The effect of venlafaxine on blood pressure and ECG in rats fed with high-fat-fructose diet

AbstractMetabolic syndrome represents one of the major health, social and economic issues nowadays, and affects more than 25% people worldwide. Being a multifactorial health problem, metabolic syndrome clusters various features, such as obesity, dyslipidemia, hyperglycemia and hypertension. Each of these disturbances represents a risk factor for developing cardiovascular disease. Moreover, patients with metabolic syndrome are more likely to suffer from depression, thus treatment with antidepressants (e.g. venlafaxine) is often neccessary. However, many of the antidepressants themselves may contribute to worsening or even development of the metabolic syndrome, thus creating a “vicious circle”. The aim of this work was to investigate on the animal model of metabolic syndrome, i.e. on hypertriacylglycerolemic rats fed high-fat-fructose diet (HFFD): 1) the effect of a change in diet from HFFD to a standard diet (SD) and the effect of venlafaxine treatment, 2) during HFFD, 3) as well as during a changed diet to SD. We focused on biometric parameters, blood pressure and selected ECG parameters. We observed the reversibility of the present metabolic and cardiovascular changes by switching the HFFD to SD in the last 3 weeks of the experiment. Switch to the standard diet led to decrease of body weight, even in the presence of venlafaxine. Administration of venlafaxine caused the decrease of heart weight/body weight index in rats fed with HFFD compared to the untreated group fed with HFFD for 8 weeks. Blood pressure, which was increased in the HFFD group showed a tendency to decrease to control values after switching to the standard diet. Administration of venlafaxine led to significant increase in all parameters of blood pressure when rats were fed with HFFD throughout the whole experiment. In untreated rats fed with HFFD for 8 weeks, we observed a shorter PQ interval and prolonged QRS complex as well as QTc interval compared to untreated rats with diet switched to SD. This effect was potentiated by venlafaxine administered not only during HFFD but even after switch to SD. Our results point to the fact that metabolic syndrome is clearly affecting the function of the cardiovascular system by modifying blood pressure and electrical activity of the heart. Moreover, administration of venlafaxine may lead to worsening of the observed changes, especially in the presence of high-fat-fructose diet.

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Dietary Melatonin Protects Against Behavioural, Metabolic, Oxidative, and Organ Morphological Changes in Mice that are Fed High-Fat, High- Sugar Diet

Endocrine Metabolic & Immune Disorders - Drug Targets ◽

10.2174/1871530319666191009161228 ◽

2020 ◽

Vol 20 (4) ◽

pp. 570-583

Author(s):

Adejoke Yetunde Onaolapo ◽

Ebenezer Oladimeji Adebisi ◽

Adegbayi Emmanuel Adeleye ◽

Anthony Tope Olofinnade ◽

Olakunle James Onaolapo

Keyword(s):

