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.

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.

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.

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.

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.

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.

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.

The Impact of Coconut Oil and Epigallocatechin Gallate on the Levels of IL-6, Anxiety and Disability in Multiple Sclerosis Patients.

BACKGROUND: Due to the inflammatory nature of multiple sclerosis (MS), interleukin 6 (IL-6) is high in blood levels, and it also increases the levels of anxiety related to functional disability. Epigallocatechin gallate (EGCG) decreases IL-6, which could be enhanced by the anti-inflammatory effect of high ketone bodies after administering coconut oil (both of which are an anxiolytic). Therefore, the aim of this study was to assess the impact of coconut oil and EGCG on the levels of IL-6, anxiety and functional disability in patients with MS. METHODS: A pilot study was conducted for four 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. Both groups followed the same isocaloric Mediterranean diet. State and trait anxiety were determined before and after the study by means of the State-Trait Anxiety Inventory (STAI). In addition, IL-6 in serum was measured using the ELISA technique and functional capacity was determined with the Expanded Disability Status Scale (EDSS) and the body mass index (BMI). RESULTS: State anxiety and functional capacity decreased in the intervention group and IL-6 decreased in both groups. CONCLUSIONS: EGCG and coconut oil improve state anxiety and functional capacity. In addition, a decrease in IL-6 is observed in patients with MS, possibly due to the antioxidant capacity of the Mediterranean diet and its impact on improving BMI.

Efficacy of a mixture of neem seed oil (Azadirachta indica) and coconut oil (Cocos nucifera) for topical treatment of tungiasis. A randomized controlled, proof-of-principle study.

BACKGROUND: Tungiasis is a neglected tropical skin disease caused by the female sand flea (Tunga penetrans), which burrows into the skin causing intense pain, itching and debilitation. People in endemic countries do not have access to an effective and safe home treatment. The aim of this study was to determine the efficacy of a traditionally used and readily available mixture of neem and coconut oil for treatment of tungiasis in coastal Kenya. METHODOLOGY: Ninety-six children aged 6-14 years with at least one embedded viable flea were randomized to be treated with either a mixture of 20% neem (Azadirachta indica) seed oil in coconut oil (NC), or with a 0.05% potassium permanganate (KMnO4) foot bath. Up to two viable fleas were selected for each participant and monitored for 6 days after first treatment using a digital microscope for signs of viability and abnormal development. Acute pathology was assessed on all areas of the feet using a previously established score. Children reported pain levels and itching on a visual scale. RESULTS: The NC was not more effective in killing embedded sand fleas within 7 days than the current standard with KMnO4, killing on average 40% of the embedded sand fleas six days after the initial treatment. However, the NC was superior with respect to the secondary outcomes of abnormal development and reduced pathology. There was a higher odds that fleas rapidly aged in response to NC compared to KMnO4 (OR 3.4, 95% CI: 1.22-9.49, p = 0.019). NC also reduced acute pathology (p<0.005), and there was a higher odds of children being pain free (OR 3.5, p = 0.001) when treated with NC. CONCLUSIONS: Whilst NC did not kill more fleas than KMnO4 within 7 days, secondary outcomes were better and suggest that a higher impact might have been observed at a longer observation period. Further trials are warranted to assess optimal mixtures and dosages. TRIAL REGISTRATION: The study was approved by the Kenya Medical Research Institute (KEMRI) Scientific and Ethical Review Unit (SERU), Nairobi (Non-SSC Protocol No. 514, 1st April 2016) and approved by and registered with the Pharmacy and Poisons Board's Expert Committee on Clinical Trials PPB/ECCT/16/05/03/2016(94), the authority mandated, by Cap 244 Laws of Kenya, to regulate clinical trials in the country. The trial was also registered with the Pan African Clinical Trial Registry (PACTR201901905832601).

Virgin coconut oil supplementation in diet modulates immunity mediated through survival signaling pathways in rats.

Background Virgin coconut oil (VCO), a cold processed form of coconut oil, is traditionally consumed in Asian countries owing to its nutritional and medicinal properties. The aim of this study was to investigate whether the health benefits of VCO involve alterations in immune responses that are regulated by intracellular signaling molecules in the spleens of rats. Methods Young male Wistar rats were fed with three doses of VCO in diet for 30 days. At the end of the treatment period, spleens were isolated and in vitro effects on immune responses (Concanavalin A [Con A]-induced lymphoproliferation and cytokine production), and direct effects of VCO treatment on intracellular signaling molecules and antioxidant status were examined. Serum was collected to measure glucose, lipid levels, and leptin. Results VCO supplementation in diet enhanced Con A-induced splenocyte proliferation and Th1 cytokine production while it suppressed the proinflammatory cytokine production. VCO increased the expression of mechanistic target of rapamycin (p-mTOR), sirtuin1 (SIRT1), liver kinase B1 (p-LKB1) p-ERK, and p-CREB in spleen. Similarly, VCO increased the activities of antioxidant enzymes while it suppressed lipid peroxidation in the spleen. VCO diet had hypolipidemic effects on the rats: an increase in high density lipoprotein cholesterol (HDL-C) levels while lowering triacylglycerol (TAG) levels. Conclusion The health benefits of VCO may be mediated through enhanced Th1 immunity through the upregulation of survival signaling pathways and inhibition of free radical generation in the spleen besides its capacity to induce hypolipidemia.

