The Potential of Spent Coffee Grounds in Functional Food Development.

Coffee is a popular and widely consumed beverage worldwide, with epidemiological studies showing reduced risk of cardiovascular disease, cancers and non-alcoholic fatty liver disease. However, few studies have investigated the health effects of the post-brewing coffee product, spent coffee grounds (SCG), from either hot- or cold-brew coffee. SCG from hot-brew coffee improved metabolic parameters in rats with diet-induced metabolic syndrome and improved gut microbiome in these rats and in humans; further, SCG reduced energy consumption in humans. SCG contains similar bioactive compounds as the beverage including caffeine, chlorogenic acids, trigonelline, polyphenols and melanoidins, with established health benefits and safety for human consumption. Further, SCG utilisation could reduce the estimated 6-8 million tonnes of waste each year worldwide from production of coffee as a beverage. In this article, we explore SCG as a major by-product of coffee production and consumption, together with the potential economic impacts of health and non-health applications of SCG. The known bioactive compounds present in hot- and cold-brew coffee and SCG show potential effects in cardiovascular disease, cancer, liver disease and metabolic disorders. Based on these potential health benefits of SCG, it is expected that foods including SCG may moderate chronic human disease while reducing the environmental impact of waste otherwise dumped in landfill.

Nannochloropsis oceanica as a Microalgal Food Intervention in Diet-Induced Metabolic Syndrome in Rats.

The microalgal genus Nannochloropsis has broad applicability to produce biofuels, animal feed supplements and other value-added products including proteins, carotenoids and lipids. This study investigated a potential role of N. oceanica in the reversal of metabolic syndrome. Male Wistar rats (n = 48) were divided into four groups in a 16-week protocol. Two groups were fed either corn starch or high-carbohydrate, high-fat diets (C and H, respectively) for the full 16 weeks. The other two groups received C and H diets for eight weeks and then received 5% freeze-dried N. oceanica in these diets for the final eight weeks (CN and HN, respectively) of the protocol. The H diet was high in fructose and sucrose, together with increased saturated and trans fats. H rats developed obesity, hypertension, dyslipidaemia, fatty liver disease and left ventricular fibrosis. N. oceanica increased lean mass in CN and HN rats, possibly due to the increased protein intake, and decreased fat mass in HN rats. Intervention with N. oceanica did not change cardiovascular, liver and metabolic parameters or gut structure. The relative abundance of Oxyphotobacteria in the gut microbiota was increased. N. oceanica may be an effective functional food against metabolic syndrome as a sustainable protein source.

Brown Seaweed Sargassum siliquosum as an Intervention for Diet-Induced Obesity in Male Wistar Rats.

The therapeutic potential of Sargassum siliquosum grown in Australian tropical waters was tested in a rat model of metabolic syndrome. Forty-eight male Wistar rats were divided into four groups of 12 rats and each group was fed a different diet for 16 weeks: corn starch diet (C); high-carbohydrate, high-fat diet (H) containing fructose, sucrose, saturated and trans fats; and C or H diets with 5% S. siliquosum mixed into the food from weeks 9 to 16 (CS and HS). Obesity, hypertension, dyslipidaemia, impaired glucose tolerance, fatty liver and left ventricular fibrosis developed in H rats. In HS rats, S. siliquosum decreased body weight (H, 547 ± 14; HS, 490 ± 16 g), fat mass (H, 248 ± 27; HS, 193 ± 19 g), abdominal fat deposition and liver fat vacuole size but did not reverse cardiovascular and liver effects. H rats showed marked changes in gut microbiota compared to C rats, while S. siliquosum supplementation increased gut microbiota belonging to the family Muribaculaceae. This selective increase in gut microbiota likely complements the prebiotic actions of the alginates. Thus, S. siliquosum may be a useful dietary additive to decrease abdominal and liver fat deposition.

Rind from Purple Mangosteen (Garcinia mangostana) Attenuates Diet-Induced Physiological and Metabolic Changes in Obese Rats.