Metabolic Syndrome ◽

Body Weight ◽

Spatial Working Memory ◽

Morphological Changes ◽

Organ Injury ◽

Standard Diet ◽

High Fat ◽

High Sugar ◽

The Metabolic Syndrome ◽

Increased Risk

Background : Metabolic syndrome is a complex pattern of disorders that occur jointly and is associated with an increased risk of cardiovascular and cerebrovascular disease. Therefore the need for more-efficient options of treatment has become imperative. Objective : This study examined the effect of dietary-melatonin in the management of behavioural, metabolic, antioxidant, and organ changes due to high-fat/high-sugar (HFHS) diet-induced metabolic syndrome in mice. Methods: Mice were randomly assigned into five groups of ten animals each. Groups were normal control [fed standard diet (SD)], HFHS control, and 3 groups of melatonin incorporated into HFHS at 2.5, 5, and 10 mg/kg of feed. Mice were fed for seven weeks, and body weight was assessed weekly. Open-field behaviours, radial-arm, and Y-maze spatial memory were scored at the end of the experimental period. Twenty-four hours after the last behavioural test, blood was taken for estimation of blood glucose levels after an overnight fast. Animals were then euthanised, and blood was taken for estimation of plasma insulin, leptin, and adiponectin levels, and serum lipid profile. The liver, kidneys, and brain were excised and processed for general histology, while homogenates of the liver and whole brain were used to assess oxidative stress parameters. Results: Results showed that dietary melatonin (compared to HFHS diet) was associated with a decrease in body weight, food intake, and novelty-induced behaviours; and an increase in spatial-working memory scores. A decrease in glucose, insulin, leptin, and malondialdehyde levels; and an increase in adiponectin levels and superoxide dismutase activity were also observed. Histomorphological/ histomorphometric examination revealed evidence of organ injury with HFHS diet, and varying degrees of amelioration with melatonin-supplemented diet. Conclusion: In conclusion, dietary melatonin supplementation may have beneficial effects in the management of the metabolic syndrome..

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7-Hydroxymatairesinol improves body weight, fat and sugar metabolism in C57BJ/6 mice on a high-fat diet

British Journal Of Nutrition ◽

10.1017/s0007114518001824 ◽

2018 ◽

Vol 120 (7) ◽

pp. 751-762 ◽

Cited By ~ 5

Author(s):

Giorgio Biasiotto ◽

Isabella Zanella ◽

Federica Predolini ◽

Ivonne Archetti ◽

Moris Cadei ◽

...

Keyword(s):

Metabolic Syndrome ◽

Body Weight ◽

High Fat Diet ◽

Sugar Metabolism ◽

Lipid Uptake ◽

High Fat ◽

Total Extract ◽

The Metabolic Syndrome ◽

Metabolic Genes

Abstract7-Hydroxymatairesinol (7-HMR) is a plant lignan abundant in various concentrations in plant foods. The objective of this study was to test HMRLignan™, a purified form of 7-HMR, and the correspondingPicea abiesextract (total extractP. abies; TEP) as dietary supplements on a background of a high-fat diet (HFD)-induced metabolic syndrome in mice and in the 3T3-L1 adipogenesis model. Mice, 3 weeks old, were fed a HFD for 60 d. Subgroups were treated with 3 mg/kg body weight 7-HMR (HMRLignan™) or 10 mg/kg body weight TEP by oral administration. 7-HMR and TEP limited the increase in body weight (−11 and −13 %) and fat mass (−11 and −18 %) in the HFD-fed mice. Epididymal adipocytes were 19 and −12 % smaller and the liver was less steatotic (−62 and −65 %). Serum lipids decreased in TEP-treated mice (−11 % cholesterol, −23 % LDL and −15 % TAG) and sugar metabolism was ameliorated by both lignan preparations, as shown by a more than 70 % decrease in insulin secretion and insulin resistance. The expression of several metabolic genes was modulated by the HFD with an effect that was reversed by lignan. In 3T3-L1 cells, the 7-HMR metabolites enterolactone (ENL) and enterodiol (END) showed a 40 % inhibition of cell differentiation accompanied by the inhibited expression of the adipogenic genesPPARγ,C/EBPαandaP2. Furthermore, END and ENL caused a 10 % reduction in TAG uptake in HEPA 1–6 hepatoma cells. In conclusion, 7-HMR and TEP reduce metabolic imbalances typical of the metabolic syndrome and obesity in male mice, whereas their metabolites inhibit adipogenesis and lipid uptakein vitro.

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Effects of chromosome 17 on features of the metabolic syndrome in the Lyon hypertensive rat

Physiological Genomics ◽

10.1152/physiolgenomics.00262.2007 ◽

2008 ◽

Vol 33 (2) ◽

pp. 212-217 ◽

Cited By ~ 15

Author(s):

S. Gilibert ◽

A. E. Kwitek ◽

N. Hubner ◽

M. Tschannen ◽

H. J. Jacob ◽

...

