Diet-induced Metabolic Syndrome In Rats Research Articles

Beneficial Effects of 6-Gingerol on Fatty Pancreas Disease in High-Fat High-Fructose Diet-Induced Metabolic Syndrome Rat Model.

To examine the effects of 6-gingerol (6-G) in overcoming fatty pancreas disease of high-fat high-fructose (HFHF) diet-induced metabolic syndrome in rats. Male Sprague-Dawley rats were randomly divided into 5 groups. The healthy-control group (normal diet, n = 5) received a standard diet. The HFHF group (HFHF; n = 20) received an HFHF diet and a single-dose intraperitoneal injection of streptozotocin (22 mg/kgBW) at week 8. Metabolic syndrome-confirmed rats received 6-G at doses of 50 (6-G 50, n = 5), 100 (6-G 100, n = 5), and 200 (6-G 200, n = 5) mg/kgBW, respectively, for 8 weeks. All rats were killed at week 16. Pancreatic tissue and blood samples were obtained for histological and amylase analysis. The serum amylase, MDA, mRNA of TNF-α, and IL-6 significantly increased, whereas GPx decreased in the HFHF group as compared with the normal diet group, respectively. Rats in the HFHF group showed pancreatic lipid accumulation and a decreased mean number of α- and β-cells in the pancreas. Meanwhile, all rats in 6-G at all dose groups showed improvement in all parameters and histopathological scores for lipid accumulation. 6-Gingerol could attenuate pancreatic lipid accumulation and improve the cell number of α- and β-cells in the pancreas, leading to improvements in fatty pancreas disease.

Japanese Quince Fruit Juice Exerts a Cardioprotective Effect in a Model of Diet-Induced Metabolic Syndrome in Rats

Summary The current study aimed to evaluate the influence of Japanese quince (Chaenomeles japonica) fruit juice (JQFJ) on the myocardium and on the coronary arteries of rats with diet-induced metabolic syndrome (MS). Male Wistar rats (n=50) were divided into 5 groups: Control, MS, MS+JQFJ2.5, MS+JQFJ5 and MS+JQFJ10. MS was induced with a high-fat high-fructose diet for 10 weeks. During that period, all animals were daily orally treated with distilled water (Control and MS groups) or with JQFJ at doses of 2.5 ml/kg, 5 ml/kg and 10 ml/kg (the other three groups, respectively). At the end of the experiment, the myocardium and coronary arteries were examined histopathologically. In group MS, necrotic endothelial cells and exposed basal membrane were observed. JQFJ at 2.5 ml/kg reduced the impairment but activated endothelial cells were still found. JQFJ at 5 ml/kg and 10 ml/kg prevented coronary artery endothelium damage, preserving the normal morphology. The myocardium in MS group presented with cardiomyocyte degeneration and increased distance between the cells. In group MS+JQFJ2.5, the degeneration was decreased. In groups MS+JQFJ5 and MS+JQFJ10, the histology of the myocardium resembled that of the control group. In the current histopathological evaluation, JQFJ prevented the MS-induced impairment of myocardium and coronary arteries.

Freshwater Macroalgae, Oedogonium, Grown in Wastewater Reduce Diet-Induced Metabolic Syndrome in Rats.

Macroalgae produce compounds with industrial, pharmaceutical and nutritional applications. In this study, biomass from the freshwater macroalgal genus Oedogonium was grown in either treated municipal wastewater (M) or ash dam water from a coal-fired power station (D). The biomass was investigated for its metabolic responses in high-carbohydrate, high-fat diet-fed rats, a model of human metabolic syndrome. The Oedogonium biomass cultured in M contained higher amounts of K, Mg, omega-3 polyunsaturated fatty acids (PUFA), insoluble fibre and β-carotene, while biomass grown in D contained higher amounts of Al, Fe, V, Zn, Mn and As. Biomass from M further increased body weight and inflammation in the heart and colon in high-carbohydrate, high-fat diet-fed rats. In contrast, biomass from D prevented changes in metabolic, cardiovascular and liver parameters without changing tissue histology. We suggest that increased intake of metals and metalloids through macroalgal biomass from D may decrease abdominal fat deposition while polysaccharides, PUFA and carotenoids from M may improve blood glucose responses in an obesogenic diet. Thus, macroalgal biomass grown in different wastewater sources could be acceptable for feed or food applications. This biomass could even provide potential health benefits in diet-induced metabolic syndrome.

Wasabi (Eutrema japonicum) Reduces Obesity and Blood Pressure in Diet-Induced Metabolic Syndrome in Rats.

