Possible Role of Butyrylcholinesterase in Fat Loss and Decreases in Inflammatory Levels in Patients with Multiple Sclerosis after Treatment with Epigallocatechin Gallate and Coconut Oil: A Pilot Study.

(1) Background. Multiple sclerosis (MS) is characterised by the loss of muscle throughout the course of the disease, which in many cases is accompanied by obesity and related to inflammation. Nonetheless, consuming epigallocatechin gallate (EGCG) and ketone bodies (especially ß-hydroxybutyrate (ßHB)) produced after metabolising coconut oil, have exhibited anti-inflammatory effects and a decrease in body fat. In addition, butyrylcholinesterase (BuChE), seems to be related to the pathogenesis of the disease associated with inflammation, and serum concentrations have been related to lipid metabolism. Objective. The aim of the study was to determine the role of BuChE in the changes caused after treatment with EGCG and ketone bodies on the levels of body fat and inflammation state in MS patients. (2) Methods. A pilot study was conducted for 4 months with 51 MS patients who were randomly divided into an intervention group and a control group. The intervention group received 800 mg of EGCG and 60 mL of coconut oil, and the control group was prescribed a placebo. Fat percentage and concentrations of the butyrylcholinesterase enzyme (BuChE), paraoxonase 1 (PON1) activity, triglycerides, interleukin 6 (IL-6), albumin and ßHB in serum were measured. (3) Results. The intervention group exhibited significant decreases in IL-6 and fat percentage and significant increases in BuChE, ßHB, PON1, albumin and functional capacity (determined by the Expanded Disability Status Scale (EDSS)). On the other hand, the control group only exhibited a decrease in IL-6. After the intervention, BuChE was positively correlated with the activity of PON1, fat percentage and triglycerides in the intervention group, whereas these correlations were not observed in the control group (4). Conclusions. BuChE seems to have an important role in lipolytic activity and the inflammation state in MS patients, evidenced after administering EGCG and coconut oil as a ßHB source.

Celecoxib exhibits therapeutic potential in experimental model of hyperlipidaemia.

Hyperlipidaemia is a major risk factor for cardiovascular diseases, the leading cause of death globally. Celecoxib attenuated hypercholesterolaemia associated with CCl4-induced hepatic injury in rats without improving liver function in our previous study. This present study investigated the lipid lowering potential of celecoxib in normal rats fed with coconut oil subjected to five deep-frying episodes. Male Sprague Dawley rats were randomly assigned to groups (n = 6 rats/group) which received physiological saline (10 mL/kg), unheated coconut oil (UO, 10 mL/kg) or heated coconut oil (HO, 10 ml/kg) for 60 days. Groups that received HO were subsequently treated with either physiological saline, atorvastatin (25 mg/kg), celecoxib (5 mg/kg) or celecoxib (10 mg/kg) in the last fifteen days of the experiment. Rats were sacrificed 24 hours after last treatment and blood and tissue samples collected for analysis. HO consumption produced significant hyperlipidaemia and elevation in marker enzymes of hepatic function. Celecoxib ameliorated the hyperlipidaemia as shown by the significantly (P<0.05) lower total cholesterol, triglycerides, low and very low density lipoprotein in the celecoxib-treated rats when compared with HO-fed rats that received saline. Celecoxib also reduced (P<0.05) alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and liver weight of hyperlipidaemic rats. Similarly, hepatocellular damage with the hyperlipidaemia was significantly reversed by celecoxib. However, serum TNF-α and IL-6 did not change significantly between the various groups. Taken together, data from this study suggest that celecoxib may exert therapeutic benefit in hyperlipidaemia and its attendant consequences.

Longitudinal study of the scalp microbiome suggests coconut oil to enrich healthy scalp commensals.

