The effect of beta-sitosterol on the metabolism of cholesterol and lipids in rats on a diet containing coconut oil.
Ontology highlight
ABSTRACT:
SUBMITTER: Gerson T
PROVIDER: S-EPMC1207053 | biostudies-other | 1965 Aug
REPOSITORIES: biostudies-other
Similar Datasets
Project description:BackgroundDiets containing fats of different proportions and types have been demonstrated to influence metabolism. These fats differ in long chain fatty acids (LCFAs) or medium chain fatty acids (MCFAs) content. In our laboratory using swimming as the training modality, MCFAs increased endurance attributed to increased activities of oxidative enzymes. How it affects whole-body metabolism remains unexplored. The present study investigated the metabolic, biochemical and genetic adaptations with treadmill running as the training modality.MethodsC57BL/6N mice were divided into untrained and trained groups and provided with low-fat (10% kcal from soybean oil), coconut oil (10% kcal from soybean oil, 20% kcal from coconut oil) or soybean oil (30% kcal from soybean oil) diet. Training was performed on a treadmill for 30 days. After recovery, whole-body metabolism at rest and during exercise, endurance, substrate metabolism, mitochondrial enzyme activities, and gene expression of training-adaptive genes in the muscle and liver were measured.ResultsAt rest, medium-fat diets decreased respiratory exchange ratio (RER) (p < 0.05). Training increased RER in all diet groups without affecting oxygen consumption (p < 0.05). During exercise, diets had no overt effects on metabolism while training decreased oxygen consumption indicating decreased energy expenditure (p < 0.05). Coconut oil without training improved endurance based on work (p < 0.05). Training improved all endurance parameters without overt effects of diet (p < 0.05). Moreover, training increased the activities of mitochondrial enzymes likely related to the increased expression of estrogen related receptor (ERR) α and ERRβ (p < 0.05). Coconut oil inhibited peroxisome proliferator-activated receptor (PPAR) β/δ activation and glycogen accumulation in the muscle but activated PPARα in the liver in the trained state (p < 0.05). Substrate utilization data suggested that coconut oil and/or resulting ketone bodies spared glycogen utilization in the trained muscle during exercise thereby preserving endurance.ConclusionOur data demonstrated the various roles of diet and fat types in training adaptation. Diets exerted different roles in PPAR activation and substrate handling in the context of endurance exercise training. However, the role of fat types in training adaptations is limited as training overwhelms and normalizes the effects of diet in the untrained state particularly on endurance performance, mitochondrial biogenesis, and ERR expression.
| S-EPMC6006686 | biostudies-literature
Project description:Background:Few trials have examined the effects of coconut oil consumption in comparison with polyunsaturated fatty acid-rich oils such as corn oil. Objective:This trial assessed the effects of consuming foods made with corn oil compared with coconut oil on lipids, glucose homeostasis, and inflammation. Methods:This was a preliminary randomized crossover study of men (n = 12) and women (n = 13) with a mean age of 45.2 y, mean body mass index (in kg/m2) of 27.7, fasting LDL cholesterol ?115 mg/dL and <190 mg/dL, and triglycerides (TGs) ?375 mg/dL. Subjects consumed muffins and rolls providing 4 tablespoons (?54 g) per day of corn oil or coconut oil as part of their habitual diets for 4 wk, with a 3-wk washout between conditions. Fasting plasma lipids and high-sensitivity C-reactive protein (hs-CRP) and glucose metabolism were assessed via an intravenous glucose tolerance test at baseline and 15 and 29 d of treatment. Responses were compared between treatments by ANCOVA. Results:Median baseline concentrations of LDL cholesterol, non-HDL cholesterol, total cholesterol (total-C), HDL cholesterol, total-C:HDL cholesterol, and TGs were 123, 144, 188, 46.0, 4.21, and 92.5 mg/dL, respectively. Changes from baseline for corn oil and coconut oil conditions, respectively, were: LDL cholesterol (primary outcome; -2.7% compared with +4.6%), non-HDL cholesterol (-3.0% compared with +5.8%), total-C (-0.5% compared with +7.1%), HDL cholesterol (+5.4% compared with +6.5%), total-C:HDL cholesterol (-4.3% compared with -3.3%), and TGs (-2.1% compared with +6.0%). Non-HDL cholesterol responses were significantly different between corn and coconut oil conditions (P = 0.034); differences between conditions in total-C and LDL cholesterol approached significance (both P = 0.06). Responses for hs-CRP and carbohydrate homeostasis parameters did not differ significantly between diet conditions. Conclusions:When incorporated into the habitual diet, consumption of foods providing ?54 g of corn oil/d produced a more favorable plasma lipid profile than did coconut oil in adults with elevated cholesterol. This trial was registered at clinicaltrials.gov as NCT03202654.
