐1), and acetyl CoA carboxylase 1 (ACACA‐1) were 8, 6, and 2‐fold greater for the MCFA pigs than LCFA and CONT pigs (P&lt; 0.05). However, apolipoprotein‐B (APO‐B) expression was not affected by treatment. These data suggest that feeding a formula rich in MCFA led to hepatic steatosis, and that fatty acid composition in liver did not reflect that of fed formulas. In addition, liver steatosis in pigs fed the MCFA rich formula is correlated with a reduction in the liver’s ability to oxidize fatty acids when compared with pigs fed an isocaloric LCFA based formula.

The Effects of Feeding Coconut Oil on Anthropometric and Biochemical Measures and Mood in Healthy Adults: A Pilot Study

Abstract Objectives Consumption studies of coconut oil on anthropometric and biochemical measures and mood are limited in healthy adults. Thus, we sought to investigate the effects of coconut oil consumption on fasting triglycerides, blood glucose and cholesterol, blood pressure, body composition, waist-to-hip measure, and mood changes in healthy adults aged 18 or older (n = 23). Methods A free-living crossover design with two seven-week treatment periods; coconut oil added (30 mL/day), a no-coconut oil control treatment, and a seven-week washout period (IRB #19–86) was utilized. Body impedance analysis measurements (Tanita), blood pressure (Omron), and waist-to-hip measurements were taken at the beginning and end of each treatment. Three randomized compliance diet recalls (n = 6) and five mood questionnaires (Profile of Mood States) (n = 10) were collected during each study period. The mood questionnaire was analyzed by chi-square; other data was analyzed by a mixed effects model (IBM SPSS Statistics 26). Results In the coconut oil treatment (treatment), total cholesterol (p = 0.037) and triglycerides (p = 0.044) significantly increased, while HDL also increased and approached significance (p = 0.084). In the no-coconut oil control (control), increased triglycerides also approached significance (p = 0.060). In the treatment, % body fat (PBF) (p = 0.034), fat mass (FM) (p = 0.033), and total body water (TBW) (p = 0.037) were significantly higher, and corrected fat free mass (FFM) FFM-TBW approached significance (p = 0.075). In the no-coconut control group, % body fat approached significance (p = 0.056). Perceived sad mood (p = 0.013) and energetic mood (p = 0.013) decreased over the five measurements in the treatment group, while the control reported significant decreased lively mood (p = 0.036) and satisfaction (p = 0.045). No other measures were significant. Conclusions Inclusion of 30 mL/day of coconut oil (240 Kcals) in the diet may raise total and HDL cholesterol. However, % body fat and fat mass also increased, and perceived sadness and perceived energy levels also decreased. More studies are needed to confirm our results. Funding Sources Virginia M. Gladney Memorial Scholarship – Academy of Nutrition and Dietetics

Effects of coconut oil on the weight and blood status of grazing cattle fed concentrate as supplementary feed

This study was conducted to determine the effect of coconut oil inclusion on thesupplementary feed intake, weight gain, haematology and serum biochemistry of grazing cattle. Twenty-five (25) White Fulani cattle weighing 138±2.21 kg were randomly allotted to five treatment groups of coconut oil administration (0 g/day, 50 g/day, 100 g/day, 150 g/day and 200 g/day) in a completely randomised design. The animals were grazed for 84 days and supplemented with concentrate throughout the experimental period. Data on feed intake, weight gain and blood profile of cattle were analysed using one-way analysis of variance. Results obtained showed that coconut oil did not affect (P&gt;0.05) the supplementary concentrate intake of grazing cattle. Lower (P&lt;0.05) weight gain was observed with animals fed coconut oil at 50 g/day (9.64 kg) but increased to 17.64 kg with 150 g/day. Packed cell volume, haemoglobin and white blood cells were not affected (P&gt;0.05) by coconut oil. Thehighest (P&lt;0.05) red blood cell (6.91×10 /L) and platelet counts (67.00×10 /L) wererecorded at 150 g/day coconut oil. Total cholesterol, HDL and LDL values were increased (P&lt;0.05) with increasing levels of coconut oil. Values obtained for HDL (166.00 mg/dL to 145.15 mg/dL) and LDL (135.00 mg/dL to 88.40 mg/dL) decreased when the level of oil was increased from 150g/day to 200g/day. Administering coconut oil up to 150 g/day is recommended as it increases the body weight gain of cattle and maintain the normal PCV and haemoglobin concentration of the animals

