Induction Of Metabolic Syndrome Research Articles

THE IMPACT OF HOP EXTRACT ACTIVE COMPONENTS ON METABOLIC DISTURBANCES IN ESTROGEN DEFICIENT FEMALE RATS WITH PREDIABETES

A number of studies have shown a greater cardiovascular risk in women with type 2 diabetes compared to men. The latter may be due to more excessive manifestations of metabolic disorders in women, in particular postmenopausal, that develop even at the stage of prediabetes. Since the use of hormone replacement therapy in women after menopause had adverse results on the progression of cardiovascular events, an alternative method of reducing cardiovascular risk in postmenopausal women with prediabetes may be the use of phytoestrogens, which possess estrogen-like activity without negative side effects specific to exogenous estrogens. The aim of our study was to evaluate the effect of hop extract on metabolic disturbances in female rats with prediabetes under estrogen deficiency. Materials and methods. The study was conducted on three-month-old intact and ovariectomized Wistar rats with metabolic syndrome (MS) induced by high calorie diet (15% lard, 25% sucrose, 1% bile salts, 59% standard feed) for eight weeks. The test substances were administered intragastrically once per day in a dose of 20 μg/kg or 200 μg/kg b.w. in recalculation on 8-prenylnaringenin for hop extract and 200 μg/kg b.w. in recalculation on estradiol for the reference drug, from the fifth week after induction of metabolic syndrome. Results. It was revealed that administration of hop extract in a dose of 200 μg/kg, similar to estradiol, led to improvement in glucose tolerance and decrease in insulin resistance (p˂0.05) in estrogen deficient rats with MS. In contrast to estradiol, hop extract had no effect on the mass of uterus in ovariectomized animals. The use of hop extract only in the dose of 200 μg/kg, similar to estradiol, was accompanied by a significant decrease in body weight gain and visceral fat, as well as normalization of the total lipids content in serum of experimental animals (p˂0.05). It is of note, that hop extract resulted in decrease of hypertriglyceridemia (p˂0.05), but did not affect the level of total cholesterol, while estradiol reduced the concentration of total cholesterol (p˂0.05), and had no effect on the level of triglycerides. Hop extract in a dose of 200 μg/kg, as well as estradiol, led to a decrease in the intensity of lipid peroxidation induced by MS under estrogen deficiency, as evidenced by reduced concentration of conjugated dienes in serum (p˂0.05). At the same time, the total antioxidant activity of serum in these animals remained elevated compared to intact group. In rats with MS and hypoestrogenia, hop extract in the highest dose and estradiol resulted in complete normalization (p˂0.05) of the decreased level of NO stable metabolites in serum and the reduced activity of NO-synthase in heart. Conclusions. The revealed cardioprotective effect of hop extract that is realized due to the improved lipid profile and reduced insulin resistance, visceral obesity, oxidative stress and endothelial dysfunction in estrogen deficient female rats with MS indicates the prospects of its use for prevention and treatment of cardiovascular complications in postmenopausal women with prediabetes.

Physicochemical Characterization of Yogurt Fortified with Microencapsulated Cinnamon (Cinnamomum zeylanicum) and Its Effects on Metabolic Syndrome Induced in Rabbits (Oryctolagus cuniculus).