| S-EPMC6168703 | biostudies-literature
Project description:Despite its 50-year history, the conventional diet-heart hypothesis holding that dietary saturated fats raise serum cholesterol, and with it, cardiovascular risk, remains controversial. Harsh chemical and physical treatment generates process contaminants, and refined oils raise serum and tissue cholesterol in vivo independent of saturated fat content. We developed an in vitro bioassay for rapidly assessing the influence of oils on cholesterol metabolism in the human liver HepG2 cell line, and tested it using coconut oil (CO) of various stages of refinement. CO was dissolved with dipalmitoyl phosphatidylcholine (DPPC) surfactant, solvent evaporated, and emulsified into fat-free cell culture media. After 24?h treatment cellular cholesterol and triacylglycerol increased; HMG-CoA Reductase (HMGCR) increased and CYP7A1 (cholesterol 7?-hydroxylase) decreased with sequential processing steps, deacidification, bleaching, deodorization, while fatty acid profiles were not affected. Glycerol-derived process contaminants glycidyl esters and monochloropropandiol (MCPD) increased with processing. Addition of glycidyl or MCPD to virgin CO (VCO) had similar effects to processing, while addition of phenolic antioxidants to fully refined CO reduced HMGCR and increased CYP7A1. We conclude that harsh processing creates contaminants that raise cholesterol levels in vitro, consistent with a role as a contributing atherosclerotic factor.
| S-EPMC6467815 | biostudies-literature
Project description:ObjectiveTo investigate and compare the effects of two common dietary phytosterols, stigmasterol and β-sitosterol, in altering lipid metabolism and attenuating nonalcoholic fatty liver disease (NAFLD).MethodsStigmasterol and β-sitosterol were administered to mice at 0.4% in a high-fat western-style diet (HFWD) for 17 weeks.ResultsStigmasterol and β-sitosterol significantly ameliorated HFWD-induced fatty liver and metabolic abnormalities, including elevated levels of hepatic total lipids, triacylglycerols, cholesterol and liver histopathology. Both phytosterols decreased the levels of intestinal bile acids, accompanied by markedly increased fecal lipid levels. In addition, they altered the expression of genes involved in lipid metabolism. β-Sitosterol was less effective in affecting most of these parameters. Lipidomic analysis of liver and serum samples showed that stigmasterol prevented the HFWD-induced elevation of some di- and triacylglycerol species and lowering of some phospholipid species. Stigmasterol also decreased serum levels of ceramides.ConclusionStigmasterol and β-sitosterol, at a dose corresponding to that suggested for humans by the FDA for lowering cholesterol levels, are shown to alleviate HFWD-induced NAFLD. Stigmasterol was more effective than β-sitosterol, possibly because of its suppression of hepatic lipogenic gene expression and modulation of circulating ceramide levels.
| S-EPMC6226309 | biostudies-literature
Project description:Elevated serum cholesterol level is generally considered to be a risk factor for the development of cardiovascular diseases which seriously threaten human health. The cholesterol-lowering effects of lactic acid bacteria have recently become an area of great interest and controversy for many researchers. In this study, we investigated the effects of two NS lactobacillus strains, Lactobacillus plantarum NS5 and Lactobacillus delbrueckii subsp. bulgaricus NS12, on lipid metabolism of rats fed a high cholesterol diet.Thirty-two SD rats were assigned to four groups and fed either a normal or a high-cholesterol diet. The NS lactobacillus treated groups received the high-cholesterol diet supplemented with Lactobacillus plantarum NS5 or Lactobacillus delbrueckii subsp. bulgaricus NS12 in drinking water. The rats were sacrificed after a 6-week feeding period. Body weights, visceral organ and fat weights, serum and liver cholesterol and lipid levels, intestinal microbiota and liver mRNA expression levels related to cholesterol metabolism were analyzed. Liver lipid deposition and adipocyte size were evaluated histologically.Compared with rats fed a high cholesterol diet, serum total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B and free fatty acids levels were decreased and apolipoprotein A-I level was increased in NS5 or NS12 strain treated rats, and with no significant change in high-density lipoprotein cholesterol level. Liver cholesterol and triglyceride levels were also significantly decreased in NS lactobacillus strains treated groups. Meanwhile, the NS lactobacillus strains obviously alleviated hepatic injuries, decreased liver lipid deposition and reduced adipocyte size of high cholesterol diet fed rats. NS lactobacillus strains restored the changes in intestinal microbiota compositions, such as the increase in Bacteroides and the decrease in Clostridium. NS lactobacillus strains also regulated the mRNA expression levels of liver enzymes related to cholesterol metabolism, including the down regulation of acyl-CoA:cholesterol acyltransferase (ACAT) and the upregulation of cholesterol 7?-hydroxylase (CYP7A1).This study suggested that the two NS lactobacillus strains may affect lipid metabolism and have cholesterol-lowering effects in rats fed a high cholesterol diet.