Impaired mitochondrial medium-chain fatty acid oxidation drives periportal macrovesicular steatosis in sirtuin-5 knockout mice

Medium-chain triglycerides (MCT), containing C8–C12 fatty acids, are used to treat several pediatric disorders and are widely consumed as a nutritional supplement. Here, we investigated the role of the sirtuin deacylase Sirt5 in MCT metabolism by feeding Sirt5 knockout mice (Sirt5KO) high-fat diets containing either C8/C10 fatty acids or coconut oil, which is rich in C12, for five weeks. Coconut oil, but not C8/C10 feeding, induced periportal macrovesicular steatosis in Sirt5KO mice. 14C–C12 degradation was significantly reduced in Sirt5KO liver. This decrease was localized to the mitochondrial β-oxidation pathway, as Sirt5KO mice exhibited no change in peroxisomal C12 β-oxidation. Endoplasmic reticulum ω-oxidation, a minor fatty acid degradation pathway known to be stimulated by C12 accumulation, was increased in Sirt5KO liver. Mice lacking another mitochondrial C12 oxidation enzyme, long-chain acyl-CoA dehydrogenase (LCAD), also developed periportal macrovesicular steatosis when fed coconut oil, confirming that defective mitochondrial C12 oxidation is sufficient to induce the steatosis phenotype. Sirt5KO liver exhibited normal LCAD activity but reduced mitochondrial acyl-CoA synthetase activity with C12. These studies reveal a role for Sirt5 in regulating the hepatic response to MCT and may shed light into the pathogenesis of periportal steatosis, a hallmark of human pediatric non-alcoholic fatty liver disease.

Efficacy of energy supplementation on growth performance and immune response of suckling pigs.

Three studies were performed to determine the effects of oral energy sources on the performance, immune status, and intestinal morphology of piglets. In Exp. 1, 50 litters were selected based on genotype and parity order to determine the optimum amount of supplemental energy for neonatal pigs. They were distributed according to a 5 × 5 Latin square design, in which columns were represented by 5 sows and rows were represented by 5 newborn weight categories. Treatments consisted of 2 oral doses of 0, 2, 4, 8, or 16 mL of rice bran oil (RBO). There was a positive response of RBO on BW with a numerical difference (P = 0.12) and a significant linear effect (P = 0.04) at weaning. In Exp. 2, litters (n = 340) were randomly allotted to a 2 × 2 factorial arrangement of treatments: RBO supplemented either through oral doses (without supplementation or with 2 mL of RBO) or through prestarter feed (without supplementation or with 2% of RBO replacing 2% of soybean oil). Piglets orally receiving RBO showed a numerical increase in BW at weaning (P = 0.101) compared with the control group. Moreover, piglets supplemented by prestarter feed tended to increase feed intake (P = 0.084). In Exp. 3, litters (n = 245) were selected based on genotype and parity order and they were distributed according to a 7 × 7 Latin square design planed in the same way as in Exp. 1. Each neonatal pig within a litter was randomly assigned to 1 of 7 treatments: 1) control (no supplementation), 2) 2 mL of RBO enriched with omega-3 fatty acids, 3) 2.33 mL of pure glycerin, 4) 1.3 mL of soybean oil, 5) 1.4 mL of linseed oil, 6) 1.68 mL of coconut oil, and 7) 2 mL of RBO. Animal performance was analyzed using 2 data sets: all data (average initial BW of 1.479 kg) and low birth weight (LBW) piglet data (≤1.220 kg initial BW with average of 0.985 kg). Body weight or BW gain (BWG) were not different among treatments (P > 0.10) when all data were analyzed. However, LBW piglets fed coconut oil tended to increase BW (P = 0.099) during the first week. In conclusion, the oral use of RBO may increase BW at weaning and the supplementation by prestarter feed may enhance the feed intake of piglets. In addition, coconut oil may increase BW of LBW piglets in the first week of life without affecting mortality, immune response, or gut morphology. The routine practice of oral supplementation of energy for newborn pigs could be an important tool in swine production.