Keyword(s):

Blood Pressure ◽

Metabolic Syndrome ◽

Body Weight ◽

Genetic Model ◽

Chromosome 17 ◽

Brown Norway ◽

Single Chromosome ◽

The Metabolic Syndrome ◽

Glucose Ratio ◽

Significant Difference

The metabolic syndrome (involving obesity, hypertension, dyslipidemia, insulin resistance, and a proinflammatory/prethrombotic state) is a major risk factor for cardiovascular disease. Its incidence continues to rise, in part because of the epidemic increase in obesity. The Lyon hypertensive (LH) rat is a model for hypertension and several other features of the metabolic syndrome, having high body weight, plasma cholesterol, and triglycerides, increased insulin-to-glucose ratio, and salt-sensitive hypertension. Previous genetic studies in LH/Mav rats and a normotensive control (LN/Mav) identified quantitative trait loci (QTLs) on rat chromosome (RNO)17 for multiple features of the metabolic syndrome. To further evaluate the role of RNO17 in the LH rat, we generated a consomic strain (LH-17BN) by substituting LH RNO17 with that of the sequenced Brown Norway (BN/NHsdMcwi) rat. Male LH and BN rats and LH-17BN rats were characterized for blood pressure and metabolic and morphological parameters. Similar to the protective effect of LN alleles, the LH-17BN rat also showed decreased body weight, triglycerides, and blood pressure; however, there was no significant difference in cholesterol or insulin-to-glucose ratio. Therefore, the substitution of the LH chromosome 17 is sufficient to recapitulate some, but not all, of the traits previously mapped to this chromosome. This could be due to the lack of a susceptible LH genome background or due to the introgression of chromosome 17 from another strain. Regardless, this study provides a single-chromosome genetic model for further dissection of blood pressure and morphological and metabolic traits on this chromosome.

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Lepidium Meyenii Supplemented Diet Modulates Neurobehavioral and Biochemical Parameters in Mice Fed High-Fat-High-Sugar Diet

Endocrine Metabolic & Immune Disorders - Drug Targets ◽

10.2174/1871530320666200821155005 ◽

2020 ◽

Vol 20 ◽

Author(s):

Anthony T. Olofinnade ◽

Abiola Alawode ◽

Adejoke Y. Onaolapo ◽

Olakunle J. Onaolapo

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Body Weight ◽

Inflammatory Markers ◽

Acetylcholinesterase Activity ◽

Standard Diet ◽

High Fat ◽

Lepidium Meyenii ◽

High Sugar ◽

Increased Risk

Background: Metabolic syndrome has been associated with increased risk of cardiovascular disease, diabetes mellitus, and neurodegenerative disorders. Known side-effects of currently-available drugs necessitate the search for possibly better treatment options. Objective: This study examined the effects of dietary lepidium meyenii (MACA) supplementation on neurobehaviour, metabolic profile, levels of inflammatory markers, and oxidative stress parameters in a mouse model of metabolic syndrome. Methodology: Mice were randomly-assigned into 8 groups of ten animals each. Groups consist of standard diet (SD) control, high fat/high sugar (HFHS) control and three groups each of lepidium meyenii incorporated into either SD or HFHS diet at 0.1, 0.2 and 0.4 %. Mice were fed for seven weeks, and body weight was measured weekly. Open-field behaviors and radial-arm/Y-maze spatial memory were scored at the end of the study. Twenty-four hours after the last behavioral test, fasting blood glucose levels were estimated. Animals were then euthanized, and blood taken for estimation of serum lipid profile. Whole brains were excised, weighed and homogenized for the estimation of levels of lipid peroxidation, inflammatory markers, antioxidant status, and acetylcholinesterase activity. Results: MACA-supplemented diet was associated with a decrease in body weight gain, an increase in food intake (at lower concentrations), suppression of grooming behavior, and decrease in acetylcholinesterase activity. MACA-supplement also reversed HFHS-induced memory impairment, anxiety, hyperglycaemia, lipid derangement, oxidative stress, and derangement of inflammatory markers. Conclusion: Dietary supplementation with MACA shows beneficial effects in mitigating the effects of metabolic syndrome on the brain in mice.