| S-EPMC3667092 | biostudies-literature
Project description:High dietary saturated fat intake is associated with higher blood concentrations of low-density lipoprotein cholesterol (LDL-C), an established risk factor for coronary heart disease. However, there is increasing interest in whether various dietary oils or fats with different fatty acid profiles such as extra virgin coconut oil may have different metabolic effects but trials have reported inconsistent results. We aimed to compare changes in blood lipid profile, weight, fat distribution and metabolic markers after four weeks consumption of 50?g daily of one of three different dietary fats, extra virgin coconut oil, butter or extra virgin olive oil, in healthy men and women in the general population.Randomised clinical trial conducted over June and July 2017.General community in Cambridgeshire, UK.Volunteer adults were recruited by the British Broadcasting Corporation through their websites. Eligibility criteria were men and women aged 50-75 years, with no known history of cancer, cardiovascular disease or diabetes, not on lipid lowering medication, no contraindications to a high-fat diet and willingness to be randomised to consume one of the three dietary fats for 4?weeks. Of 160 individuals initially expressing an interest and assessed for eligibility, 96 were randomised to one of three interventions; 2 individuals subsequently withdrew and 94 men and women attended a baseline assessment. Their mean age was 60 years, 67% were women and 98% were European Caucasian. Of these, 91 men and women attended a follow-up assessment 4?weeks later.Participants were randomised to extra virgin coconut oil, extra virgin olive oil or unsalted butter and asked to consume 50?g daily of one of these fats for 4?weeks, which they could incorporate into their usual diet or consume as a supplement.The primary outcome was change in serum LDL-C; secondary outcomes were change in total and high-density lipoprotein cholesterol (TC and HDL-C), TC/HDL-C ratio and non-HDL-C; change in weight, body mass index (BMI), waist circumference, per cent body fat, systolic and diastolic blood pressure, fasting plasma glucose and C reactive protein.LDL-C concentrations were significantly increased on butter compared with coconut oil (+0.42, 95%?CI 0.19 to 0.65 mmol/L, P<0.0001) and with olive oil (+0.38, 95%?CI 0.16 to 0.60?mmol/L, P<0.0001), with no differences in change of LDL-C in coconut oil compared with olive oil (-0.04, 95%?CI -0.27 to 0.19?mmol/L, P=0.74). Coconut oil significantly increased HDL-C compared with butter (+0.18, 95%?CI 0.06 to 0.30?mmol/L) or olive oil (+0.16, 95%?CI 0.03 to 0.28?mmol/L). Butter significantly increased TC/HDL-C ratio and non-HDL-C compared with coconut oil but coconut oil did not significantly differ from olive oil for TC/HDL-C and non-HDL-C. There were no significant differences in changes in weight, BMI, central adiposity, fasting blood glucose, systolic or diastolic blood pressure among any of the three intervention groups.Two different dietary fats (butter and coconut oil) which are predominantly saturated fats, appear to have different effects on blood lipids compared with olive oil, a predominantly monounsaturated fat with coconut oil more comparable to olive oil with respect to LDL-C. The effects of different dietary fats on lipid profiles, metabolic markers and health outcomes may vary not just according to the general classification of their main component fatty acids as saturated or unsaturated but possibly according to different profiles in individual fatty acids, processing methods as well as the foods in which they are consumed or dietary patterns. These findings do not alter current dietary recommendations to reduce saturated fat intake in general but highlight the need for further elucidation of the more nuanced relationships between different dietary fats and health.NCT03105947; Results.