Reconstituted HDL (Milano) Treatment Efficaciously Reverses Heart Failure with Preserved Ejection Fraction in Mice.

Heart failure with preserved ejection fraction (HFpEF) represents a major unmet therapeutic need. This study investigated whether feeding coconut oil (CC diet) for 26 weeks in female C57BL/6N mice induces HFpEF and evaluated the effect of reconstituted high-density lipoprotein (HDL)Milano (MDCO-216) administration on established HFpEF. Eight intraperitoneal injections of MDCO-216 (100 mg/kg protein concentration) or of an equivalent volume of control buffer were executed with a 48-h interval starting at 26 weeks after the initiation of the diet. Feeding the CC diet for 26 weeks induced pathological left ventricular hypertrophy characterized by a 17.1% (p < 0.0001) lower myocardial capillary density and markedly (p < 0.0001) increased interstitial fibrosis compared to standard chow (SC) diet mice. Parameters of systolic and diastolic function were significantly impaired in CC diet mice resulting in a reduced stroke volume, decreased cardiac output, and impaired ventriculo-arterial coupling. However, ejection fraction was preserved. Administration of MDCO-216 in CC diet mice reduced cardiac hypertrophy, increased capillary density (p < 0.01), and reduced interstitial fibrosis (p < 0.01). MDCO-216 treatment completely normalized cardiac function, lowered myocardial acetyl-coenzyme A carboxylase levels, and decreased myocardial transforming growth factor-β1 in CC diet mice. In conclusion, the CC diet induced HFpEF. Reconstituted HDLMilano reversed pathological remodeling and functional cardiac abnormalities.

Comparative Effect of Dietary Soybean Oil, Fish Oil, and Coconut Oil on Performance, Egg Quality and Some Blood Parameters in Laying Hens

Two hundred and sixteen 28-wk-old Hy-line laying hens were randomly distributed to three dietary treatments and fed 1of 3 diets containing 8% soybean oil, fish oil, or coconut oil from 28 to 47 wk of age to investigate comparative effect of dietary soybean oil, fish oil, and coconut oil on the performance, egg quality and blood malondialdehyde (MDA), aspartate transaminase (AST) and uric acid (UA). Hens fed fish oil showed poor performance compared with soybean oil or coconut oil, and especially egg weight throughout the trial was significantly and consistently decreased (P < 0.05) due to dietary fish oil. Unexpectedly, shell reflectivity throughout the majority of the trial was consistently and significantly higher (P < 0.05) when hens fed fish oil than that when fed soybean oil or coconut oil. Dietary treatments affected (P < 0.05) shell shape at 4 of 8 time points tested. Average shell shape in fish oil treatment was higher (P < 0.05) than that of coconut oil group. Albumen height, Haugh unit and yolk color were influenced by dietary treatments only at 1 or 2 time points. However, average albumen height and Haugh unit in fish oil treatment were higher (P < 0.05) than that of soybean oil or coconut oil treatments and average yolk color in coconut oil treatment was higher (P < 0.05) than that of soybean oil group. Serum MDA, AST and UA concentrations were increased (P < 0.05) by fish oil during the majority of the first 2 mo of the trial. These data suggested that the inclusion of fish oil into feed may reduce the performance of laying hens, especially the egg weight, decrease the intensity of egg brown color and increase blood MDA, AST and UA levels compared with soybean oil or coconut oil. As a result, hens fed fish oil may lay smaller, longer and lighter-brown eggs whereas those fed coconut oil produce blunter and darker-brown eggs relative to soybean oil.