The pulp of the purple mangosteen, Garcinia mangostana, is a popular tropical fruit but the rind containing xanthones such as α-mangostin together with procyanidins and anthocyanidins is usually discarded as waste. However, this rind has been used in South-East Asia for diarrhoea, dysentery, skin infections and wounds. As xanthones have reported anti-inflammatory and antioxidant responses, this study has determined the bioactive compounds and evaluated the effects of G. mangostana rind on physiological, metabolic, liver and cardiovascular parameters in rats with diet-induced metabolic syndrome. Rats fed a diet with increased simple sugars and saturated fats developed obesity, hypertension, increased left ventricular stiffness, dyslipidaemia and fatty liver. Administration of G. mangostana rind as 5% of the food to rats with diet-induced metabolic syndrome gave a dose of 168 mg/kg/day α-mangostin, 355 mg/kg/day procyanidins, 3.9 mg/kg/day anthocyanins and 11.8 mg/kg/day hydroxycitric acid for 8 weeks which reduced body weight and attenuated physiological and metabolic changes in rats including decreased abdominal fat deposition, decreased abdominal circumference and whole-body fat mass, improved liver structure and function and improved cardiovascular parameters such as systolic blood pressure, left ventricular stiffness and endothelial function. These responses were associated with decreased infiltration of inflammatory cells, decreased deposition of collagen in both heart and liver and decreased mean adipocyte size in retroperitoneal adipose tissues. We conclude that, in rats with diet-induced metabolic syndrome, chronic intake of G. mangostana rind decreased infiltration of inflammatory cells which decreased physiological, metabolic, liver and cardiovascular symptoms.

Caulerpa lentillifera (Sea Grapes) Improves Cardiovascular and Metabolic Health of Rats with Diet-Induced Metabolic Syndrome.

Caulerpa lentillifera (sea grapes) is widely consumed in South-East Asia as a low-energy food with high contents of vitamins and minerals. This study investigated dried sea grapes containing 16.6% insoluble fibre commercially produced in Vietnam as an intervention. We hypothesised that insoluble fibre is the primary metabolite that will reverse diet-induced metabolic syndrome. Male Wistar rats (n = 48) were randomly allocated to four groups in a 16 week protocol. Two groups were fed either corn starch (C) or high-carbohydrate, high-fat (H) diets for the full 16 weeks. The other two groups received C and H diets for eight weeks and then received C. lentillifera added to these diets for the final eight weeks (CCL and HCL, respectively). High-carbohydrate, high-fat diet-fed rats developed obesity, hypertension, dyslipidaemia, fatty liver disease and increased left ventricular collagen deposition. C. lentillifera supplementation in HCL rats decreased body weight, systolic blood pressure, plasma concentrations of total cholesterol and non-esterified fatty acids, inflammatory cells in heart and liver, and visceral adiposity. The Firmicutes to Bacteroidetes ratio decreased in the gut microbiota of HCL rats. Therefore, C. lentillifera attenuated cardiovascular and metabolic symptoms of metabolic syndrome in rats, possibly by preventing infiltration of inflammatory cells together with modulating gut microbiota.

Tropical foods as functional foods for metabolic syndrome.

Tropical foods are an integral part of the traditional diet and form part of traditional medicine in many countries. This review examines the potential of tropical foods to treat signs of metabolic syndrome, defined as a chronic low-grade inflammation leading to obesity, hypertension, impaired glucose tolerance, insulin resistance, dyslipidaemia and fatty liver. It is a major risk factor for cardiovascular and metabolic disease as well as osteoarthritis and some cancers. Tropical foods such as seaweeds and tropical fruits including indigenous fruits such as Davidson's plums are effective in reducing these signs of metabolic syndrome in rats, as well as reducing degeneration of bone cartilage and altering gut microbiome. Further, waste products from tropical fruits including mangosteen rind, coffee pulp and spent coffee grounds provide further options to reduce metabolic syndrome. Production of local tropical foods and local recovery of food waste from these foods could allow the development of commercial, sustainable and cost-effective functional foods in tropical countries. The aim is to develop these functional foods to reduce the incidence of metabolic syndrome and decrease the risk of costly chronic cardiovascular and metabolic disorders locally and globally.

Saskatoon Berry Amelanchier alnifolia Regulates Glucose Metabolism and Improves Cardiovascular and Liver Signs of Diet-Induced Metabolic Syndrome in Rats.