Feasibility of cultivation of Spinibarbus sinensis with coconut oil and its effect on disease resistance (nonspecific immunity, antioxidation and mTOR and NF-kB signaling pathways).

Application of traditional bait in aquaculture caused environment pollution and disease frequent occurrence. Residual coconut could be re-utilized to culture Spinibarbus sinensis as dietary supplement. Therefore, a novel integrated system of the improvement of yield, antioxidant and nonspecific immunity of Spinibarbus sinensis by dietary residual coconut was proposed and investigated. Spinibarbus sinensis could grow well in all supplement residual coconut groups. Survival rate, yield, whole fish body composition under 15-45% groups were increased compared with control group (CK). Bioactive substances (polyphenols and vitamin) in residual coconut enhanced AKP, ACP, phagocytic, SOD, CAT activities through up-regulating AKP, ACP, SOD, CAT genes expression levels. Theoretical analysis showed bioactive substances regulated these genes expressions and enzyme activities as stimulus signal, component, active center. Moreover, residual coconut improved mTOR and NF-kB signaling pathway. Furthermore, residual coconut inhibited Aeromonas hydrophila that increased resistance to diseases. This technology completed the solid waste recovery and the Spinibarbus sinensis culture simultaneously.

Acute Caffeine and Coconut Oil Intake, Isolated or Combined, Does Not Improve Running Times of Recreational Runners: A Randomized, Placebo-Controlled and Crossover Study.

The aim was to evaluate the effect of caffeine (CAF) and extra virgin coconut oil (CO), isolated or combined, on running performance in runners. Methods: A randomized, placebo-controlled, and crossover study was conducted with thirteen recreational runners aged 18-40. All volunteers performed a 1600 m time trial at a 400 m track, each ingesting four different substances: (1) placebo (water), (2) decaffeinated coffee plus isolated CAF (DECAF + CAF), (3) decaffeinated coffee plus isolated CAF plus soy oil (DECAF + CAF + SO), and (4) decaffeinated coffee plus isolated CAF plus extra virgin coconut oil (DECAF + CAF + CO). The substances were ingested 60 min before the trials, the order of the situations was randomized, and there were one-week intervals between them. At the end of the trials, the Borg scale was applied to evaluate the rating of perceived exertion (RPE) and the time was measured. Results: Our data did not show differences in running time among the trials (placebo: 7.64 ± 0.80, DECAF + CAF: 7.61 ± 1.02, DECAF + CAF + SO: 7.66 ± 0.89, and DECAF + CAF + CO: 7.58 ± 0.74 min; p = 0.93), nor RPE (placebo: 6.15 ± 2.03, DECAF + CAF: 6.00 ± 2.27, DECAF + CAF + SO: 6.54 ± 2.73, and DECAF + CAF + CO: 6.00 ± 2.45 score; p = 0.99). Lactate concentrations (placebo: 6.23 ± 2.72, DECAF + CAF: 4.43 ± 3.77, DECAF + CAF + SO: 5.29 ± 3.77, and DECAF + CAF + CO: 6.17 ± 4.18 mmol/L; p = 0.55) also was not modified. Conclusion: Our study shows that ingestion of decaffeinated coffee with the addition of isolated CAF and extra virgin CO, either isolated or combined, does not improve 1600 m running times, nor influence RPE and lactate concentrations in recreational runners. Thus, combination of coffee with CO as a pre-workout supplement seems to be unsubstantiated for a short-distance race.

Moringa oleifera seed oil or virgin coconut oil supplementation abrogates cerebral neurotoxicity induced by antineoplastic agent methotrexate by suppression of oxidative stress and neuro-inflammation in rats.