6-(Methylsulfinyl)hexyl isothiocyanate (6-MSITC) has several biological functions. The present study aimed to evaluate the composition of hydroponically grown Tasmanian wasabi (Eutrema japonicum (Miq.) Koidz.) for 6-MSITC in all plant tissues and investigate the influence of wasabi (rhizome and stem blend) in high-carbohydrate, high-fat (H) diet-fed rats. Male Wistar rats were fed either a corn starch (C) or H diet. After the initial 8 weeks, half of the animals on the C and H diets were given 5% (w/w) wasabi powder in their respective diets for an 8-week duration (CW and HW). The control animals received diets without supplementation throughout the 16-week experiment. Our findings demonstrated that wasabi grown under hydroponic conditions contained 6-MSITC in all parts of the plant such as the stem, leaf and flower, as well as the commonly used rhizome, albeit at lower concentrations. Rats treated with wasabi showed reductions in body weight (H, 460.0 ± 9.5; HW, 416.0 ± 3.6 g), fat mass (H, 178 ± 14; HW, 120 ± 23 g), plasma triglycerides (H, 1.7 ± 0.3; HW, 0.9 ± 0.3 mmol/L) and total cholesterol (H, 1.5 ± 0.1; HW, 1.0 ± 0.04 mmol/L), and the plasma activities of aspartate transaminase. Systolic blood pressure and the area under the curve of blood glucose concentration were decreased by wasabi treatment. Thus, wasabi may be a novel alternative treatment to assist in the management of obesity and related metabolic disorders.

Rosuvastatin and co-enzyme Q10 improve high-fat and high-fructose diet-induced metabolic syndrome in rats via ameliorating inflammatory and oxidative burden

The prevalence of metabolic syndrome (MetS) has been rising alarmingly and it has now become a global concern causing an enormous economic burden on the health care system. MetS is generally linked to complications in lipid metabolism, oxidative stress and low grade inflammation. The aim of the current study was to evaluate the effect of rosuvastatin, co-enzyme Q10 (CoQ10), and their combination on blood pressure, blood sugar, dyslipidemia, and liver function in rats with MetS induced by high fructose and high fat diet (HF-HFD) and the possible underlying mechanism. Oral administration of rosuvastatin (10 mg/kg/day), CoQ10 (10 mg/kg/day) and their combination for 4 weeks in HF-HFD-fed rats elevated serum high density lipoprotein and reduced glutathione. On the other hand, treatment with rosuvastatin, CoQ10 or their combination decreased the serum levels of malondialdehyde, triglycerides, total cholesterol, and low density lipoprotein-cholesterol as well as systolic blood pressure, body weight and fasting blood glucose level. In addition, the drugs or their combination declined serum pro-inflammatory cytokines, namely tumor necrosis factor-α and interleukin-1β. In conclusion, our results showed that rosuvastatin or CoQ10 protected against HF-HFD-induced MetS through the regulation of dyslipidemia, elevated blood glucose, elevated blood pressure, antioxidant defenses and inflammatory response. Rosuvastatin or CoQ10 also alleviated the impairment of liver function that was induced by HF-HFD. Interestingly, CoQ10 augmented rosuvastatin's effect in ameliorating MetS, via exerting synergistic modulatory effects on oxidative stress and inflammation. Thus, rosuvastatin and CoQ10 combination therapy may have possible applications in ameliorating metabolic disorders.

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.

Solasodine with Coenzyme Q10 Supplementation Ameliorates High Fat Diet-Induced Metabolic Syndrome in Rats by Modulating Adipokines and Lipid Peroxidation

Solasodine with Coenzyme Q10 Supplementation Ameliorates High Fat Diet-Induced Metabolic Syndrome in Rats by Modulating Adipokines and Lipid Peroxidation

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.

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.

Pelargonidin 3-glucoside-enriched strawberry attenuates symptoms of DSS-induced inflammatory bowel disease and diet-induced metabolic syndrome in rats.

To determine whether the anthocyanin, pelargonidin 3-glucoside (P3G), attenuates symptoms of inflammatory bowel disease (IBD) and metabolic syndrome in rats. We tested P3G-enriched strawberry in two models of chronic inflammation in rats, chronic IBD induced by 0.5% dextran sodium sulphate in the drinking water for 12weeks (D) and metabolic syndrome induced by a high-carbohydrate, high-fat diet (H) for 16weeks. P3G-enriched strawberry was added to the diet for the final 6weeks in IBD rats (DP) or 8weeks in H rats (HP) to provide a dose of 8mg P3G/kg/day. D rats had marked diarrhoea, bloody stools, erosion of mucosal epithelium, crypt atrophy, loss of villi and goblet cells, and inflammatory cell infiltration. These symptoms were reversed by P3G with healthy stools and mucosal lining of ileum and colon including increased villi, crypts and goblet cells and reduced inflammation. H rats developed hypertension, dyslipidaemia, central obesity, increased ventricular stiffness, cardiac and liver inflammation, and steatosis. P3G treatment in H rats improved systolic blood pressure, ventricular stiffness, and cardiac and liver structure, and reduced abdominal fat, abdominal circumference and body weight gain. Our study indicates that dietary P3G decreased inflammation to decrease the symptoms of IBD, and to improve cardiovascular, liver and metabolic functions in metabolic syndrome.