| S-EPMC5855206 | biostudies-other
Project description:BackgroundThe purpose of this study is to investigate the effects of a high-fat diet from perilla oil on serum lipids, hepatic lipid metabolism and insulin sensitivity.MethodsMale Sprague-Dawley (SD) rats were fed either a control (CT) diet or a diet high in perilla oil (HP). After 16 weeks of feeding, the serum lipids were measured, and the gene expressions involved in hepatic fatty acid oxidation and synthesis were determined. In addition, hepatic fat deposition was detected, and insulin sensitivity was evaluated by means of euglycemic-hyperinsulinemic clamp.ResultsCompared with the rats in the CT group, the HP-feeding significantly decreased the levels of triglyceride (TG), total cholesterol (TCH) and HDL-cholesterol (HDL-c). HP-feeding did not change the levels of LDL-cholesterol (LDL-c), free fatty acid (FFA), intrahepatic lipids or body weight. Moreover, the HP-feeding dramatically increased the mRNA expressions of fatty acid oxidation markers (PPAR-alpha, CPT1A) and fatty acid synthesis markers (SREBP-1, FASN and ACC) in the liver. The HP-feeding induced increased protein levels of CPT1A, while reducing the protein levels of FASN and ACC in the liver. However, the glucose infusion rate significantly increased in the HP group compared with the CT group.ConclusionsOur data show that, in rats, excessive perilla oil intake may significantly lower serum lipids, strengthen hepatic fatty acid oxidation, and inhibit hepatic fatty acid synthesis, but at the same time may also lead to insulin resistance.
| S-EPMC3904189 | biostudies-literature
Project description:The gut microbiota influences many aspects of host metabolism. We have previously shown that the presence of a gut microbiota remodels lipid composition. Here we investigated how interaction between gut microbiota and dietary lipids regulates lipid composition in the liver and plasma, and gene expression in the liver. Germ-free and conventionally raised mice were fed a lard or fish oil diet for 11 weeks. We performed lipidomics analysis of the liver and serum and microarray analysis of the liver. As expected, most of the variation in the lipidomics dataset was induced by the diet, and abundance of most lipid classes differed between mice fed lard and fish oil. However, the gut microbiota also affected lipid composition. The gut microbiota increased hepatic levels of cholesterol and cholesteryl esters in mice fed lard, but not in mice fed fish oil. Serum levels of cholesterol and cholesteryl esters were not affected by the gut microbiota. Genes encoding enzymes involved in cholesterol biosynthesis were downregulated by the gut microbiota in mice fed lard and were expressed at a low level in mice fed fish oil independent of microbial status. In summary, we show that gut microbiota-induced regulation of hepatic cholesterol metabolism is dependent on dietary lipid composition.
| S-EPMC4766996 | biostudies-literature
Project description:Indigofera zollingeriana Miq (I.zollingeriana) is a widely grown tree in Vietnam. It is used to cure various illnesses. The purpose of this study was to investigate the chemical constituents of an I. zollingeriana extract and test its anticancer activity on hepatocellular cells (Huh7 and HepG2). The experimental results of the analysis of the bioactive compounds revealed that β-sitosterol (β-S) and β-sitosterol-glucoside (β-SG) were the main ingredients of the I.zollingeriana extract. Regarding anticancer activity, the β-S and β-SG of I. zollingeriana were found to exhibit cytotoxic effects against HepG2 and Huh7 cells, but not against normal human primary fibroblasts. The β-S was able to inhibit the proliferation of HepG2 and Huh7 cells in a dose-dependent manner with half-maximal inhibitory concentration (IC50) values of 6.85 ± 0.61 µg/mL and 8.71 ± 0.21 µg/mL, respectively (p < 0.01), whereas the β-SG IC50 values were 4.64 ± 0.48 µg/mL for HepG2 and 5.25 ± 0.14 µg/mL for Huh7 cells (p < 0.01). Remarkably, our study also indicated that β-S and β-SG exhibited cytotoxic activities via inducing apoptosis and activating caspase-3 and -9 in these cells. These findings demonstrated that β-S and β-SG from I.zollingeriana could potentially be developed into promising therapeutic agents to treat liver cancer.
| S-EPMC7411723 | biostudies-literature
Project description: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.
| S-EPMC8552221 | biostudies-literature