Methotrexate (MTX) is an effective antineoplastic drug associated with wide organ toxicity. Accumulating evidence implicates oxidative stress to be a leading underlying mechanism of MTX-induced neurotoxicity. The study explores antioxidant potential of virgin coconut oil (VCO) or Moringa oleifera seed oil (MOO) in MTX-induced oxidative stress-mediated cerebral neurotoxicity and inflammation in rats. Rats treated with VCO or MOO (5 ml/kg bw) for 17 days were administered MTX (20 mg/kg, intraperitoneally) on day 14 only. Cerebral activities of acetylcholinesterase, antioxidant enzymes, lipid peroxidation, reduced glutathione and nitric oxide levels as well as cytokines were evaluated. MTX-induced neurotoxic alterations were significantly abrogated by MOO and VCO supplementation via inhibition of cholinesterase, oxidative stress, and anti-inflammatory mechanisms. VCO and MOO showed comparable antioxidant potentials with the standards in DPPH and FRAP assays. VCO and MOO are promising natural oils for modulating MTX neurotoxicity in cancer patients. PRACTICAL APPLICATIONS: Methotrexate chemotherapy induces neurotoxicity in cancer patients, and this is a source of worry for clinicians. This study reports, for the first time, the beneficial health effects of functional food oils, Moringa oleifera seed oil, and virgin coconut oil against anticancer drug methotrexate-induced cerebral neurotoxicity. Supplementation of these natural oils may be beneficial in the prevention of cerebral neurotoxic side effect in cancer patients undergoing methotrexate chemotherapy.

Short-term supplement of virgin coconut oil improves endothelial-dependent dilation but not exercise-mediated hyperemia in young adults.

Virgin coconut oil (VCO) is high in antioxidants, which reduce reactive oxygen species-induced conversion of vascular endothelial-derived nitric oxide (NO) to toxic peroxynitrite. As such, flow-mediated dilation (FMD, a surrogate marker of NO bioavailability) and exercise-mediated hyperemia may be enhanced following VCO treatment. Animal research supports these findings, but direct assessments of FMD after short-term VCO use in humans are unknown. We tested the hypotheses that a 4-week VCO supplement (30 mL·d-1) would improve popliteal artery (PA) FMD and the hyperemic response to aerobic exercise. Thirty-four young adults were divided into VCO (n = 19, 9 women, 22 ±â€¯2 years, 24 ±â€¯3 kg·m-2) and control (CON: n = 15, 7 women, 24 ±â€¯2 years, 24 ±â€¯3 kg·m-2) groups. PA-FMD and blood flow were assessed via high-resolution duplex ultrasonography (Vivid i, GE Healthcare, Mississauga, Ontario, Canada). PA blood flow was measured at rest and for 5 minutes following a 10-minute bout of moderate-intensity (60% heart rate reserve) cycling exercise. Total PA blood volume was calculated as the integral of the 5-minute postexercise PA blood flow response. After 4 weeks, PA-FMD increased (P = .04) following VCO supplementation (4.9% ±â€¯0.9% to 5.5% ±â€¯1.2%) with no change (P > .9) in the CON group (5.7% ±â€¯2.1% to 5.8% ±â€¯1.9%). There were no differences (both P > .28) in the postexercise total PA blood volume response in either group (VCO: 495 ±â€¯355 to 598 ±â€¯384 mL; CON: 562 ±â€¯362 to 488 ±â€¯229 mL). Short-term VCO supplementation does not alter aerobic exercise-mediated blood flow responses in young adults. However, the augmented popliteal FMD response observed in the VCO supplement group indicates that short-term VCO supplementation improves vascular endothelial function in young, healthy adults.

Changes in the diet composition of fatty acids and fiber affect the lower gastrointestinal motility but have no impact on cardiovascular parameters: In vivo and in vitro studies.

BACKGROUND: Food and diet are central issues for proper functioning of the cardiovascular (CV) system and gastrointestinal (GI) tract. We hypothesize that different types of dietary FAs affect CV parameters as well as GI motor function and visceral sensitivity. METHODS: Male Wistar rats were fed with control diet (CTRL), diet supplemented with 7% soybean oil (SOY), SOY + 3.5% virgin coconut oil (COCO), and SOY + 3.5% evening primrose oil (EP) for 4 weeks. The content of insoluble fiber in CTRL was higher than in SOY, COCO, or EP. Body weight gain and food/water intake were measured. At day 28, biometric, biochemical, CV parameters, GI motor function (X-ray and colon bead expulsion test), and visceral sensitivity were evaluated. Changes in propulsive colonic activity were determined in vitro. The colon and adipose tissue were histologically studied; the number of mast cells (MCs) in the colon was calculated. RESULTS: SOY, COCO, and EP had increased body weight gain but decreased food intake vs CTRL. Water consumption, biometric, biochemical, and CV parameters were comparable between groups. SOY increased the sensitivity to colonic distention. All groups maintained regular propulsive neurogenic contractions; EP delayed colonic motility (P < 0.01). SOY, COCO, and EP displayed decreased size of the cecum, lower number and size of fecal pellets, and higher infiltration of MCs to the colon (P < 0.001). CONCLUSIONS AND INFERENCES: Dietary FAs supplementation and lower intake of insoluble fiber can induce changes in the motility of the lower GI tract, in vivo and in vitro, but CV function and visceral sensitivity are not generally affected.