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3-Amino-1,2,4-Triazole Induces Quick and Strong Fat Loss in Mice with High Fat-Induced Metabolic Syndrome

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/3025361 ◽

2020 ◽

Vol 2020 ◽

pp. 1-14 ◽

Cited By ~ 1

Author(s):

Valéria Nunes-Souza ◽

Nelson Miguel Dias-Júnior ◽

Marcos Antônio Eleutério-Silva ◽

Vanessa P. Ferreira-Neves ◽

Fabiana Andréa Moura ◽

...

Keyword(s):

Blood Pressure ◽

Metabolic Syndrome ◽

Body Weight ◽

Nonesterified Fatty Acid ◽

High Fat ◽

Fat Loss ◽

Heme Synthesis ◽

Expression Of Genes ◽

Lower Body Weight ◽

Marked Atrophy

Background. Obesity is a growing epidemic with limited effective treatments and an important risk factor for several diseases such as metabolic syndrome (MetS). In this study, we aimed to investigate the effect of 3-amino-1,2,4-triazole (ATZ), an inhibitor of catalase and heme synthesis, in a murine model for MetS. Methods. Male C57BL/6 mice with high-fat diet-induced MetS received ATZ (500 mg·kg-1·24 h-1) for 12 weeks. Results. The HFD group showed increased blood pressure and body weight, enhanced fat deposition accompanied by an increase in adipocyte diameter, and decreased lipolysis in white adipose tissue (WAT). The expression of genes related to inflammation was increased in WAT of the HFD group. Concurrently, these mice exhibited an increase in leptin, nonesterified fatty acid (NEFA), insulin, and glucose in plasma, coupled with glucose intolerance and insulin resistance. Strikingly, ATZ prevented the increase in blood pressure and the HFD-induced obesity as observed by lower body weight, WAT index, triglycerides, NEFA, and leptin in plasma. ATZ treatment also prevented the HFD-induced increase in adipocyte diameter and even induced marked atrophy and the accumulation of macrophages in this tissue. ATZ treatment also improved glucose metabolism by increasing glucose tolerance and insulin sensitivity, GLUT4 mRNA expression in WAT in parallel to decreased insulin levels. Conclusions. In the context of HFD-induced obesity and metabolic syndrome, the fat loss induced by ATZ is probably due to heme synthesis inhibition, which blocks adipogenesis by probably decreased RevErbα activity, leading to apoptosis of adipocytes and the recruitment of macrophages. As a consequence of fat loss, ATZ elicits a beneficial systemic antiobesity effect and improves the metabolic status.

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Effectiveness of Ascophyllum nodosum and Fucus vesiculosus on Metabolic Syndrome Components: A Real-World, Observational Study

Journal of Diabetes Research ◽

10.1155/2021/3389316 ◽

2021 ◽

Vol 2021 ◽

pp. 1-8

Author(s):

Antonio Nicolucci ◽

Maria Chiara Rossi ◽

Massimiliano Petrelli

Keyword(s):