Dandruff is a recurrent chronic scalp disorder, affecting majority of the population worldwide. Recently a metagenomic study of the Indian scalp microbiome described an imperative role of bacterial commensals in providing essential vitamins and amino acids to the scalp. Coconut oil and its formulations are commonly applied on the scalp in several parts of the world to maintain scalp health. Thus, in this study we examined the effect of topical application of coconut oil on the scalp microbiome (bacterial and fungal) at the taxonomic and functional levels and their correlation with scalp physiological parameters. A 16-weeks-long time-course study was performed including 12-weeks of treatment and 4-weeks of relapse phase on a cohort of 140 (70 healthy and 70 dandruff) Indian women, resulting in ~ 900 metagenomic samples. After the treatment phase, an increase in the abundance of Cutibacterium acnes and Malassezia globosa in dandruff scalp was observed, which were negatively correlated to dandruff parameters. At the functional level, an enrichment of healthy scalp-related bacterial pathways, such as biotin metabolism and decrease in the fungal pathogenesis pathways was observed. The study provides novel insights on the effect of coconut oil in maintaining a healthy scalp and in modulating the scalp microbiome.

Coconut Oil Supplementation Does Not Affect Blood Pressure Variability and Oxidative Stress: A Placebo-Controlled Clinical Study in Stage-1 Hypertensive Patients.

Exploring an alternative to improve the clinical management of hypertension, we tested the hypothesis that food supplementation with coconut oil (EVCO), alone or combined with aerobic exercise training, could exert an antihypertensive effect (primary outcome) in patients with stage 1 hypertension. Forty-five hypertensive volunteers of both genders participated in a placebo-controlled clinical trial. The volunteers were submitted to 24-hour ambulatory blood pressure monitoring, analysis of blood pressure variability (BPV), measurement of serum malondialdehyde (MDA) and nutritional assessment. Results indicate that EVCO consumption had no adverse effects. The supplementation did not increase the caloric intake compared with placebo, and the dietary constituents were similar between groups, except for the saturated fats, especially lauric acid. The analysis of blood pressure indicated absence of antihypertensive effect of EVCO alone or combined with physical training. Furthermore, no effects on blood pressure variability and oxidative stress were observed in the supplemented hypertensive patients. Thus, despite the results observed in pre-clinical studies, the current clinical study did not provide evidence to support the use of coconut oil as an adjuvant in the management of hypertension in humans.

Health effects of coconut oil: Summary of evidence from systematic reviews and meta-analysis of interventional studies.

BACKGROUND AND AIMS: Systemic review (SR) and meta-analysis (MA) of interventional studies are considered as the highest level of evidence for clinical decision making. Therefore, we systematically summarized all high-quality evidence on the usage of coconut oil for health-related benefits from SRs and MA. METHODS: PubMed®, Web of science®, SciVerse Scopus®, and EMBASE® databases were systematically searched to select SRs and SRs with MA of interventional studies reporting health-related clinical outcomes of coconut oil. Similar studies were grouped based on their respective clinical areas. A methodological quality appraisal was conducted for all included SRs and SRs with MA using the Critical Appraisal Checklist for Systematic Reviews. RESULTS: A total of seven papers were selected for inclusion in this review, consisting of three MA and one SR on cardio-metabolic health, one SR on oral health, and one SR and one MA each on skin health. Coconut oil significantly increases serum total cholesterol, low-density- and high-density- lipoprotein cholesterol levels compared to poly- and mono-unsaturated oils. Limited studies showed that topical use of coconut oil helps in the prevention and treatment of atopic dermatitis and oil pulling for the prevention of dental caries. All four studies on cardiometabolic health and the SR on oral health had a high score in the quality assessment, SR with MA on skin health fulfilled high-quality scoring whereas the SR on the same topic had a low-quality scoring. CONCLUSIONS: In summary, consistent and strong evidence shows that coconut oil has an adverse effect on the lipids parameters associated with cardio-metabolic health, with limited studies to conclude the effects of atopic dermatitis and oil pulling.

Coconut oil supplementation during development reduces brain excitability in adult rats nourished and overnourished in lactation.