Saskatoon berry (Amelanchier alnifolia) is a potential functional food containing anthocyanins and flavonols, as well as ellagitannins and phenolic acids. We have determined the potential therapeutic effects of Saskatoon berry in diet-induced metabolic syndrome. Nine- to ten-week-old male Wistar rats were randomly assigned to four groups. Two groups were fed on control diets, either corn starch (C) or high-carbohydrate, high-fat diet (H) respectively, for 16 weeks. Two further groups were fed on C or H diet for 16 weeks with Saskatoon berry powder added to the diet for the final 8 weeks (CSSK, HSSK). After 16 weeks, H rats showed symptoms of metabolic syndrome, including increased body weight, visceral adiposity, systolic blood pressure, cardiac fibrosis, plasma concentrations of triglycerides and non-esterified fatty acids, and plasma activities of alanine transaminase and aspartate transaminase. Saskatoon berry intervention normalised body weight and adiposity, improved glucose tolerance, decreased systolic blood pressure, improved heart and liver structure and function with decreased infiltration of inflammatory cells, and decreased plasma total cholesterol. Further, Saskatoon berry normalised liver expression of hexokinase 1 and glycogen phosphorylase and increased glucose 6-phosphatase relative to H rats. These results suggest that Saskatoon berry regulates glycolysis, gluconeogenesis and glycogenesis to improve metabolic syndrome.

Modulation of gut microbiota by spent coffee grounds attenuates diet-induced metabolic syndrome in rats.

Coffee brewing produces spent coffee grounds as waste; few studies have investigated the health benefits of these grounds. This study investigated responses to spent coffee grounds in a diet-induced rat model of metabolic syndrome. Male Wistar rats aged 8-9 weeks were fed either corn starch-rich diet or high-carbohydrate, high-fat diet for 16 weeks, which were supplemented with 5% spent coffee grounds during the last 8 weeks. Rats fed non-supplemented diets were used as controls. High-carbohydrate, high-fat diet-fed rats developed metabolic syndrome including abdominal obesity, impaired glucose tolerance, dyslipidemia, and cardiovascular and liver damage. Body weight, abdominal fat, total body fat mass, systolic blood pressure, and concentrations of plasma triglycerides and non-esterified fatty acids were reduced by spent coffee grounds along with improved glucose tolerance and structure and function of heart and liver. Spent coffee grounds increased the diversity of the gut microbiota and decreased the ratio of Firmicutes to Bacteroidetes. Changes in gut microbiota correlated with the reduction in obesity and improvement in glucose tolerance and systolic blood pressure. These findings indicate that intervention with spent coffee grounds may be useful for managing obesity and metabolic syndrome by altering the gut microbiota, thus increasing the value of this food waste.

Carrageenans from the Red Seaweed Sarconema filiforme Attenuate Symptoms of Diet-Induced Metabolic Syndrome in Rats.

Carrageenans are thickening and gelling agents that may provide health benefits. Iota (ι)-carrageenan, a linear sulfated polysaccharide, is produced by the red seaweed, Sarconema filiforme. This study investigated the potential of this seaweed as a functional food for the reversal of metabolic syndrome and possible mechanisms. Male Wistar rats were divided into four groups in a 16-week protocol: corn starch diet-fed rats (C); C rats supplemented with 5% S. filiforme for the last 8 weeks (CSF); high-carbohydrate, high-fat diet-fed rats (H); and H rats supplemented with 5% S. filiforme for the last 8 weeks (HSF). S. filiforme was produced in tank-based aquaculture yielding 27 g dry weight/day/m2 of culture area. H rats developed obesity, hypertension, dyslipidaemia, glucose intolerance, fatty liver and increased left ventricular collagen deposition. S. filiforme supplementation decreased body weight, abdominal and liver fat, systolic blood pressure, plasma total cholesterol concentrations, and plasma activities of alanine transaminase and aspartate transaminase. S. filiforme supplementation modulated gut microbiota without changing the Firmicutes to Bacteroidetes ratio. S. filiforme improved symptoms of high-carbohydrate, high-fat diet-induced metabolic syndrome in rats. Possible mechanisms include a reduced infiltration of inflammatory cells into organs as well as prebiotic actions in the gastrointestinal tract.

Triacylglycerol-Lowering Effect of Docosahexaenoic Acid Is Not Influenced by Single-Nucleotide Polymorphisms Involved in Lipid Metabolism in Humans.