Chronic noncommunicable diseases are a global health problem causing increased rates of mortality and sick leaves, which can be reduced by controlling dyslipidemia and hyperglycemia. Experimental and clinical studies have demonstrated the antidiabetic, lipid-lowering, antiobesogenic, anti-inflammatory, and antihypertensive properties of cinnamon; therefore, its use in yogurt can help reverse the effects of these diseases. Our study aims to evaluate the effect of a microencapsulated aqueous extract of cinnamon (Cinnamomum zeylanicum) (MCE Cz) incorporated in a yogurt drink on metabolic syndrome (MS) in a rabbit (Oryctolagus cuniculus). Physicochemical, microbiological, and proximal chemical characterization; total phenol, flavonoid, and 2,2-diphenyl-1-picrylhydrazil activity quantification; intestinal bioaccessibility; sensory analysis; MS induction through diet; and treatment with 5, 10, and 20 mg/kg of flavonoids contained in the MCE Cz were performed to help evaluate morphological, biochemical, and lipid peroxidation measurements in the liver and heart. The results show that the addition of MCE Cz in the yogurt modified the yogurt texture, increased its adhesiveness and firmness, and imparted a characteristic cinnamon color and biological value by providing intestinally bioaccessible antioxidants with antioxidant potential by reducing lipoperoxidation in the liver and heart after treatment. MCE Cz reduced the weight of the animals by up to 38.5% and the abdominal circumference by 29%. Biochemically, it decreased glucose levels by 24.38%, total cholesterol levels by 69.2%, triglyceride levels by 72.69%, and low-density lipoprotein levels by 89.25%; it increased high-density lipoprotein levels by 67.08%. Therefore, adding MCE Cz in doses of 5 and 10 mg of flavonoids in drinkable yogurt can be an alternative to preparing functional foods with physicochemical attributes and biological properties that can be consumed at all stages of life without undesirable effects. Moreover, it can act as a potential adjuvant in the treatment of comorbidities related to MS.

Aronia melanocarpa fruit juice prevents hepatic impairment in rats subjected to metabolic syndrome

AbstractThis study evaluated the effects of Aronia melanocarpa fruit juice (AMFJ) on the liver in a model of high-fat, high-fructose (HFHF) diet-induced metabolic syndrome (MS). Fifty rats were allocated to five groups – Control, MS, MS+AMFJ2.5, MS+AMFJ5, and MS+AMFJ10. The control group was fed a standard diet, while the other groups were provided a HFHF diet. During MS induction, daily oral treatment was performed. Control and MS groups received 10.0 mL kg−1 distilled water, while the other three groups received AMFJ at doses of 2.5, 5.0, and 10.0 mL kg−1, respectively. After 10 weeks, liver samples were collected and inspected histologically as well as immunohistochemically to determine the expression of Bax, Bcl-2, and MAC387. Bax/Bcl-2 ratio was calculated. In MS rats, steatotic, inflammatory and degenerative alterations of the liver were detected, Bax and MAC387 were markedly elevated, while Bcl-2 was non-significantly reduced. The Bax/Bcl-2 ratio significantly increased. The histopathological alterations were prevented by the AMFJ treatment. Compared to MS group, Bax and MAC387 values were significantly lower and Bcl-2 value was higher resulting in significantly lower (P < 0.001) Bax/Bcl-2 ratio in all AMFJ-treated groups. AMFJ, administered during MS induction in rats, prevented the occurrence of inflammatory, steatotic, degenerative, and pro-apoptotic changes in the liver.

Effects of probiotics in rats with experimental metabolic syndrome and periodontitis: An investigation of the intestine-adipose tissue axis.

This study evaluated the systemic (intestine and adipose tissue) and local (periodontal tissues) impact of probiotic therapy in rats with metabolic syndrome (MS) associated or not with periodontitis (PE). Forty-eight rats received a high-fat diet for induction of MS for 16weeks. They were subdivided into groups with (+) and without (-) PE, receiving (*) or not (**) receiving probiotics (PROB): MS (-**), MSP (-*), MSPE (+**), and MSPEP (+*). PROB administration (Bifidobacterium animalis subsp. lactis HN019) started on the 8th week of the study and PE was induced on the 14th week by placing ligature on the animals' lower first molars. Euthanasia occurred in the 16th week. Biomolecular, immunoenzymatic assays, and histomorphometric analyses were performed. The data obtained were statistically analyzed (ANOVA, Tukey, p<0.05). The MSPEP group exhibited reduced alveolar bone loss when compared with the MSPE group, as well as lower levels of hepatic steatosis and proteinuria (p<0.05). In the intestinal environment, the MSPE group exhibited significantlylower villus height and crypt depth, as well as a greater increase in Bacillota when compared with the MSPEP group (p<0.05). The MSPEP group showed lower adipokine gene expression (LEPR, NAMPT, and FABP4) in adipose tissue than the MSPE group (p<0.05). The probiotic B. lactis HN019 reduced the severity of experimental periodontitis and modulated the expression of lipogenic genes and intestinal morphological and microbiological parameters in rats with MS.