INTRODUCTION: Coconut oil has been considered as a therapeutic alternative in several pathologies, but there is limited information regarding its effects on brain functioning. OBJECTIVE: This study analyzed whether early virgin coconut oil (VCO) supplementation interferes with electrical activity of the adult rat brain and its lipid peroxidation. Moreover, it investigated whether the putative effect on brain electrophysiology could be affected by overnutrition occurring during lactation, and/or by environmental enrichment (EE). Electrophysiology was measured through cortical spreading depression (CSD), a phenomenon related to brain excitability. METHODS: Wistar rats were suckled in litters of either nine or three pups, forming nourished (N) or overnourished (ON) groups, respectively. Between the 7th and 30th days of life, half of the animals in each group received VCO (10 mg kg-1 d-1; by gavage). The other half received an equivalent amount of vehicle (V, 0.009% cremophor). On day 36, animals from both groups were subjected to EE for 4 weeks. At 105 ± 15 days of life, each animal was subjected to CSD recordings and lipid peroxidation analyses. RESULTS: Overnutrition during lactation enhanced body and brain weights. VCO decelerated the CSD propagation velocity (control - 3.57 ± 0.23 mm min-1versus VCO - 3.27 ± 0.18 mm min-1; p < 0.001), regardless of whether subjected to overnourishment or EE exposure. Neither VCO nor EE modified the cerebral lipid peroxidation (p > 0.05). CONCLUSION: VCO supplementation impaired the spreading of CSD, indicating reduction of brain excitability. VCO effects occurred regardless of the nutritional state during lactation.

Low-Dose Coconut Oil Supplementation Induces Hypothalamic Inflammation, Behavioral Dysfunction, and Metabolic Damage in Healthy Mice.

SCOPE: Coconut oil (CO) diets remain controversial due to the possible association with metabolic disorder and obesity. This study investigates the metabolic effects of a low amount of CO supplementation. METHODS AND RESULTS: Swiss male mice are assigned to be supplemented orally during 8 weeks with 300 µL of water for the control group (CV), 100 or 300 µL of CO (CO100 and CO300) and 100 or 300 µL of soybean oil (SO; SO100 and SO300). CO led to anxious behavior, increase in body weight gain, and adiposity. In the hypothalamus, CO and SO increase cytokines expression and pJNK, pNFKB, and TLR4 levels. Nevertheless, the adipose tissue presented increases macrophage infiltration, TNF-α and IL-6 after CO and SO consumption. IL-1B and CCL2 expression, pJNK and pNFKB levels increase only in CO300. In the hepatic tissue, CO increases TNF-α and chemokines expression. Neuronal cell line (mHypoA-2/29) exposed to serum from CO and SO mice shows increased NFKB migration to the nucleus, TNF-α, and NFKBia expression, but are prevented by inhibitor of TLR4 (TAK-242). CONCLUSIONS: These results show that a low-dose CO changes the behavioral pattern, induces inflammatory pathway activation, TLR4 expression in healthy mice, and stimulates the pro-inflammatory response through a TLR4-mediated mechanism.

Effects of virgin coconut oil consumption on metabolic syndrome components and asymmetric dimethylarginine: A randomized controlled clinical trial.

BACKGROUND AND AIMS: There is some promising evidence regarding the beneficial effect of coconut oil on cardiometabolic risk factors. This study aimed to assess the effects of virgin coconut oil (VCO) consumption on metabolic syndrome (MetS) components, as well as, asymmetric dimethylarginine (ADMA) in adults with MetS. METHODS AND RESULTS: In this randomized controlled trial, 48 subjects, aged 20-50 years, with MetS were allocated into two groups; the intervention group was given 30 ml of VCO per day to substitute the same amounts of fat in their usual diet for four weeks. The control group was advised to follow their usual diet. VCO consumption significantly reduced serum levels of triglyceride (TG) (P = 0.001), very low-density lipoprotein (VLDL) (P = 0.001), and fasting blood sugar (FBS) (P = 0.015) compared to the control group. The levels of high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and total cholesterol (TC) were significantly increased in the VCO group when compared to the control group (P = 0.001). Circulatory ADMA also increased in the VCO group compared to the control group (P = 0.003). No significant differences were observed in the LDL-C/HDL-C ratio, anthropometric parameters, and blood pressure measurements between the two groups at the end of the study (P > 0.05). CONCLUSION: VCO consumption increased the values of HDL-C while reduced TG and FBS levels. Blood pressure and waist circumference did not change. However, levels of TC, LDL-C, and ADMA elevated by VCO consumption. Caution is warranted until the results of further studies become available to explain the long-term effects of VCO consumption. REGISTRATION NUMBER: IRCT20131125015536N11.