The triacylglycerol (TAG)-lowering effects of long-chain n-3 fatty acids, and in particular docosahexaenoic acid (DHA), are well documented, although these effects manifest large interindividual variability. The objective of this secondary analysis is to investigate whether common single-nucleotide polymorphisms (SNP) in genes involved in DHA synthesis and TAG metabolism are associated with the responsiveness of blood lipids, lipoprotein, and apolipoprotein concentration to dietary treatment by DHA supplied in high-oleic canola oil (HOCO). In a randomized, crossover-controlled feeding trial, 129 subjects with metabolic syndrome received high-oleic canola oil (HOCO) and high-oleic canola oil supplemented with DHA (HOCO-DHA), each for 4 weeks. During the HOCO-DHA phase, the intake of DHA ranged from 1 to 2.5 g/day. The subjects were genotyped for apolipoprotein E (APOE) isoforms, and SNP including FADS1-rs174561, FADS2-rs174583, ELOVL2-rs953413, ELOVL5-rs2397142, CETP-rs5882, SCD1-rs2234970, PPARA-rs6008259, and LIPF-rs814628 were selected as important genes controlling fatty acid metabolism. Overall, consumption of HOCO-DHA oil reduced blood concentrations of TAG by 24% compared to HOCO oil. The reduction in TAG was independent of genetic variations in the studied genes. Similarly, no treatment-by-gene interactions were evident in the response to other lipids, lipoproteins, or apolipoproteins to DHA supplementation. Nevertheless, a lower interindividual variation in the TAG response to DHA supplementation compared to other studies was observed in this analysis. The TAG-lowering effect of a supplemental body-weight-based dose of DHA was not influenced by genetic variations in APOE, FADS1, FADS2, ELOVL2, ELOVL5, CETP, SCD1, PPARA, and LIPF.

Achacha (Garcinia humilis) Rind Improves Cardiovascular Function in Rats with Diet-Induced Metabolic Syndrome.

Garcinia humilis is a fruit known as achachairú. It is native to South American countries such as Bolivia, Peru, and Brazil, but it is also cultivated as achacha in northern Australia. The aim of this study was to determine the phytochemicals in achacha rind and pulp and to investigate these components as potential treatments for the symptoms of metabolic syndrome. Both rind and pulp contain procyanidins and citric acid rather than hydroxycitric acid. Male Wistar rats (8⁻9 weeks old) were fed with either high-carbohydrate, high-fat, or corn starch diets for 16 weeks. Intervention groups were fed with either diet supplemented with 1.5% G. humilis rind powder or 2.0% G. humilis pulp for the last 8 weeks of the protocol. Rats fed a high-carbohydrate, high-fat diet exhibited hypertension, dyslipidemia, central obesity, impaired glucose tolerance, and non-alcoholic fatty liver disease. G. humilis rind decreased systolic blood pressure, diastolic stiffness, left ventricular inflammatory cell infiltration, and collagen deposition in high-carbohydrate, high-fat diet-fed rats. However, there was no change in glucose tolerance, body weight, or body composition. Therefore, G. humilis rind, usually a food by-product, but not the edible pulp, showed potential cardioprotection with minimal metabolic changes in a rat model of diet-induced metabolic syndrome.

Attenuation of Metabolic Syndrome by EPA/DHA Ethyl Esters in Testosterone-Deficient Obese Rats.

Inducing testosterone deficiency, as the standard treatment of prostate cancer, may cause metabolic disorders including insulin resistance, dyslipidemia, central obesity, cardiovascular diseases, and type 2 diabetes. This study measured responses to testosterone deficiency in high-carbohydrate, high-fat (H) diet-fed rats. We then tested whether eicosapentaenoic acid (EPA)/docosahexaenoic acid (DHA) ethyl esters (Omacor) reversed these metabolic changes. Male Wistar rats (8⁻9 weeks old) were divided into eight groups with four groups fed corn starch and four groups fed H diet. For each diet, one group received diet only; one group was orchidectomized; one group was given leuprolide (gonadotrophin-releasing hormone agonist, 2 mg/kg every 4th week); and the last group was treated with leuprolide and their diet was supplemented with 3% Omacor for the last eight weeks. The protocol was for 16 weeks. Leuprolide worsened metabolic syndrome symptoms and cardiovascular function, and orchidectomy produced greater responses. In H fed leuprolide-treated rats, Omacor decreased systolic blood pressure and left ventricular diastolic stiffness, reduced infiltration of inflammatory cells and collagen deposition in the heart, and reduced lipid accumulation and inflammatory cell infiltration without improving liver damage. These results suggest that Omacor has potential to attenuate metabolic complications in prostate cancer patients with induced testosterone deprivation.

Nutraceuticals in rodent models as potential treatments for human Inflammatory Bowel Disease.

Inflammatory Bowel Disease (IBD) is characterized by chronic inflammation of all or part of the digestive tract. Nutraceuticals include bioactive compounds such as polyphenols with anti-inflammatory activities, thus these products have the potential to treat chronic inflammatory diseases. We have emphasized the role of nutraceuticals in ameliorating the symptoms of IBD in rodent models of human IBD through modulation of key pathogenic mechanisms including dysbiosis, oxidative stress, increased inflammatory cytokines, immune system dysregulation, and inflammatory cell signaling pathways. Nutraceuticals have an important role in IBD patients as a preventive approach to extend remission phases and as a therapeutic intervention to suppress active IBD. Further clinical trials on nutraceuticals with positive results in rodent models are warranted.