Maternal coconut oil intake on lactation programs for endocannabinoid system dysfunction in adult offspring.

Maternal exposure to coconut oil metabolically programs adult offspring for overweight, hyperphagia and hyperleptinemia. We studied the neuroendocrine mechanisms by which coconut oil supplementation during breastfeeding as well as continued exposure of this oil throughout life affect the feeding behavior of the progeny. At birth, pups were divided into two groups: Soybean oil (SO) and Coconut oil (CO). Dams received these oils by gavage (0.5 g/kg body mass/day) during lactation. Half of the CO group continued to receive CO in chow throughout life (CO + C). Adult CO and CO + C groups had overweight; the CO group had hyperphagia, higher visceral adiposity, and hyperleptinemia, while the CO + C group had hypophagia only. The CO group showed higher DAGLα (endocannabinoid synthesis) but no alteration of FAAH (endocannabinoid degradation) or CB1R. Leptin signaling and GLP1R were unchanged in the CO group, which did not explain its phenotype. Hyperphagia in these animals can be due to higher DAGLα, increasing the production of 2-AG, an orexigenic mediator. The CO + C group had higher preference for fat and lower hypothalamic GLP1R content. Continuous exposure to coconut oil prevented an increase in DAGLα. The CO + C group, although hypophagic, showed greater voracity when exposed to a hyperlipidemic diet, maybe due to lower GLP1R, since GLP1 inhibits short-term food intake.

Effects of lespedeza condensed tannins alone or with monensin, soybean oil, and coconut oil on feed intake, growth, digestion, ruminal methane emission, and heat energy by yearling Alpine doelings.

Fifty-four Alpine doelings (initial BW and age of 31.7 ± 0.38 kg and 306 ± 1.9 d, respectively) were allocated to nine treatments individually fed for ad libitum intake of 25% concentrate and 75% forage diets (DM basis). Alfalfa was the forage in the control diet. Other diets contained Sericea lespedeza as the forage, with 1.25% DM of quebracho extract included in the concentrate fraction for a dietary condensed tannin level of 8.4%. Lespedeza treatments were no additive (L) and inclusion of monensin (I) at 22 mg/kg DM (L-I), soybean oil at 3% (L-S), coconut oil at 3% (L-N), I and 3% soybean oil (L-I-S), I and 3% coconut oil (L-I-N), 1.5% soybean oil and 1.5% coconut oil (L-S-N), and I, 1.5% soybean oil, and 1.5% coconut oil (L-I-S-N). The experiment was 12 wk with two 6-wk periods. Gas exchange was determined in weeks 6 and 12, and other measures occurred in weeks 5 and 11. The control diet offered averaged 2.67% nitrogen, 43.8% neutral detergent fiber, and 8.8% acid detergent lignin, and the L diet offered averaged 2.03% nitrogen, 42.8% neutral detergent fiber, and 13.2% acid detergent lignin. There were no treatment × period interactions for digestibilities (P ≥ 0.770) or methane emission (P ≥ 0.324). There were differences (P < 0.001) between the control treatment and diets with lespedeza in intake of DM (1.46, 1.23, 1.30, 1.18, 1.32, 1.10, 1.02, 1.20, and 1.01 kg/d; SEM = 0.059), digestibility of OM (57.4%, 50.9%, 51.8%, 52.7%, 50.3%, 52.1%, 52.1%, 51.9%, and 49.8%; SEM = 1.42), and digestibility of nitrogen (59.1%, 31.2%, 32.5%, 37.1%, 31.6%, 38.3%, 30.4%, 38.4%, and 34.1% for control, L, L-I, L-S, L-N, L-I-S, L-I-N, L-S-N, and L-I-S-N, respectively; SEM = 2.21). Ruminal methane emission was less (P < 0.001) for diets with lespedeza than for the control in MJ/d (1.36, 0.76, 0.84, 0.71, 0.71, 0.66, 0.65, 0.68, and 0.68; SEM = 0.048) and relative to intake of gross energy (5.92%, 3.27%, 3.49%, 3.19%, 2.84%, 2.91%, 3.20%, 3.20%, and 3.27%; SEM = 0.165) and digestible energy (11.19%, 6.98%, 7.40%, 6.38%, 5.90%, 5.69%, 6.37%, 6.38%, and 6.70% for control, L, L-I, L-S, L-N, L-I-S, L-I-N, L-S-N, and L-I-S-N, respectively; SEM = 0.400). In conclusion, the magnitude of effect of condensed tannins from lespedeza and quebracho extract on ruminal methane emission by Alpine doelings did not diminish over time and was not markedly influenced by dietary inclusion of monensin, soybean oil, or coconut oil.