Linseed Components Are More Effective Than Whole Linseed in Reversing Diet-Induced Metabolic Syndrome in Rats.

Linseed is a dietary source of plant-based ω–3 fatty acids along with fiber as well as lignans including secoisolariciresinol diglucoside (SDG). We investigated the reversal of signs of metabolic syndrome following addition of whole linseed (5%), defatted linseed (3%), or SDG (0.03%) to either a high-carbohydrate, high-fat or corn starch diet for rats for the final eight weeks of a 16–week protocol. All interventions reduced plasma insulin, systolic blood pressure, inflammatory cell infiltration in heart, ventricular collagen deposition, and diastolic stiffness but had no effect on plasma total cholesterol, nonesterified fatty acids, or triglycerides. Whole linseed did not change the body weight or abdominal fat in obese rats while SDG and defatted linseed decreased abdominal fat and defatted linseed increased lean mass. Defatted linseed and SDG, but not whole linseed, improved heart and liver structure, decreased fat vacuoles in liver, and decreased plasma leptin concentrations. These results show that the individual components of linseed produce greater potential therapeutic responses in rats with metabolic syndrome than whole linseed. We suggest that the reduced responses indicate reduced oral bioavailability of the whole seeds compared to the components.

Green coffee ameliorates components of diet-induced metabolic syndrome in rats

Abstract Metabolic syndrome, especially obesity, increases the risk of type 2 diabetes and cardiovascular disease. We hypothesised that green coffee will attenuate metabolic, cardiovascular and liver parameters in high-carbohydrate high-fat diet-fed rats. Male Wistar rats (8–9 weeks old) were divided into 6 groups and fed for 16 weeks with either corn starch diet (C), C with either 5% green or decaffeinated green coffee in food for the last 8 weeks, high-carbohydrate high-fat diet (H) or H with either 5% green or decaffeinated green coffee in food for the last 8 weeks. Green coffee contained chlorogenic acids, trigonelline, caffeine and diterpenoids; decaffeinated green coffee contained these compounds but no caffeine. Green coffee attenuated body weight, systolic blood pressure, inflammation in the heart and liver and diastolic stiffness without improving glucose sensitivity or plasma lipids. We suggest that chlorogenic acids, trigonelline and diterpenoids in green coffee attenuate diet-induced abnormalities in heart and liver.

Queen Garnet plum juice and raspberry cordial in mildly hypertensive obese or overweight subjects: A randomized, double-blind study

Abstract The anthocyanin, cyanidin 3-glucoside, in Queen Garnet (QG) plums reduced cardiovascular parameters, obesity and inflammation in diet-induced metabolic syndrome in rats. We have now assessed whether QG juice improves cardiovascular and metabolic risk factors and markers of inflammation in mildly hypertensive overweight or obese humans. The 32 subjects were randomly divided into two groups consuming either QG juice or Placebo (raspberry cordial) drinks for 12 weeks. QG juice decreased systolic blood pressure by 12 ± 3 mmHg, diastolic blood pressure by 9 ± 2 mmHg, insulin by 6 ± 3 pmol/L, and leptin by 4 ± 2.5 ng/ml, and increased adiponectin by 3.62 ± 0.28 µg/ml. Cyanidin 3-glucoside is the likely active component of the plum juice, with possible additive effects of other flavonoids such as quercetin glycosides. Thus, QG juice decreased blood pressure and attenuated some risk factors of metabolic syndrome after 12 weeks suggesting that daily consumption could attenuate the development of cardiovascular and metabolic diseases.

I1-imidazoline receptor-mediated cardiovascular and metabolic effects in high-fat diet-induced metabolic syndrome in rats.