Kappaphycus alvarezii as a Food Supplement Prevents Diet-Induced Metabolic Syndrome in Rats.

The red seaweed, Kappaphycus alvarezii, was evaluated for its potential to prevent signs of metabolic syndrome through use as a whole food supplement. Major biochemical components of dried Kappaphycus are carrageenan (soluble fiber ~34.6%) and salt (predominantly potassium (K) 20%) with a low overall energy content for whole seaweed. Eight to nine week old male Wistar rats were randomly divided into three groups and fed for 8 weeks on a corn starch diet, a high-carbohydrate, high-fat (H) diet, alone or supplemented with a 5% (w/w) dried and milled Kappaphycus blended into the base diet. H-fed rats showed symptoms of metabolic syndrome including increased body weight, total fat mass, systolic blood pressure, left ventricular collagen deposition, plasma triglycerides, and plasma non-esterified fatty acids along with fatty liver. Relative to these obese rats, Kappaphycus-treated rats showed normalized body weight and adiposity, lower systolic blood pressure, improved heart and liver structure, and lower plasma lipids, even in presence of H diet. Kappaphycus modulated the balance between Firmicutes and Bacteroidetes in the gut, which could serve as the potential mechanism for improved metabolic variables; this was accompanied by no damage to the gut structure. Thus, whole Kappaphycus improved cardiovascular, liver, and metabolic parameters in obese rats.

Selenium, Vanadium, and Chromium as Micronutrients to Improve Metabolic Syndrome.

Trace metals play an important role in the proper functioning of carbohydrate and lipid metabolism. Some of the trace metals are thus essential for maintaining homeostasis, while deficiency of these trace metals can cause disorders with metabolic and physiological imbalances. This article concentrates on three trace metals (selenium, vanadium, and chromium) that may play crucial roles in controlling blood glucose concentrations possibly through their insulin-mimetic effects. For these trace metals, the level of evidence available for their health effects as supplements is weak. Thus, their potential is not fully exploited for the target of metabolic syndrome, a constellation that increases the risk for cardiovascular disease and type 2 diabetes. Given that the prevalence of metabolic syndrome is increasing throughout the world, a simpler option of interventions with food supplemented with well-studied trace metals could serve as an answer to this problem. The oxidation state and coordination chemistry play crucial roles in defining the responses to these trace metals, so further research is warranted to understand fully their metabolic and cardiovascular effects in human metabolic syndrome.

Cyanidin 3-glucoside improves diet-induced metabolic syndrome in rats.

Increased consumption of dark-coloured fruits and vegetables may mitigate metabolic syndrome. This study has determined the changes in metabolic parameters, and in cardiovascular and liver structure and function, following chronic administration of either cyanidin 3-glucoside (CG) or Queen Garnet plum juice (QG) containing cyanidin glycosides to rats fed either a corn starch (C) or a high-carbohydrate, high-fat (H) diet. Eight to nine-week-old male Wistar rats were randomly divided into six groups for 16-week feeding with C, C with CG or QG, H or H with CG or QG. C or H were supplemented with CG or QG at a dose of ∼ 8 mg/kg/day cyanidin glycosides from week 8 to 16. H rats developed signs of metabolic syndrome including visceral adiposity, impaired glucose tolerance, hypertension, cardiovascular remodelling, increased collagen deposition in left ventricle, non-alcoholic fatty liver disease, increased plasma liver enzymes and increased inflammatory cell infiltration in the heart and liver. Both CG and QG reversed these cardiovascular, liver and metabolic signs. However, no intact anthocyanins or common methylated/conjugated metabolites could be detected in the plasma samples and plasma hippuric acid concentrations were unchanged. Our results suggest CG is the most likely mediator of the responses to QG but that further investigation of the pharmacokinetics of oral CG in rats is required.

Modulation of tissue fatty acids by L-carnitine attenuates metabolic syndrome in diet-induced obese rats.