Effect of Ethanolic Extract of Moringa oleifera, Lam. Roots on Expression of Cyclin D1 in Testicular Tissue of Metabolic Syndrome Induced Wistar Rats

Background: Metabolic syndrome (MS) impacts on inhibition process of spermatogenesis by damaging various components of cell cycle proteins. Cyclin D1 protein which plays role in regulating the cell cycle of spermatogenic cells is depleted due to the metabolic syndrome. Variation results of M. oleifera studies on fertility are interesting for further research. This study aimed to determine the effect of ethanolic extract of M. oleifera roots towards expression of testicular cyclin D1 of metabolic syndrome induced Wistar rats.Subjects and Method: This study was an experimental laboratory. Thirty subjects of male Wistar rats were randomly divided into 5 groups consisted of 6 rats, control group (K1), MS group (K2), and treatment groups (K3, K4, and K5) which were given doses of 150, 250, and 350 mg/kgBW, respectively for 28 days. Induction of MS was achieved by high-fat diet for 28 days and injection of streptozotocin-nicotinamide (STZ-NA) on day 25. Cyclin D1 data was calculated using Intensity Distribution Score (IDS) and analyzed using one-way ANOVA test followed by post hoc multiple comparisons with Tukey HSD. Simple liniar regression test conducted on cyclin D1 data of K2, K3, K4, and K5.Results: One-way ANOVA test showed that the administration of ethanolic extract M. oleifera Lam. roots with doses of 150, 250, and 350 mg/kgBW in 28 days increased cyclin D1 significantly (p= 0.000). There were significant differences between K1 and K2 (p= 0.000), K2 and K3 (p= 0.000), K2 and K4 (p= 0.000), K2 and K5 (P= 0.000). Liniar regression test showed significant (p= 0.000) and moderate effect (R2= 0.65) of doses of ethanolic extract of M. oleifera roots on the expression of cyclin D1.Conclusion: The administration of ethanolic extract Moringa oleifera Lam. roots with doses of 150, 250, and 350 mg/kgBW for 28 days increased cyclin D1 in testicular rats.

Antihypertensive, antidyslipidemic, and renoprotective effects of Bursera simaruba on metabolic syndrome.

Metabolic syndrome is associated with the development of chronic kidney disease. Bursera simaruba "chaca" is a medicinal plant used in Mexico for hypertension and empirical therapy. In this study, were examined the effects of ethanol extract of B. simaruba on metabolic syndrome. For induction of metabolic syndrome, 20% fructose was used, and it was administered in the water and food to male Wistar rats for 12 weeks, after administering ethanol extract of B. simaruba intragastrically (100 and 200 mg/kg/day) for 6 weeks, blood pressure was determined. In plasma, glucose, cholesterol, triglycerides, angiotensin II, oxide nitric, and angiotensin 1-7 were quantified. In the kidney was performed histological study and the activity of anti-oxidant enzymes was quantified. Rats with metabolic syndrome developed obesity, arterial hypertension, dyslipidemia, and kidney damage characterized by proliferative glomerulonephritis, necrosis, and reduced activity of anti-oxidant enzymes. These alterations were significantly ameliorated by ethanol extract of B. simaruba. The ethanolic extract of B. simaruba showed antidyslipidemic, antihypertensive, anti-oxidant, and renoprotective effects.

Effect of the Lingzi or Reishi Medicinal Mushroom Ganoderma lucidum (Agaricomycetes) on Hyperglycemia and Dyslipidemia with Experimental Metabolic Syndrome.