Blood Pressure ◽

Metabolic Syndrome ◽

Body Weight ◽

Blood Glucose ◽

Waist Circumference ◽

Real World ◽

Fasting Blood Glucose ◽

Ascophyllum Nodosum ◽

Fucus Vesiculosus ◽

The Metabolic Syndrome

Introduction. Gdue is a nutraceutical obtained from the association of two marine algae, Ascophyllum nodosum and Fucus vesiculosus, in addition to chromium picolinate, which could be useful for the treatment of dysglycemia, overweight, and the other components of the metabolic syndrome. The aim of the study was to assess the real-world effectiveness and safety of Gdue when administered to subjects with one or more components of the metabolic syndrome. Methods. A longitudinal, retrospective, observational study, conducted among primary care physicians, nutritionists, and specialists from various disciplines. The impact of 180 days of administration of Gdue was assessed on body weight, waist circumference, fasting blood glucose, HbA1c, lipid profile, and blood pressure levels. The likelihood of experiencing a first major cardiovascular event over ten years was estimated using Italian risk charts. General linear models for repeated measures were applied to assess changes in the parameters of interest during the follow-up. Results are expressed as estimated marginal means with their 95% confidence interval. Results. Overall, 505 patients were enrolled by 282 physicians. After 6 months of treatment with Gdue, body weight was reduced on average by 7.3 kg (-8.0; -6.6), waist circumference by 7.5 cm (-8.2; -6.8), fasting blood glucose by 16.3 mg/dL (-17.8; -14.7), HbA1c by 0.55% (-0.62; -0.49), systolic and diastolic blood pressure by 7.1 mmHg (-8.3; -6.0) and 4.2 mmHg (-5.0; -3.5), respectively, LDL cholesterol by 18.2 mg/dL (-21.2; -15.3), and triglycerides by 39 mg/dL (-45; -32). HDL cholesterol was significantly increased by 2.9 mg/dL (0.7; 5.0). The 10-year risk of cardiovascular events significantly decreased by 1.8%, corresponding to a relative risk reduction of 27.7%. Conclusion. Our real-world study shows that 6 months of treatment with Gdue have an impact on all the components of the metabolic syndrome, thus offering the potential for decreasing the cardiovascular risk associated with metabolic syndrome.

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Abstract 018: Neuronal (Pro)renin Receptor Deletion Prevents High-fat Diet Induced High Blood Pressure and Type II Diabetes

Hypertension ◽

10.1161/hyp.70.suppl_1.018 ◽

2017 ◽

Vol 70 (suppl_1) ◽

Author(s):

Caleb J Worker ◽

Wencheng Li ◽

Yumei Feng

Keyword(s):

Blood Pressure ◽

Metabolic Syndrome ◽

Body Weight ◽

Insulin Sensitivity ◽

Angiotensin Ii ◽

Glucose Tolerance ◽

High Fat Diet ◽

Fasting Blood Glucose ◽

Renin Angiotensin System ◽

High Fat

We recently reported that the (pro)renin receptor (PRR) is a key component of the brain renin-angiotensin system, mediating the majority of Ang II formation, and plays a pivotal role in the development of hypertension. Its importance in obesity-related metabolic syndrome is, however, unknown. We hypothesize that brain PRR plays a regulatory role in high-fat diet (HFD) induced metabolic syndrome. To test our hypothesis, neuron-specific PRR knockout (PRRKO) mice and wildtype (WT) littermates were fed with either HFD (60% calories from fat) or normal fat chow (NFD, 10% calories from fat) with matching calories for 16 weeks. Weekly body weight (BW) and monthly fasting blood glucose (FBG) measurements were recorded and end point glucose tolerance (GTT) and insulin sensitivity tests (IST) were performed. Blood pressure (BP) was recorded using radiotelemetry in conscious free moving mice. We observed no difference in BW or food intake between genotypes in either HFD or NFD. The baseline BP and heart rate (HR) were similar between PRRKO and WT mice; however, following 16 weeks HFD the BP (101±6 vs. 111±3 mmHg, P=0.035) and HR (536±12 vs. 578±4 BPM, P=0.046) were significantly lower in PRRKO compared with WT mice. Interestingly, neuronal PRR deletion attenuated the elevation of FBG (127.12±10.46 vs. 167.77±16.57 mg/dl, P=0.039) induced by HFD. Glucose tolerance was significantly improved in PRRKO compared with WT following 16 weeks of HFD (AUC: 20557±894 vs. 29994±2976, P=0.006), while there was no difference in the IST between the groups. We also found that HFD mice had higher levels of plasma (pro)renin (9.95±1.83 vs. 2.74± 0.47 ng/ml, P=0.005) and brain angiotensin II (656.8±94.9 vs. 375.3±32.0 pg/g, P=0.02), as well as higher cardiac (ΔHR to propranolol: -150±6 vs. -82±15 bpm , P=0.0054) and vasomotor (ΔBP to chlorisondamine: -44±3 vs. -22±3 mmHg, P=0.0004) sympathetic tone, suggesting that the HFD-induced rise in BP is sympathetically mediated and associated with elevation of brain angiotensin II. Our data indicates that PRR deletion in the neurons protects against glucose intolerance and BP elevation in HFD mice with no effect on insulin sensitivity or body weight. We conclude that neuronal PRR plays a role in the development of obesity-related metabolic syndrome.