Obesity and dyslipidaemia are metabolic defects resulting from impaired lipid metabolism. These impairments are associated with the development of cardiovascular disease and non-alcoholic fatty liver disease. Correcting the defects in lipid metabolism may attenuate obesity and dyslipidaemia, and reduce cardiovascular risk and liver damage. L-Carnitine supplementation was used in this study to enhance fatty acid oxidation so as to ameliorate diet-induced disturbances in lipid metabolism. Male Wistar rats (8-9 weeks old) were fed with either corn starch or high-carbohydrate, high-fat diets for 16 weeks. Separate groups were supplemented with L-carnitine (1.2% in food) on either diet for the last 8 weeks of the protocol. High-carbohydrate, high-fat diet-fed rats showed central obesity, dyslipidaemia, hypertension, impaired glucose tolerance, hyperinsulinaemia, cardiovascular remodelling and non-alcoholic fatty liver disease. L-Carnitine supplementation attenuated these high-carbohydrate, high-fat diet-induced changes, together with modifications in lipid metabolism including the inhibition of stearoyl-CoA desaturase-1 activity, reduced storage of short-chain monounsaturated fatty acids in the tissues with decreased linoleic acid content and trans fatty acids stored in retroperitoneal fat. Thus, L-carnitine supplementation attenuated the signs of metabolic syndrome through inhibition of stearoyl-CoA desaturase-1 activity, preferential ß-oxidation of some fatty acids and increased storage of saturated fatty acids and relatively inert oleic acid in the tissues.

Cardioprotective and hepatoprotective effects of ellagitannins from European oak bark (Quercus petraea L.) extract in rats.

BACKGROUND: Red wine contains many potentially bioactive polyphenols including resveratrol, catechins, anthocyanins and flavonoids as well as tannins derived from oak during maturation. This study examined the effects of a mixture of ellagitannins from oak bark (Quercus petraea L.) on cardiovascular, metabolic and liver changes in high-carbohydrate, high-fat diet-fed rats and in Spontaneously Hypertensive Rats (SHR). METHODS: First, 8-week-old male Wistar rats were divided into four groups and given either cornstarch diet, cornstarch diet + oak bark extract (0.5 mL/kg food), high-carbohydrate, high-fat diet or high-carbohydrate, high-fat diet + oak bark extract (0.5 mL/kg food) for 16 weeks. Oak bark extract was added to the diets for last 8 weeks of the feeding period. Secondly, SHR aged 42 weeks fed on standard chow diet were divided into two groups with and without oak bark extract treatment for 12 weeks (0.5 mL/kg food). RESULTS: The high-carbohydrate, high-fat diet induced signs of metabolic syndrome along with cardiovascular remodelling and non-alcoholic steatohepatitis. Oak bark extract attenuated the signs of metabolic syndrome in high-carbohydrate, high-fat diet-fed rats and improved the structure and function of the heart and the liver. SHR after oak bark extract treatment for 12 weeks showed lower systolic blood pressure, lower cardiac fibrosis and cardiac stiffness and improved vascular reactivity. CONCLUSIONS: Oak bark extract containing ellagitannins improved cardiovascular, metabolic and liver parameters in these rat models of human disease, suggesting that part of the benefits attributed to red wine may be produced by these ellagitannins.

Effects of ALA, EPA and DHA in high-carbohydrate, high-fat diet-induced metabolic syndrome in rats.

We compared the cardiovascular, hepatic and metabolic responses to individual dietary n-3 fatty acids (α-linolenic acid, ALA; eicosapentaenoic acid, EPA; and docosahexaenoic acid, DHA) in a high-carbohydrate, high-fat diet-induced model of metabolic syndrome in rats. Additionally, we measured fatty acid composition of plasma, adipose tissue, liver, heart and skeletal muscle in these rats. The same dosages of ALA and EPA/DHA produced different physiological responses to decrease the risk factors for metabolic syndrome. ALA did not reduce total body fat but induced lipid redistribution away from the abdominal area and favorably improved glucose tolerance, insulin sensitivity, dyslipidemia, hypertension and left ventricular dimensions, contractility, volumes and stiffness. EPA and DHA increased sympathetic activation, reduced the abdominal adiposity and total body fat and attenuated insulin sensitivity, dyslipidemia, hypertension and left ventricular stiffness but not glucose tolerance. However, ALA, EPA and DHA all reduced inflammation in both the heart and the liver, cardiac fibrosis and hepatic steatosis. These effects were associated with complete suppression of stearoyl-CoA desaturase 1 activity. Since the physiological responses to EPA and DHA were similar, it is likely that the effects are mediated by DHA with EPA serving as a precursor. Also, ALA supplementation increased DHA concentrations but induced different physiological responses to EPA and DHA. This result strongly suggests that ALA has independent effects in metabolic syndrome, not relying on its metabolism to DHA.