The effect of Ganoderma lucidum hot water extract of submerged cultivated mycelium suspensia on carbohydrate metabolism and lipid profile during fructose-induced metabolic syndrome in rats was studied. The outbred white male Wistar rats, in which metabolic syndrome was induced by consuming a 10% fructose solution instead of drinking water for 42 days, were used. After the induction of metabolic syndrome, the mycelium of G. lucidum in the form of water suspension (a dose of 1 g/kg of the animal's body weight) was administered to animals per os for 7 and 14 days. Glucose concentration was determined using the glucose oxidase method. The content of glycosylated hemoglobin in erythrocytes was determined by the colorimetric method. The concentration of triglycerides, cholesterol, high-density lipoproteins, and low-density lipoproteins in blood plasma was determined by enzymatic methods. A significant decrease in the content of glycosylated hemoglobin was established in animals with metabolic syndrome against the background of administration of the studied suspension. Under the conditions of experimental metabolic syndrome, the administration of mycelium for 7 and 14 days led to a decrease in the concentration of triglycerides by 17.8 and 44.8%, cholesterol by 10.7 and 21.3%, low-density lipoproteins by 14.8 and 28.4%, and to an increase in high-density lipoproteins concentration by 11.9 and 21.5%, compared with metabolic syndrome. The obtained results demonstrate the corrective effect of the suspension of the G. lucidum powdered mycelium on carbohydrate and lipid metabolism, which was directly proportional to the duration of administration.

Omega-3 Effects on Ligature-Induced Periodontitis in Rats with Fructose-Induced Metabolic Syndrome.

Both periodontal disease (PD) and metabolic syndrome (MS) represent disorders of concern worldwide. Current evidence indicates that PD and MS might negatively influence each other, increasing the risk for cardiovascular diseases (CVD), via mutual inflammatory pathways. A failure of the inflammation resolution mechanisms is crucial for these comorbidities. Fish oil-derived omega-3 has been linked with resolution-driven responses in different pathological conditions during the last years. This study evaluated the impacts of omega-3 supplementation in a rat model combining ligature-induced PD and 10% fructose intake-elicited MS. Our main findings show that 10% fructose ingestion led to an elevation of Lee index and white adipose tissue (WAT) weight, along with hepatic alterations, accompanied by an increase of leptin, and a decrement of adiponectin serum amounts, regardless of PD induction. Noteworthy, the co-induction of PD and MS resulted in higher levels of glycemia and triglycerides, being this latter effect lessened by omega-3 supplementation. In this case, the beneficial effects of omega-3 might be associated with its ability to recover the decline of serum adiponectin levels in rats with PD plus MS. As expected, PD induction led to alveolar bone loss, independent of MS induction. However, the supplementation with omega-3 restored alveolar bone in PD control animals, but not in the rats with PD combined with MS. Our study extends the knowledge about PD and MS as comorbidities, showing novel effects of omega-3 supplementation in this context.

The therapeutic effects of distinct exercise types on metabolic syndrome-induced reproductive system impairment in male rats: Potential contribution of mitochondria-related genes.

A sedentary lifestyle and high fructose dietary habits cause diseases, such as metabolic syndrome (MS). The study was aimed to investigate the potential ameliorative effects of different exercise interventions on high fructose-induced MS-mediated reproductive system disruption of male rats. Rats were divided into four groups (n=6): Control, MS, MS+aerobic exercise (AE) and MS+anaerobic exercise (ANE). MS was induced by using tap water containing 30% fructose for 8weeks. After the induction of MS, AE/ANE implementations were started for 6weeks. Testis tissue and serum samples of rats were stored for biochemical and molecular analyses. Serum total antioxidant status level increased in the MS+AE group compared to all groups. Also, serum total oxidant status level, which increased by MS, decreased with AE, but not altered with ANE. Moreover, MS markedly decreased serum luteinizing hormone, but not changed the follicle-stimulating hormone. However, serum hormone levels were similar to the control group in both MS+AE and MS+ANE groups. MS upregulated mitochondria-related genes' mRNA expressions (MFN2, PGC1A, PPARG, PARP2 and TXNL4B). These increases, except for PPARG, were normalized with both exercise types. These results revealed that mitochondria-related genes may have a crucial role in MS-mediated male reproductive impairment and therapeutic effects of exercises.