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Results of adding metformin and orlistat to complex treatment of stable angina associated with metabolic syndrome

Kazan medical journal ◽

10.17816/kmj1956 ◽

2013 ◽

Vol 94 (4) ◽

pp. 492-496

Author(s):

R L Dashdamirov

Keyword(s):

Blood Pressure ◽

Metabolic Syndrome ◽

Body Weight ◽

Glucose Level ◽

Stable Angina ◽

Serum Glucose ◽

Serum Glucose Level ◽

Fasting Serum ◽

Fasting Serum Glucose Level ◽

Body Weight Index

Aim. To evaluate the complex therapy with the addition of metformin and orlistat in treatment of II-III functional class stable angina associated with metabolic syndrome. Methods. The study included 143 patients with stable angina at the age of 36 to 70 years (mean age 54.2±3.6). Of these, 59 patients (control group) received standard treatment (isosorbide 5-mononitrate 40 mg/day, amlodipine 5 mg/day, acetylsalicylic acid 100 mg/day, carvedilol 25 mg/day, atorvastatin 20 mg/day, eprosartan 600 mg/day), and 84 patients (study group) were additionally administered metformin 1000 mg/day and orlistat 360 mg/day. Clinical and laboratory examinations (serum glucose and lipid level measurements) as well as instrumental examinations (electrocardiography, Doppler echocardiography, 24-hour electrocardiography and blood pressure monitoring) were performed before the treatment, 3, 6 and 12 months after the treatment start. Results. After 12 months of treatment mean systolic blood pressure in patients of the main group reduced by 24.5%, diastolic - by 18.8%, fasting serum glucose level - by 14.3% compared to the baseline level. Cholesterol level reduced by 13.8%, triglycerides - by 14.7%, low density lipoproteins - by 14.0%, blood level of high density lipoproteins increased by 11.6%. Body weight index reduced by 10.3%. Conclusion. Adding of 1000 mg of metformin and 360 mg of orlistat daily decreased the fasting serum glucose level by 14.3%, body weight index by 10.3%, and reduced the number of angina episodes by 19.6%, of painless myocardial ischemia by 36.3%, as well as increased physical ability tolerance by 26.5%.

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Diet-induced insulin resistance precedes other aspects of the metabolic syndrome

Journal of Applied Physiology ◽

10.1152/jappl.1998.84.4.1311 ◽

1998 ◽

Vol 84 (4) ◽

pp. 1311-1315 ◽

Cited By ~ 125

Author(s):

R. James Barnard ◽

Christian K. Roberts ◽

Shira M. Varon ◽

Joshua J. Berger

Keyword(s):