Protective Effects of Cocos Nucifera Oil in Paraphenylene Diamine Toxicity.

BACKGROUND: Paraphenylenediamine (PPD) is a highly toxic compound used for hair-dyeing worldwide. PPD self-poisoning had significantly increased in recent times with increased mortality rates. OBJECTIVE: This study aims to evaluate the toxic effects of PPD and the protective potential of its prospective antidote Virgin Coconut Oil (Cocos nucifera). METHODS: PPD was identified and validated by FT-IR and UV mass spectrometer. PPD toxicity was induced in-vivo by single intraperitoneal injection (40 mg/kg and 60 mg/kg). Single-injection of Virgin Coconut Oil (VCO) was administered in the presence of PPD at doses of 5 mg/kg and 10 mg/kg. Blood was analyzed for renal, hepatic and cardiac biomarkers. Relevant organs were collected, weighed and preserved for histopathological examination. Statistical analysis was carried out to note mortality rate, survival duration and serum biochemical parameter. Molecular docking studies were performed to assess attachment of PPD with histaminergic receptors. RESULTS: PPD injection achieved 100% mortality rate with short survival span, and disturbed hepatic, renal, and cardiac serum markers with marked histopathological changes. VCO notably decreased mortality rate, raised treatment time window with marked adjustment in hepatic, renal, and cardiac markers. Docking studies proved that PPD attaches robustly with histaminergic receptors. CONCLUSION: The study concludes that VCO possesses lifesaving protection against PPD toxicity and can be a suitable antidote.

Postprandial lipaemia following consumption of a meal enriched with medium chain saturated and/or long chain omega-3 polyunsaturated fatty acids. A randomised cross-over study.

BACKGROUND & AIMS: Postprandial lipaemic response has emerged as a risk factor for cardiovascular disease. Dietary fats such as medium-chain saturated fatty acids (MCSFA) and long-chain omega-3 polyunsaturated fatty acids (LCn-3PUFA) are known to reduce postprandial lipaemic responses. The combination of the two could potentially have complementary and/or synergistic effects for optimising cardiovascular health. This study aims to investigate the effects of MCSFA (coconut oil) with or without LCn-3PUFA (fish oil) inclusion in the test meal on postprandial blood lipids in healthy adults. METHODS: In a randomised, double-blinded, placebo-controlled, 2 × 2 factorial cross-over study, participants (n = 15) were randomised to receive four standardised isocaloric test meals. Test meals include: placebo [PL, containing no fish oil (0 g EPA & DHA) or coconut oil (0 g MCSFA)], fish oil [FO, 6 g fish oil (3.85 g EPA & DHA), containing no coconut oil (0 g MCSFA)], coconut oil [CO, 18.65 g coconut oil (15 g MCSFA), containing no fish oil (0 g EPA & DHA)] and coconut oil + fish oil [COFO, 18.65 g coconut oil (15 g MCSFA) + 6 g fish oil (3.85 g EPA & DHA)]; all providing a total fat content of 33.5 g. Participants received all four treatments on four separate test days with at least 3 days washout in between. Blood parameters were measured by finger pricks at 7 timepoints between 0 and 300min. The primary outcome of this study was the change in postprandial triglycerides (TG) concentrations with secondary outcomes as total cholesterol, high-density lipoprotein cholesterol and blood glucose concentrations. RESULTS: TG area under the curve (AUC) (mmol/L/min) was significantly lower for FO (383.67, p = 0.0125) and COFO (299.12, p = 0.0186) in comparison to PL (409.17) only. TG incremental area under the curve (iAUC) (mmol/L/min) was significantly lower with COFO (59.67) in comparison to CO (99.86), (p = 0.0480). Compared to PL, the change in absolute TG concentrations (mmol/L) from baseline to post TG peak time (180min) after FO were significantly less at 240min (0.39 vs 0.15), 270min (0.2 vs 0.1), and 300min (0.28 vs 0.06), and after COFO was significantly less at 300min (0.28 vs 0.16) (p < 0.05). No significant differences in postprandial AUC and iAUC for any other blood parameters were reported. CONCLUSIONS: Our study demonstrated that LCn-3PUFA with or without MCSFA but not MCSFA alone are effective in reducing postprandial TG in healthy individuals.