Metabolic syndrome improves cardiovascular dysfunction and survival during cecal ligation and puncture-induced mild sepsis in mice

AimsSepsis is a potentially fatal systemic inflammatory response and its underlying pathophysiology is still poorly understood. Studies suggest that obesity, a component of metabolic syndrome (MS), is associated with sepsis survival. Therefore, this study focused on investigating the influence of MS on mortality and cardiovascular dysfunction induced by sublethal cecal ligation and puncture (SL-CLP). Main methodsNewborn Swiss mice received monosodium glutamate (MSG) (4 mg kg−1 day−1, s.c.) during the first 5 d of life for MS induction, while the control pups received equimolar saline solution. On the 75th day, SL-CLP was used to induce mild sepsis (M-CLP) in the MS (MS-M-CLP) and control (SAL-M-CLP) mice. The effect of MS on sepsis in mice was assessed by determining the survival rate and quantification of nitric oxide (NO) in the plasma, and associating this data with hematological and cardiovascular parameters. Key findingsMS improved the survival of septic mice, preventing impairment to hematological and cardiovascular parameters. In addition, MS attenuated plasmatic NO increase, which is a typical feature of sepsis. SignificanceThese findings provide new insights into the relationship between obesity and mild sepsis in mice, thus revealing an approach in favor of the “obesity paradox.”

Abstract 1125: Altered therapeutic response to metronomic chemotherapy in a metabolic syndrome model of mice bearing a mammary adenocarcinoma: Implication of intestinal ABC transporters

Abstract Breast cancer is one of the most prevalent and deadly cancers worldwide. Its prognosis depends on the cell type, as well as the age and comorbidities of each patient. A novel therapeutic approach is metronomic chemotherapy (MCT) characterized by chronic, low dose drug administration with therapeutic efficacy andlow or null toxicity as majoradvantages. The comorbidity that worsens cancer prognosis is metabolic syndrome (MS) characterized by obesity, insulinresistance, hyperglycemia, hypertriglyceridemia and hypercholesterolemia, and a chronic systemic inflammatory state. These conditions influence the intestinal biochemical barrier, altering the multidrug resistance-associated protein 2 (Mrp2) and P-glycoprotein (P-gp activities. Significantly, these two efflux pumps transport chemotherapeutics drugs such as cyclophosphamide (Cy). Our aim was to evaluate the effectiveness and toxicity of MCT with Cy in mice with metabolic syndrome bearing a mammary adenocarcinoma. Simultaneously, the activities of the intestinal efflux transporters were assessed. CBi male mice (5 weeks n=20/group), were fed with a chow diet (C) and a diet with 40% calories of fat (HFD) throughout the experiment. At 16 weeks, the development of MS was confirmed by biochemical and morphological parameters. The Mrp2 and P-gp activities were evaluated using the in vitro model of everted intestinal sacs. Once the MS features were settled, mice werechallenged s.c. with triple negative M-406 mammary adenocarcinoma (day 0); when the tumor was palpable, mice were distributed into 4 groups (n=8/group):GI: C no treatment, GII:C+Cy (30 mg/kg/day in drinking water), GIII: HFD no treatment and GIV: HFD+Cy. Efflux of Mrp2 substrate DNP-SG decreased 64% in HFD respect to C (P&amp;lt;0.05); transport rate of rhodamine 123 by P-gp decreased 55% in HFD vs C (P&amp;lt;0.05). At the end of the experiment (day 22), the tumor volume was lower in GIIvsGI and in GIVvsGIII (P&amp;lt;0.0001).The % inhibition of tumor growth in GII was higher than thatof GIV (P=0.052). The activity of Mrp2 or P-gpit was not modified by the tumor or MCT and remained decreased. It was observed a 30% decrease in body weight and leukopenia in GIV, indicating toxicity. We conclude that the induction of MS impairs the intestinal Mrp2 and P-gp activities bringing about differences in Cy absorption, leading to toxicity; in addition, MCT has lower antitumor effectiveness in animals with MS. The age-related changes and metabolic syndrome comorbid conditions urge to reconsider the therapeutics. Citation Format: María Manuela Barranco, Martín Habib, Bianca Di Carlo, Nicolás Sigal, María Sylvestre Begnis, Felipe Zechinatti, Antonela Del Giudice, María Jose Rico, Viviana Rosa Rosados, O. Graciela Scharovsky, Silvina Stella Maris Villanueva, Fabiana García, Leandro E Mainetti. Altered therapeutic response to metronomic chemotherapy in a metabolic syndrome model of mice bearing a mammary adenocarcinoma: Implication of intestinal ABC transporters [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 1125.