Insulin Resistance ◽

Blood Pressure ◽

Metabolic Syndrome ◽

Body Weight ◽

Glucose Transport ◽

Serum Insulin ◽

Fat Cell ◽

Plasma Triglycerides ◽

The Metabolic Syndrome ◽

Muscle Glucose Transport

This study was designed to examine the effects of a high-fat refined-sugar (HFS) or a low-fat complex-carbohydrate (LFCC) diet on insulin-stimulated skeletal muscle glucose transport, plasma insulin, blood pressure, plasma triglycerides, plasma glycerol, body weight, and body fat in female Fischer rats. Insulin-stimulated glucose transport was significantly reduced in the HFS group at 2 wk, 2 mo, and 2 yr, whereas serum insulin was significantly elevated at all time points. Blood pressure was not significantly elevated in the HFS group until 12 mo, and all HFS animals were hypertensive by 18 mo. Glycerol, triglycerides, and abdominal fat cell size were not significantly different at 2 wk but were significantly elevated in the HFS rats at 2 and 6 mo. Body weight was similar in both groups until 20 wk on the diet, when the HFS rats started to gain more weight. These results demonstrate that insulin resistance and hyperinsulinemia occur before the other manifestations of the metabolic syndrome and that diet, not obesity, is the underlying cause.

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Etlingera elatior (Jack) R.M, Sm Containing Diet Normalizes some Metabolic Syndrome Markers due to High-Fat High-Fructose Diet in Wistar Rats

Current Nutrition & Food Science ◽

10.2174/1573401316666201208101359 ◽

2020 ◽

Vol 16 ◽

Author(s):

Nur Islami Dini Hanifah ◽

Retno Murwani ◽

Achmad Zulfa Juniarto

Keyword(s):

Metabolic Syndrome ◽

Body Weight ◽

Total Cholesterol ◽

Wistar Rats ◽

Density Lipoprotein ◽

Standard Diet ◽

High Fat ◽

High Fructose Diet ◽

High Fructose ◽

Etlingera Elatior

Background: Etlingera elatior (Ee) contains phytochemical compounds that are rich in antioxidants, which may reduce several biochemical markers of metabolic syndrome (MetS). Objective: We aimed to study the effect of fresh Etlingera elatior (FEe) and steamed Etlingera elatior (SEe) as a part of rat diet on the body weight, serum lipid, and malondialdehyde (MDA) level in Wistar rats with MetS induced by a highfat, high-fructose diet. Method: Our research was a true experimental randomized control group design with pre- and post-test. A total of 24 male Wistar rats were divided randomly into the following four groups: 1) Control, fed standard rat diet during the whole duration of the study, 2) HFFr-Sd, fed high-fat high-fructose (HFFr) diet for 29 days, followed by 29 days of the standard diet, 3) HFFr-FEe, fed HFFr diet for 29 days, followed by 29 days of a standard diet containing 33.3% FEe, and 4) HFFrSEe, fed HFFr diet for 29 days, followed by 29 days of a standard diet containing 33.3% SEe. The HFFr diet was given at 15 g/day along with fructose drink (20% pure fructose) at 100 ml/day. The diets in each group after the MetS induction period is referred to as intervention diets. Data at the end of HFFr (pre) and intervention diets (post) were analyzed by paired t-test. The data among groups were analyzed by one-way analysis of variance followed by post hoc test. Results: HFFr diet for 29 days induced MetS in Wistar rats fulfilling the criteria of obesity (Lee Index), hypertriglyceridemia, and decreased high-density lipoprotein cholesterol (HDL-C). Also, there was a significant increase in serum total cholesterol, low-density lipoprotein cholesterol (LDL-C), and MDA level (p < 0.05). Feeding a diet contaning FEe or SEe can significantly reduce body weight, serum triglyceride, total cholesterol, LDL-C, and MDA, and increase HDL-C levels (p < 0.05). The effect of FEe was more pronounced in ameliorating body weight and lipid profile than SEe. Conclusion: Fresh Ee and Steamed Ee can ameliorate obesity, dyslipidemia, and oxidative stress in MetS Wistar rats induced by a high-fat high-fructose diet. It suggests that dietary Ee accounting for one-third of daily standard diet can assist in normalizing some MetS markers in rats.

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