Diets enriched with coconut, fish, or olive oil modify peripheral metabolic effects of ozone in rats.

Dietary factors may modulate metabolic effects of air pollutant exposures. We hypothesized that diets enriched with coconut oil (CO), fish oil (FO), or olive oil (OO) would alter ozone-induced metabolic responses. Male Wistar-Kyoto rats (1-month-old) were fed normal diet (ND), or CO-, FO-, or OO-enriched diets. After eight weeks, animals were exposed to air or 0.8 ppm ozone, 4 h/day for 2 days. Relative to ND, CO- and OO-enriched diet increased body fat, serum triglycerides, cholesterols, and leptin, while all supplements increased liver lipid staining (OO > FO > CO). FO increased n-3, OO increased n-6/n-9, and all supplements increased saturated fatty-acids. Ozone increased total cholesterol, low-density lipoprotein, branched-chain amino acids (BCAA), induced hyperglycemia, glucose intolerance, and changed gene expression involved in energy metabolism in adipose and muscle tissue in rats fed ND. Ozone-induced glucose intolerance was exacerbated by OO-enriched diet. Ozone increased leptin in CO- and FO-enriched groups; however, BCAA increases were blunted by FO and OO. Ozone-induced inhibition of liver cholesterol biosynthesis genes in ND-fed rats was not evident in enriched dietary groups; however, genes involved in energy metabolism and glucose transport were increased in rats fed FO and OO-enriched diet. FO- and OO-enriched diets blunted ozone-induced inhibition of genes involved in adipose tissue glucose uptake and cholesterol synthesis, but exacerbated genes involved in adipose lipolysis. Ozone-induced decreases in muscle energy metabolism genes were similar in all dietary groups. In conclusion, CO-, FO-, and OO-enriched diets modified ozone-induced metabolic changes in a diet-specific manner, which could contribute to altered peripheral energy homeostasis.

''Anti-lice Protector Shampoo'': Clinical Study Shows Lack of Efficacy of Coconut Oil Derivatives in the Elimination of Head Louse Infestation.

OBJECTIVE: Coconut oil and its derivatives are widely thought to kill head lice by occlusion and asphyxiation. There is no evidence in support of coconut derivative-based products sold to treat pediculosis. This study was designed to test one such product. METHODS: This was an open-label clinical study in 31 people. The treatment was shampoo containing 1% fractionated coconut oil. Treatment was given on day 0 and day 8. Efficacy was measured using a detection comb on day 1, day 8 and day 16 after the first treatment. The trial was registered in the current controlled trials database, under number ISRCTN79136319. RESULTS: The first application of the product eliminated the lice from 7/31 participants, and 12/31 (38.7%) people had no lice at the end of the study. Lice of all development stages were found post treatment at all assessments on one or more participants. This indicates that the treatment failed to kill all stages of the life cycle of head lice. CONCLUSION: Two applications of the modified coconut shampoo were not effective at killing head lice or their eggs. The results confirm other studies that show little intrinsic activity in vegetable oils and modified oils. Most of the activity in shampoos is probably due to other product components, such as high levels of detergents.

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 ß-oxidation pathway, as Sirt5KO mice exhibited no change in peroxisomal C12 ß-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.

Neurochemical, neurobehavioral and histochemical effects of therapeutic dose of l-dopa on striatal neurons in rats: Protective effect of virgin coconut oil.