Оксидантный стресс и тканевая гипоксия как факторы, способствующие развитию дисфункции предстательной железы и мочевого пузыря при метаболическом синдроме

Introduction. The development of oxidative stress and nonspecific inflammation is one of the leading factors in the development of benign prostatic hyperplasia (BPH) and associated urination disorders in metabolic syndrome (MS). However, the specific mechanisms of these processes are not entirely clear. The purpose of the study. To study the activity of reactive oxygen species production and the functional state of mitochondria in the prostate and bladder and their role in the dysfunction of these organs using an experimental model of MS induction in rats. Material and methods. In 10 adult mongrel male rats MS was induced by keeping them on a high-calorie diet with an increased content of carbohydrates and fats for 3 months. 10 rats kept on a standard vivarium diet served as controls. The development of MS was confirmed by characteristic changes in the biochemical analysis of blood (hyperglycemia, hyperuricemia, dyslipidemia, hyperinsulinemia). In both series of rats, sections of the native prostate and bladder were examined by laser confocal microscopy and stained with fluorescent probes that characterize the activity of the production of reactive oxygen species (dichlorofluorescein-DCF) and the functional state of the mitochondria (tetramethylrodamine ether – TMRE). The activity of a number of intracellular enzymes (AST, ALT. Alkaline phosphatase, LDH) was investigated in the tissues and urine. Results. In rats with MS, the development of BPH and hypertrophy of the bladder were revealed, confirmed histologically. The study of sections of both organs by confocal microscopy revealed a significant increase in the production of reactive oxygen species by their cells and a decrease in the functional activity of mitochondria, which indicated the development of oxidant stress and tissue hypoxia. In the prostate, this was accompanied by a decrease in the secretory activity of the prostate glands, and in the bladder – the release of cytoplasmic enzymes from damaged cells into the urine, indicating cell damage. Conclusion. The causes of the development of a non-specific inflammatory process in the prostate and bladder, leading to dysfunction of these organs in MS, are increased production of reactive oxygen species and the development of tissue hypoxia.

Exercise and Caloric Restriction Improves Liver Damage in Metabolic Syndrome Model

Objective: Detecting the level of antioxidant and tissue damage that can occur in liver tissue induced metabolic syndrome by a high fructose diet in rats and the changes after exercise and/or caloric restriction. Materials and Methods: Sprague-Dawley male rats were divided into five groups: control (C), metabolic syndrome (M), metabolic syndrome with exercise (ME), metabolic syndrome with caloric restriction (MCR), and metabolic syndrome with exercise and caloric restriction (MECR). To induce metabolic syndrome, a 10% fructose solution was given to rats in drinking water for 3 months. Exercise and caloric restriction were applied to the related groups for 6 weeks after the induction of metabolic syndrome. Glucose in the blood, lipid peroxidation (LPO), sialic acid (SA), hexosamine, mucin, fucose, glutathione (GSH) levels, alkaline phosphatase (ALP), tissue factor (TF), superoxide dismutase (SOD), catalase (CAT), and glutathione-Stransferase (GST) activities were measured in rat liver homogenates. Results: In the liver, LPO levels increased and TF activities decreased in the M group compared to the C group and increased in the MCR and MECR groups compared to M group. GSH levels, SOD, and CAT activities decreased in M compared to C group and increased more significantly in MECR group compared to M group. SA levels increased in MCR and MECR groups compared with M group. Fucose levels also increased in MECR compared with the all others. Conclusion: Liver tissue damage that occurs after a fructose diet and decreased antioxidant levels was shown to improve best in combined exercise and caloric restriction treatment (MECR group).