The objective of this study was to investigate the effects of a new I1-imidazoline receptor-selective pyrroline compound on the hemodynamic, metabolic and microvascular alterations in a high-fat diet (HFD)-induced model of metabolic syndrome in rats. In total, twenty adult male Wistar rats were fed a high-fat diet (HFD, n = 20) for 20 weeks. Thereafter, the rats received a new pyrroline compound selective for I1-imidazoline receptors (LNP599; 10 mg/kg/day) or vehicle (n = 10/group) orally by gavage for 4 weeks. Functional microcirculation was assessed using intravital video microscopy, and structural microcirculation was evaluated using histochemical analysis. LNP599 induced concomitant reductions in the SBP, HR and plasma catecholamine levels. The animals treated with this new antihypertensive compound also presented an improvement in body weight and the metabolic parameters related to metabolic syndrome, such as the glucose and lipid profiles. These effects were accompanied by a reversal of the functional and structural capillary rarefaction in the skeletal muscle. The modulation of the sympathetic nervous system by a selective agonist for I1-imidazoline receptors improves the hemodynamic and metabolic parameters in an experimental model of metabolic syndrome. LNP599 can also contribute to the restoration of microcirculatory parameters.

Betulinic acid improves insulin sensitivity, hyperglycemia, inflammation and oxidative stress in metabolic syndrome rats via PI3K/Akt pathways

This study investigated the influence of betulinic acid on high-fructose diet-induced metabolic syndrome in rats. Oral administration of betulinic acid significantly reversed high-fructose diet-mediated increase in body mass index and blood glucose. Furthermore, betulinic acid restored high-fructose diet-mediated alterations in metabolic hormones (insulin, leptin and adiponectin). Betulinic acid-mediated upregulation of protein kinase B (Akt) and phosphoinositde-3 kinase (PI3K) anulled high-fructose diet mediated depletion. Also, elevated tumour necrosis factor-α, interleukin-6 and -8 were significantly lowered. Administration of betulinic acid restored high-fructose diet-mediated increase in the levels of lipid profile parameters and indices of atherosclerosis, cardiac and cardiovascular diseases. High-fructose diet-mediated decrease in activities of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose 6-phosphate dehydrogenase) and increase in oxidative stress biomarkers (reduced glutathione, lipid peroxidation products, protein oxidation and fragmented DNA) were significantly restored by the phenolic acids. Conclusively, betulinic acid improves insulin sensitivity, elevated blood glucose, inflammation and dyslipidaemia and oxidative stress in high-fructose diet-induced metabolic syndrome through the PI#Kand Akt pathways .

In vitro antioxidant activity, α-glucosidase inhibitory potential and in vivo protective effect of Asparagus stipularis Forssk aqueous extract against high-fructose diet-induced metabolic syndrome in rats

The study was carried out to evaluate the in vitro antioxidant, α-glucosidase inhibitory potential and the protective effect of Asparagus stipularis Forssk aqueous extract against high-fructose diet (HFD; 10% fructose solution for 5 months) induced metabolic syndrome in rats. An A. stipularis shoots decoction (ASD) was administered orally (100 and 300 mg/kg body weight), daily for 4 weeks. Controls were performed using metformin (150 mg/kg) as a standard drug. HPLC-MS analysis showed hydroxycinnamoyl derivatives and flavonoid glycosides as the major constituents of ASD. Fructose fed rats showed hyperglycemia, dyslipidemia, impaired glucose tolerance and an increase of inflammation markers (alkaline phosphatase, aspartate transaminase and alanine transaminase) together with higher values of lipid peroxidation and lowered activities of antioxidants enzymes in liver. Hepatic histopathological examinations were performed. Variable sized fat vacuoles and diffuse lymphocytic infiltration were observed. ASD treatment prevented these abnormalities, demonstrating its protective effect against HFD-induced metabolic syndrome in rats.

Pioglitazone Reduces Oxidative Stress in Kidney Against High Sucrose Diet-Induced Metabolic Syndrome in Rats