Effect of Mouse Strain on Dietary CLA and Coconut Oil‐Induced Lipolysis

Dietary conjugated linoleic acid (CLA)‐induced lipolysis and body fat loss are enhanced in mice fed coconut oil (CO); however, differences between mouse strains have been observed. This study was designed to evaluate the response to CLA and oil source in 4 common mouse strains. Male CF‐1, ICR, NIH, and Swiss Webster mice (3‐wk‐old, n = 24 per strain) were fed diets containing either soy oil (SO) or CO for 6 weeks, followed by 0 or 0.5% CLA (replacing base oil w/w) for 12 days. Tissue weights were measured for the calculation of a body fat index (BFI): epididymal + retroperitoneal fat pads/body weight*100. Epididymal and retroperitoneal fat pads were pooled and used for ex vivo lipolysis analysis and real time RT‐PCR. We detected an oil*CLA interaction (P = 0.03) on BFI where SO‐fed mice were the fattest and CO+CLA‐fed mice were the leanest, and a main effect of strain (P &lt; 0.001) where Swiss Webster mice were the fattest and NIH mice the leanest, but no diet by strain interactions. Lipolysis was stimulated by both CO (P &lt; 0.001) and CLA (P = 0.002) with no effect of strain. No differences in the mRNA expressions of UCP1, UCP2, UCP3, or CPT1 were detected but UCP1 expression was positively correlated (r = 0.26, P = 0.01) with lipolysis. As expected, the BFI was negatively correlated (r = ‐0.43, P &lt; 0.001) with lipolysis but positively correlated (r = 0.35, P = 0.001) with serum NEFA. In conclusion, we found that mouse strain does not significantly impact the response to CLA and/or CO and no evidence of increased UCP expression in the adipose tissue of CLA‐fed mice.

Effects of feeding lauric acid or coconut oil on ruminal protozoa numbers, fermentation pattern, digestion, omasal nutrient flow, and milk production in dairy cows

The objectives of this study were to evaluate the feeding of coconut oil (CO), in which lauric acid (La) comprises about 50% of the fatty acid composition, as a practical rumen protozoa (RP) suppressing agent, to assess whether the source of La affects ruminal fermentation and animal performance and to test whether suppressing RP improves N utilization, nutrient digestion, nutrient flow at the omasal canal, and milk production. Fifteen multiparous Holstein cows (3 fitted with ruminal cannulas) and 15 primiparous Holstein cows (3 fitted with ruminal cannulas) were used in a replicated 3×3 Latin square experiment with 14d of adaptation and 14d of sample collection. Diets were fed as total mixed ration and contained (dry matter basis) 10% corn silage, 50% alfalfa silage, and 40% concentrate. The control diet contained 3% (dry matter basis) calcium soaps of palm oil fatty acids (Megalac, Church & Dwight Co. Inc., Princeton, NJ) as a ruminally inert fat source and had no added La or CO. Diets with La and CO were formulated to contain equal amounts of La (1.3%, dry matter basis). Dry matter intake was not affected by treatment. Both CO and La reduced RP numbers by about 40%. Lauric acid reduced yield of milk and milk components; however, CO did not affect yield of milk and yields of milk components. Both La and CO caused small reductions in total VFA concentration; CO increased molar proportion of ruminal propionate, reduced ruminal ammonia and branched-chain volatile fatty acids, suggesting reduced protein degradation, and reduced milk urea N and blood urea N concentrations, suggesting improved protein efficiency. Lauric acid reduced total-tract apparent digestibility of neutral detergent fiber and acid detergent fiber as well as ruminal apparent digestibility of neutral detergent fiber and acid detergent fiber as measured at the omasal canal; however, CO did not alter fiber digestion. Microbial protein flow at the omasal canal, as well as the flow of N fractions at the omasal canal, did not differ among treatments. Results from this experiment have confirmed that dietary La is not a practical agent for suppressing RP population in dairy cows, mainly because of its negative effects on fiber digestion and ruminal fermentation. Intake of CO appeared to reduce ruminal and improve protein efficiency, but did not improve milk production, milk composition, or increase microbial outflow from the rumen. Based on the results of this study, a 40% reduction of RP population is not sufficient to improve N utilization in dairy cows.