Diagnostic Criteria for Metabolic Syndrome in Diet-Induced Rodent Models: A Systematic Review.

Thousands of publications in recent years have addressed the induction of metabolic syndrome (MetS) in rodents. However, the criteria and the reference values for diagnosing this disease have not been defined. Our main objective was to carry out a systematic review to gather evidence about the criteria for biochemical and anthropometric parameters in which scientific studies have relied on to report that rats developed MetS from a previous dietary manipulation. We compiled characteristics and findings of diet-induced MetS with high-fat, high-carbohydrate, high-fat/high-carbohydrates, and cafeteria diet from PubMed and Science Direct databases published in the last 5 years. The results on the principal determinants for the syndrome, published in the reviewed articles, were chosen to propose reference values in the rat models of food induction. The values obtained will serve as reference cut-of points in the development of the disease; in addition, the compilation of data will be useful in planning and executing research protocols in animal models.

The effects of two types of Western diet on the induction of metabolic syndrome and cardiac remodeling in obese rats

Metabolic syndrome (MetS) include obesity as a critical feature and is strongly associated with risk of cardiovascular disease (CVD). Insights into mechanisms involved in the pathophysiology of these clinical manifestations are essential for the development of therapeutic strategies. Thus, Western diets (WD) have been widely employed in diet-induced obesity (DIO) model. However, there are variations in fat and sugar proportions of such diets, making comparisons challenging. We aimed to assess the impact of two types of the WD on metabolic status and cardiac remodeling, to achieve a DIO model that better mimics the human pathogenesis of MetS-induced CVD. Male Wistar rats were distributed into three groups: control diet, Western diet fat (WDF), and Western diet sugar (WDS) for 41 weeks. Metabolic and inflammatory parameters and cardiac changes were characterized. WDF and WDS feeding promoted higher serum triglycerides, glucose intolerance, and insulin resistance, while just WDF presented inflammation in adipose tissue. WDF-fed rats showed increased catalase activity and malondialdehyde (MDA) and carbonyl protein levels, suggesting cardiac oxidative stress, while WDS-fed rats only raised MDA. Both WD equally elevated protein expressions involved in lipid metabolism, but only WDF downregulated the glycolysis pathway. Furthermore, the mechanical myocardial function was impaired in obese rats, being more relevant in WDF. In conclusion, both WD effectively triggered MetS features, although inflammation was detected just on the WDF-fed animals. Moreover, the WDF promoted a more pronounced functional, metabolic, and oxidative cardiac disorder, suggesting to be an adequate model for studying CVD in the scenario of MetS.

The Effect of Dipeptidyl Peptidase-4 Inhibitors or Curcumin on Diet Induced Metabolic Syndrome with Cardiac Dysfunction in Rats

ABSTRACT Background: Metabolic syndrome (MS) increases the risk of developing cardiovascular diseases (CVDs) which are the leading cause of death worldwide. Objective: This study is aiming to investigate the curative effects ofdipeptidyl peptidase-4 inhibitorsand the prophylactic effects of curcumin on diet induced metabolic syndrome which is associated with cardiac dysfunction in rats. Methodology: sixty adult male albino rats were divided into six groups: Group I: (control). Group II: (MS induced). Group III: (Vildagliptin only). Group IV: (Curcumin only). Group V (therapeutic):Vildagliptin treated rats after 8 weeks of MS to the end of 12 weeks. Group VI (prophylactic): Curcumin is administered with MS induction concomitantly for 12 weeks. Transthoracic echocardiogram was done while rats were alive. At the end of the experiment, blood was collected and biochemical analysis (blood glucose, serum insulin, lipid profile and cardiac enzymes) was done. Heart tissues were used for oxidative stress parameters (cardiac mitochondrial reactive oxygen species (ROS) and cardiac mitochondrial complex I and complex II) beside histopathological examination. Results: High fat diet (HFD)administration resulted in a significant increase in blood glucose, serum insulin, homeostasis model assessment of IR (HOMA- IR) index with disturbed lipid profile. Significant increase in serum cardiac enzymes and oxidative stress tissue markers were also noticed. Echocardiography revealed structural and functional cardiomyopathy. Histopathological examination showed cellular infiltrations with fat cells and collagen fibers accumulation. DPP- 4 inhibitors and curcuminresulted in a significant decrease in glucose, insulin, and HOMA- IR index, partial amelioration of lipid profile, cardiac enzymes, and cardiac oxidative stress markers. Echocardiography revealed alleviation of cardiomyopathy. Histopathological examination also revealed highly manifested structural improvement. Conclusion: The current study revealed that both DPP- 4 inhibitors and curcumin improve cardiomyopathy resulted from HFD administration with a diversity of mechanisms including anti-inflammatory, anti-apoptotic and anti-oxidative ways.