Amac: Metabolik sendrom (MS), kronik bobrek hastaliginin ilerlemesinde onemli bir risk faktorudur. Tiyazolidindionlar (TZDs) muhtemelen MS’de renovaskuler koruma saglar. Bununla birlikte, yuksek sukroz baslangicli MS’de pioglitazonun bobrege ait oksidatif stres uzerine etkisinin aciklanmasiyla ilgili calismalar devam etmektedir. Bu calismanin amaci pioglitazonun MS’li sicanlarin bobreklerindeki oksidatif stres belirleyicileri uzerine etkisinin incelenmesidir. Materyal ve Metot: Calismada erkek Wistar turu sicanlar (200-250 g agirlikta) kullanildi. Onlar kontrol grup, MS grup (935 mM sukroz icme sularina katilarak) ve pioglitazon uygulanmis MS grup (MSP); MS grubun 18. haftasindan baslayarak 2 hafta pioglitazon (30 mg/kg/gun, gavajla) uygulandi. Aspartate amino transferaz (AST), laktat dehidrojenaz (LDH), toplam oksidan durum (TOS), toplam antioksidan durum (TAS) seviyeleri ticari kitler kullanilarak olculdu. Tiyobarbiturik asit reaktif maddeler (TBARS), indirgenmis glutatyon (GSH), ure, urik asit and kreatin olculdu. Tiyoredoksin 1 (TRX1) duzeyi sitoplazma ve hucre zarinda western blot ile olculdu. TRX1 aktivitesi sitoplazma ve hucre zarinda ticari kit kullanilarak oculdu. Bulgular: Kontrol sicanlari ile karsilastirildiginda, sukroz ile beslenmis olan sicanlar abdominal obezite, insulin direnci, hiperinsulinemi, ve hipertrigliseridemi iceren MS’nin bir cok ozelligini gostermistir. Bunun yaninda, MS’de degismis olan AST, LDH, TOS, TAS, TBARS, GSH, ure, urik asit and kreatin, TRX1 aktivitesi ve protein duzeyleri pioglitazon uygulamasiyla kontrol seviyelerine donmustur. Sonuc: Pioglitazon, MS’li sicanlarin bobreklerinde artmis olan oksidatif stresi azaltmistir.

Dietary phenolic acids reverse insulin resistance, hyperglycaemia, dyslipidaemia, inflammation and oxidative stress in high-fructose diet-induced metabolic syndrome rats

This study investigated the influence of caffeic, ferulic, gallic and protocatechuic acids on high-fructose diet-induced metabolic syndrome in rats. Oral administration of the phenolic acids significantly reversed high-fructose diet-mediated increase in body mass index and blood glucose. Furthermore, phenolic acids restored high-fructose diet-mediated alterations in metabolic hormones (insulin, leptin and adiponectin). Similarly, elevated tumour necrosis factor-α, interleukin-6 and -8 were significantly lowered. Administration of phenolic acids restored High-fructose diet-mediated increase in the levels of lipid parameters and indices of atherosclerosis, cardiac and cardiovascular diseases. High-fructose diet-mediated decrease in activities of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose 6-phosphate dehydrogenase) and increase in oxidative stress biomarkers (reduced glutathione, lipid peroxidation products, protein oxidation and fragmented DNA) were significantly restored by the phenolic acids. The result of this study shows protective influence of caffeic acid, ferulic acid, gallic acid and protocatechuic acid in high-fructose diet-induced metabolic syndrome.

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.

Coconut Products Improve Signs of Diet-Induced Metabolic Syndrome in Rats.

Increasing prevalence of obesity and metabolic syndrome warrants identification of potential therapeutic options for intervention. This study tested commercially available Virgin Coconut Oil and Coconut Nourish, as coconuts are rich sources of lauric and myristic acids. Male Wistar rats were fed either corn starch diet (C); high-carbohydrate, high-fat diet (H); high-carbohydrate, high-virgin coconut oil diet (HV); or high-carbohydrate, high-coconut Nourish diet (HN) for 16weeks. Metabolic, liver, and cardiovascular health parameters were measured during and at the end of the study. Virgin coconut oil lowered body weight (C 386±8g, H 516±13g, HV 459±10g), blood glucose concentrations (C 4.2±0.1mmol/L, H 5.4±0.2mmol/L, HV 4.6±0.2mmol/L), systolic blood pressure (C 127±5mmHg, H 149±4mmHg, HV 133±3mmHg,) and diastolic stiffness (C 25.0±1.7, H 31.4±1.2, HV 25.2±2.3,) with improved structure and function of the heart and liver. Coconut Nourish increased total body lean mass (C 255±10g, H 270±16g, HN 303±15g) and lowered plasma total cholesterol concentrations (C 1.6±0.2mmol/L, H 1.7±0.1mmol/L, HN 1.0±0.0mmol/L), systolic blood pressure (C 127±5mmHg, H 149±4mmHg, HN 130±3mmHg) and diastolic stiffness (C 25.0±1.7, H 31.4±1.2, HN 26.5±1.0), improved structure and function of the heart and liver but increased plasma concentrations of triglycerides (C 0.3±0.1mmol/L, H 1.1±0.4mmol/L, HN 1.8±0.2mmol/L) and non-esterified fatty acids (C 1.2±0.3mmol/L, H 3.3±0.8mmol/L, HN 5.6±0.4mmol/L). Thus, the fiber and protein in coconut Nourish and the medium-chain saturated fatty acids in virgin coconut oil may improve cardiovascular and liver complications in obesity.