The Peroxisomal Enzyme L-PBE Is Required to Prevent the Dietary Toxicity of Medium-Chain Fatty Acids

Specific metabolic pathways are activated by different nutrients to adapt the organism to available resources. Although essential, these mechanisms are incompletely defined. Here, we report that medium-chain fatty acids contained in coconut oil, a major source of dietary fat, induce the liver ω-oxidation genes Cyp4a10 and Cyp4a14 to increase the production of dicarboxylic fatty acids. Furthermore, these activate all ω- and β-oxidation pathways through peroxisome proliferator activated receptor (PPAR) α and PPARγ, an activation loop normally kept under control by dicarboxylic fatty acid degradation by the peroxisomal enzyme L-PBE. Indeed, L-pbe(-/-) mice fed coconut oil overaccumulate dicarboxylic fatty acids, which activate all fatty acid oxidation pathways and lead to liver inflammation, fibrosis, and death. Thus, the correct homeostasis of dicarboxylic fatty acids is a means to regulate the efficient utilization of ingested medium-chain fatty acids, and its deregulation exemplifies the intricate relationship between impaired metabolism and inflammation.

Dietary CLA‐induced Lipolysis Is Delayed in Soy Oil‐Fed Mice Compared to Coconut Oil‐Fed Mice

Conjugated linoleic acid (CLA) has been shown to cause a reduction in obesity in several species. CLA-induced body fat loss is enhanced when mice are fed coconut oil (CO) and involves increased lipolysis. The objective of this paper was to determine if the CLA-induced lipolysis in mice fed with different oil sources was time-dependent. Mice were fed 7% soybean oil (SO) or CO diets for 6week and then supplemented with 0 or 0.5% CLA for 3, 7, 10 or 14days. Body fat and ex-vivo lipolysis was determined. Body fat was reduced by CO on day 7 (P<0.01) and in both CO and SO-fed mice (P<0.05) in response to CLA on d14. Lipolysis was increased by CLA in CO-fed mice (P<0.01) but not in SO-fed mice on day 7 and 10, but on day 14 CLA increased lipolysis in both CO- and SO-fed mice (P<0.001). Expression and activation level of proteins involved in lipolysis and lipogenesis was determined by western blotting and real-time PCR, respectively. No significant differences were detected in protein expression. CO-fed mice had greater fatty acid synthase and stearyl CoA desaturase 1 mRNA expression and less acetyl CoA carboxylase mRNA expression (P<0.01). Sterol regulatory binding protein 1c was decreased by CLA in CO-fed mice and increased in SO-fed mice (P<0.05). Malic enzyme expression was increased by CLA (P<0.001) and CO (P<0.01). Therefore, CLA-induced lipolysis occurs more rapidly in CO vs SO-fed mice and lipogenesis is decreased in CO-fed mice with CLA supplementation.

Mice do not accumulate muscle lipid in response to dietary conjugated linoleic acid1

Dietary CLA decreases body fat in several species and in pigs this is accompanied by increased muscle lipid. Our objective was to determine if mice could be used as a model for CLA-induced increased marbling in pigs. We used our model of enhanced CLA response, where mice fed coconut oil (CO) lose more body fat than mice fed soy oil (SO). Mice (21 d old; Imprinting Control Region [ICR]) were fed SO or CO diets for 6 wk followed by 12 d of 0 or 0.5% mixed isomer CLA. Ether extraction determined that thigh muscle lipid content was reduced by both CLA and CO (P = 0.007 and P = 0.006, respectively). Conjugated linoleic acid also caused a reduction (P = 0.016) in carnitine palmitoyltransferase (CPT) enzyme activity, so less fatty acid oxidation appeared to be occurring. Lumbar muscle, which is more similar to the longissimus dorsi tested in pigs, did not differ in lipid content between mice (56 d old; ICR) fed SO or SO+CLA for 14 d. Therefore, CLA-fed mice do not appear to be accumulating excess lipid in their muscle. However, CLA addition to CO diets increased (P = 0.007) the mRNA expression of PPAR-γ in the thigh muscle to the level of SO-fed mice, indicating that intramuscular adipocyte differentiation may be increasing. On the other hand, liver lipid was increased (P < 0.0001) by CO and tended to be increased (P = 0.099) by CLA. Liver CPT activity was decreased (P = 0.018) in SO+CLA-fed mice but not CO+CLA. It appears that mice may accumulate lipid in their livers preferentially over muscle when fed CLA and therefore are not a good model for CLA-induced muscle lipid accumulation.