Despite the fact that levodopa has proven its effectiveness in treating the symptoms of Parkinson's disease (PD), increasing concerns have emerged about its possible long-term toxic effects on dopamine (DA) neurons. The study investigated the possible ameliorative effect of virgin coconut oil against l-dopa- induced neurotoxicity in adult rats. A total number of 40 rats were divided into four groups. Briefly, the first served as control, the second was orally administered virgin coconut oil (1.42 mL/kg), the third group was administered a single daily dose of l-dopa/carbidopa (100/10 mg/kg/day, p.o) and the fourth group pre-treated with virgin coconut oil then administered a single daily dose of l-dopa/carbidopa. The different treatments were extended for 30 days. l-dopa treated group exhibited aggressive behavior and behavioral abnormalities in open field test compared to control group. In addition, l-dopa treatment caused significant increase in the levels of striatal dopamine and norepinephrine and their metabolites with concomitant decrease of serotonin and its metabolite. Moreover, l-dopa treatment increased histamine and GABA levels. In addition, l-dopa treatment induced oxidative stress and energy crisis. The histological and immunohistochemical studies showed that l-dopa caused a remarkable neurodegeneration and increased glial fibrillary acidic protein (GFAP) immunoexpression in the striatal area. Virgin coconut oil co-treatment significantly minimized the harmful effects of l-dopa. In conclusion, the present study revealed that virgin coconut oil provided a notable protection against l-dopa's untoward effects.

Effect of coconut oil on weight loss and metabolic parameters in men with obesity: a randomized controlled clinical trial.

Coconut oil appears to help in weight loss and improve metabolic parameters associated with obesity. We evaluate the influence of coconut oil on the body composition, lipid profile and glycemia in men with obesity. A controlled, randomized clinical trial was performed with 29 adult men affected by obesity. They were randomized between two groups receiving a daily intake of 1 tablespoon (12 mL) of extra virgin coconut oil (CO, n = 15) or soybean oil (SO, n = 14), and an isoenergetic balanced diet. The anthropometric profile, lipid profile and glycaemia were evaluated at the baseline and 45 days after intervention. The Mann-Whitney test was performed to compare the groups, and the Wilcoxon test was performed to compare the times. We considered a value of p < 0.05 as significant. There was no difference in anthropometric variables between the groups before and after intervention. The level of HDL cholesterol increased (3.67 ± 8.08 versus-3.79 ± 10.98, p = 0.02) and the TC/HDL cholesterol ratio decreased (-0.63 ± 0.82 versus 0.23 ± 0.80, p = 0.03) in the CO group, compared to the SO group. Coconut oil included in the isoenergetic balanced diet could increase HDL cholesterol and decrease the TC/HDL cholesterol ratio in men with obesity.

Black soldier fly larvae oil as an alternative fat source in broiler nutrition.

The present study was conducted to investigate growth performance, carcass characteristics, short-chain fatty acids, fatty acid composition in abdominal fat, and serum parameters in broiler chickens fed diets containing corn oil, coconut oil, or black soldier fly larvae (BSFL) oil at the level of 50 g per kg of diet during the 30-day-feeding period. A total 450 one-day-old male broiler chicks (Ross 308) were randomly allocated to one of 3 dietary groups. Each treatment had 10 replicates with 15 chicks per replicate. Feed conversion ratio was decreased in the coconut and BSFL oil group compared with the corn oil group. Dietary BSFL oil increased ileal weight-to-length ratio at day 30 after hatch. Dietary BSFL oil increased significantly ileal branched-chain fatty acid (P < 0.05) and moderately total short-chain fatty acid in 15-day-old broilers (P = 0.074). At day 30, ileal propionate was highest in the coconut oil group but cecal propionate was highest (P < 0.05) in the BSFL oil group. Fatty acid composition of abdominal fat was affected by dietary fat sources. Especially, chickens fed diets containing coconut oil or BSFL oil had higher contents (P < 0.05) of saturated fatty acid being dominant in lauric and myristic acids compared with those fed on corn oil. On the other hand, the reverse trend was noted (P < 0.05) as to polyunsaturated fatty acids being dominant in corn oil compared with coconut oil and BSFL oil. Coconut oil vs. corn oil significantly increased total and high-density lipoprotein cholesterol. Finally, BSFL oil vs. corn oil significantly increased total antioxidant capacity in chickens. It is concluded that dietary BSFL oil improves feed conversion ratio and increases the incorporation of medium-chain fatty acids into abdominal fat pad and serum antioxidant capacity in broiler chickens.

Effect of diet supplemented with coconut essential oil on performance and villus histomorphology in broiler exposed to avian coccidiosis.