Effects of some edible oils on renal function in rats

This work was done to investigate the effects of palm oil, groundnut oil and coconut oil on kidney function. Biochemical analysis carried out includes the determinations of creatinine, urea, sodium, potassium, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and alkaline phosphatase (ALP) levels. Measurement of kidney weight, body weight, feed intake, faecal output as well as histological examination were also carried out. Consequently, 32 albino rats were divided into 4 groups of 8 rats each, the control rats were fed rats&#8217; chow only while others were given 90% rats&#8217; chow supplemented with 10% of palm oil, coconut oil or groundnut oil. They were given these diets along with water for six weeks ad libitum. Results showed that body and kidney weight were not significantly altered compared with control. Also urea and sodium levels were not significantly altered although potassium levels were significantly reduced compared with control. Creatinine levels were significantly increased in all the test rats. ALT levels were significantly increased in rats fed groundnut and palm oil based diet while AST levels were significantly increased only in those rats fed coconut oil &#8211; based diet. Histological examination shows the presence of chronic inflammatory cells. These results suggest that renal function was compromised when rats were given these oil-based diets.Keywords: Kidney; Creatinine; Urea; Aminotransferases; Histological analysis

Coconut Oil Enhances Tomato Carotenoid Tissue Accumulation Compared to Safflower Oil in the Mongolian Gerbil (Meriones unguiculatus)

Evidence suggests that monounsaturated and polyunsaturated fats facilitate greater absorption of carotenoids than saturated fats. However, the comparison of consuming a polyunsaturated fat source versus a saturated fat source on tomato carotenoid bioaccumulation has not been examined. The goal of this study was to determine the influence of coconut oil and safflower oil on tomato carotenoid tissue accumulation in Mongolian gerbils ( Meriones unguiculatus ) fed a 20% fat diet. Coconut oil feeding increased carotenoid concentrations among many compartments including total carotenoids in the serum (p = 0.0003), adrenal glandular phytoene (p = 0.04), hepatic phytofluene (p = 0.0001), testicular all-trans-lycopene (p = 0.01), and cis-lycopene (p = 0.006) in the prostate-seminal vesicle complex compared to safflower oil. Safflower oil-fed gerbils had greater splenic lycopene concentrations (p = 0.006) compared to coconut oil-fed gerbils. Coconut oil feeding increased serum cholesterol (p = 0.0001) and decreased hepatic cholesterol (p = 0.0003) compared to safflower oil. In summary, coconut oil enhanced tissue uptake of tomato carotenoids to a greater degree than safflower oil. These results may have been due to the large proportion of medium-chain fatty acids in coconut oil, which might have caused a shift in cholesterol flux to favor extrahepatic carotenoid tissue deposition.

Effect of conjugated linoleic acid on fatty acid synthesis in soy and coconut oil fed mice

Dietary conjugated linoleic acid (CLA) causes a body fat loss, which is enhanced when mice are fed coconut oil (CO), in part due to increased lipolysis. Our objective was to determine the effect of CLA supplementation on the mRNA expression of genes involved in fatty acid synthesis in mice fed soy oil (SO) or CO. Male mice (ICR; n=80; 3 wk‐old) were fed 7% SO or CO diets for 6wk, then 0 or 0.5% CLA for 3,7,10, or 14d. The liver relative mRNA expression of Fatty Acid Synthase (FAS), Acetyl‐CoA Carboxylase (ACC), Malic Enzyme (ME), Sterol Regulatory Element Binding Protein (SREBP), and Stearoyl‐CoA Desaturase (SCD) were determined via real time RT‐PCR and normalized to Acidic Ribosomal Protein. FAS enzyme activity was also determined as NADPH disappearance. CO increased the expression of ME (P &lt; 0.01), FAS (P &lt; 0.001), and SCD (P &lt; 0.001) but decreased the expression of ACC (P &lt; 0.01). CLA increased the expression of ME (P &lt; 0.001). Specifically, the CO+CLA‐fed mice had increased (P &lt; 0.05) ME and SCD mRNA and decreased (P &lt; 0.05) ACC mRNA vs all other diet groups. There was also an effect of day on SCD mRNA, where SCD expression increased (P &lt; 0.01) with increasing days on feed. SREBP mRNA and FAS enzyme activity were not different. It appears that CO‐feeding may cause an increase in fatty acid turnover that could contribute to the greater loss of body fat observed when these mice are fed CLA.