The current research study was designed to determine the inclusion of 2% dietary essential coconut oil with and without coccidiosis challenge on performance, carcass characteristics, and intestinal histomorphology in broilers. A total of 560 broiler chicks were divided into 4 groups and then subdivided into 5 replicates. Coconut oil was used at 2% in feed, whereas coccidiosis challenged was introduced using 30,000 oocysts. The other four groups were designated as G1 (without coconut oil and without oocysts), G2 (without coconut oil with oocysts), G3 (with coconut oil without oocysts), and G4 (with coconut oil and with oocysts). The results revealed that the overall feed consumption was significantly (P < 0.01) increased in G1 and G2 than G3 and G4 groups. Overall weight gain was significantly (P < 0.01) higher in G3 compared with all other groups. Significantly (P < 0.01) better feed conversion ratio was recorded at the finisher phase in G3 and G4 groups in comparison with G1 and G2. The villus length, width, and surface area were higher (P < 0.01) in G3 compared with G2. Based on the findings of the present study, it was concluded that the use of 2% coconut oil in broiler feed improved growth performance and villus histology during coccidial challenge.

Investigation of the effects of dietary modification in experimental obesity: low dose of virgin coconut oil has a potent therapeutic value.

There is no report in literature on possible physiological changes that accompany dietary modification in obese condition. Moreover, there is no conclusive evidence on the optimal amount of virgin coconut oil (VCO) that could be of health benefit, although it is known to enhance lipid metabolism. Therefore, we investigated the antiobesitogenic action of graded doses of VCO (200, 400 and 600 mg/kg) in obese rats fed with normo/hyper-lipidaemic diet. Sixty rats (n = 10) were divided into 6 groups and treated as follows: the control and high fat diet (HFD) groups were administered normal saline (0.1 mL/day, p.o.) during the last four weeks of the study, and were fed with normal and HFD respectively throughout the twenty weeks duration of the experiment. Groups 3-6 were fed with HFD for 16 weeks, then normal diet during the next 4 weeks. While group - 3 received saline (0.1 mL/day, p.o.) during the last four weeks, groups 4-6 received graded doses of VCO. The results showed that HFD-induced obesity caused impaired glucose homeostasis, distorted hepatic histoarchitecture, selected deviations in hepatic function indices, pro-inflammatory, pro-oxidant, and dsylipidaemic effects. There were evidence of escalated and reversed pathological actions following the replacement of HFD with normal diet. VCO showed no effect on glucose, insulin, insulin resistance, total protein, uric acid and TAC; but equitable effects on CAT, IL-6, CRP, ALT, AST & GGT, irrespective of the dose. Compared to the effects of VCO at 400 and 600 mg/kg, at 200 mg/kg, VCO had more significant therapeutic effects on LDH, MDA, SOD, GPX, TC, TG, LDL-C, total bilirubin, atherogenic and lee indices and hepatic histoarchitecture. Conclusively, VCO, preferably at a low dose could be used to reverse hepatic structural alteration and some biochemical deviations following dietary modifications in obese condition.

Effect of vegetable oils on the experimental infection of mice with Trypanosoma congolense.

Vegetable oils are frequently used as solvents for lipophilic materials; accordingly, the effects of their components should be considered in animal experiments. In this study, the effects of various vegetable oils on the course of Trypanosoma congolense infection were examined in mice. C57BL/6J mice were orally administered four kinds of oils (i.e., coconut oil, olive oil, high oleic safflower oil, and high linoleic safflower oil) with different fatty acid compositions and infected with T. congolense IL-3000. Oil-treated mice infected with T. congolense showed significantly higher survival rates and lower parasitemia than those of control mice. Notably, coconut oil, which mainly consists of saturated fatty acids, delayed the development of parasitemia at the early stage of infection. These results indicated that vegetable oil intake could affect T. congolense infection in mice. These findings have important practical implications; for example, they suggest the potential effectiveness of vegetable oils as a part of the regular animal diet for controlling tropical diseases and indicate that vegetable oils are not suitable solvents for studies of the efficacy of lipophilic agents against T. congolense.