Interaction of unsaturated fat or coconut oil with monensin in lactating dairy cows fed 12 times daily. I. Protozoal abundance, nutrient digestibility, and microbial protein flow to the omasum

Monensin (tradename: Rumensin) should reduce the extent of amino acid deamination in the rumen, and supplemental fat should decrease protozoal abundance and intraruminal N recycling. Because animal-vegetable (AV) fat can be biohydrogenated in the rumen and decrease its effectiveness as an anti-protozoal agent, we included diets supplemented with coconut oil (CNO) to inhibit protozoa. In a 6 × 6 Latin square design with a 2 × 3 factorial arrangement of treatments, 6 rumen-cannulated cows were fed diets without or with Rumensin (12g/909kg) and either no fat (control), 5% AV fat, or 5% CNO. The log10 concentrations (cells/mL) of total protozoa were not different between control (5.97) and AV fat (5.95) but were decreased by CNO (4.79; main effect of fat source). Entodinium and Dasytricha decreased as a proportion of total cells from feeding CNO, whereas Epidinium was unchanged in total abundance and thus increased proportionately. Total volatile fatty acid concentration was not affected by diet, but the acetate:propionate ratio decreased for CNO (1.85) versus control (2.95) or AV fat (2.58). Feeding CNO (23.8%) decreased ruminal neutral detergent fiber digestibility compared with control (31.1%) and AV fat (30.5%). The total-tract digestibility of NDF was lower for CNO (45.8%) versus control (57.0%) and AV fat (54.6%), with no difference in apparent organic matter digestibility (averaging 69.8%). The omasal flows of microbial N and non-ammonia N were lower for CNO versus control and AV fat, but efficiency of microbial protein synthesis was not affected. The dry matter intake was 4.5kg/d lower with CNO, which decreased milk production by 3.1kg/d. Main effect means of dry matter intake and milk yield tended to decrease by 0.7 and 1.2kg/d, respectively, when Rumensin was added. Both percentage and production of milk fat decreased for CNO (main effect of fat source). An interaction was observed such that AV decreased milk fat yield more when combined with Rumensin. Using large amounts of supplemental fat, especially CNO, to decrease abundance of protozoa requires further research to characterize benefits versus risks, especiallywhen combined with Rumensin.

Link between lipid metabolism and voluntary food intake in rainbow trout fed coconut oil rich in medium-chain TAG

We examined the long-term effect of feeding coconut oil (CO; rich in lauric acid, C12) on voluntary food intake and nutrient utilisation in rainbow trout (Oncorhynchus mykiss), with particular attention to the metabolic use (storage or oxidation) of ingested medium-chain TAG. Trout were fed for 15 weeks one of the four isoproteic diets containing fish oil (FO) or CO as fat source (FS), incorporated at 5% (low fat, LF) or 15% (high fat, HF). Fat level or FS did not modify food intake (g/kg(0·8) per d), despite higher intestinal cholecystokinin-T mRNA in trout fed the HF-FO diet. The HF diets relative to the LF ones induced higher growth and adiposity, whereas the replacements of FO by CO resulted in similar growth and adiposity. This, together with the substantial retention of C12 (57% of intake), suggests the relatively low oxidation of ingested C12. The down-regulation of carnitine palmitoyl-transferase-1 (CPT-1) confirms the minor dependency of medium-chain fatty acids (MCFA) on CPT-1 to enter the mitochondria. However, MCFA did not up-regulate mitochondrial oxidation evaluated using hepatic hydroxyacyl-CoA dehydrogenase as a marker, in line with their high retention in body lipids. At a low lipid level, MCFA increased mRNA levels of fatty acid synthase, elongase and stearoyl-CoA desaturase in liver, showing the hepatic activation of fatty acid synthesis pathways by MCFA, reflected by increased 16 : 0, 18 : 0, 16 : 1, 18 : 1 body levels. The high capacity of trout to incorporate and transform C12, rather than to readily oxidise C12, contrasts with data in mammals and may explain the absence of a satiating effect of CO in rainbow trout.