The protective effects of eugenol on metabolic-syndrome, renal damages

Introduction: Metabolic syndrome consists of a group of abnormities which is involved with chronic kidney disease and nephropathy. Eugenol is an important phenolic component, which is present in many plants’ essential oils such as cloves oil with antioxidant effects. Objectives: Our study planned to demonstrate eugenol’s effects over nephrotoxicity derived from metabolic syndrome. Materials and Methods: Thirty-five male Wistar rats were picked accidentally and then divided into five groups including 1) tap water; 2) water with fructose10%; 3) water with fructose + sweet almond oil and administered intraperitoneally; 4) water with fructose+ eugenol 50 mg/kg/d and administered intraperitoneally; 5) water with fructose+ eugenol 100 mg/kg/d administered intraperitoneally. This regime lasted for 60 days, and at the beginning of day 31st, injections started for 30 days. Assessment of serum, urine and renal parameters (in homogenized kidney tissue) were conducted in the last step. Results: The results argued that the induction of metabolic syndrome following renal injury has significantly increased serum blood urea nitrogen (BUN) and creatinine (Cr) levels in the fructose group. Consumption of eugenol resulted in a significant reduction in the level of these two biochemical factors (P &lt; 0.05). The renal level of malondialdehyde (MDA) increased in the fructose group while treatment with a dose of 50 eugenol decreasing its level (P &lt; 0.05). Proteinuria and kidney tissue damage score (KTDS) increased in the fructose group compared with the tap water group (P &lt; 0.001). It is noteworthy that treatment with eugenol did not affect the level of proteinuria and KTDS with any of the used doses. Conclusion: Our results indicated the improvement of renal functioning and decrease in lipid peroxidation, although eugenol doses used in this study did not reduce proteinuria and KTDS.

Exercise and caloric restriction improve cardiovascular and erectile function in rats with metabolic syndrome.

The aim of this study is to examine the possible benefits of exercise and caloric restriction (CR) on cardiovascular hemodynamics, erectile function, and antioxidant system in metabolic syndrome (MS). Sixty male Spraque-Dawley rats were divided into five groups; control, MS, MS + CR, MS + exercise (EXC), and MS + CR + EXC. To induce MS, 10% fructose solution was applied for 3 months. Thereafter, in CR groups calorie was restricted 40% and in EXC groups swimming was performed for 6 weeks. Body weight, blood glucose, and blood pressure (BP) levels were measured before and after MS induction and at the end of the experiment. After decapitation, tumor necrosis factor (TNF)-α, adiponectin (ADP), and plasminogen activator inhibitor (PAI)-1 levels were investigated in blood, oxidative stress parameters were examined in heart, aorta, and corpus cavernosum (CC) tissues. Isometric contraction in isolated tissue bath was studied in aorta and CC tissues. Animals subjected to exercise and CR had decreased BP and blood glucose levels. Impaired contraction-relaxation responses in MS group were improved with exercise and CR. MS-induced increase in TNF-α, PAI-1, malondialdehyde (MDA), and decrease in ADP, glutathione (GSH), and superoxide dismutase (SOD) were normalized with exercise and CR. Exercise and CR may be beneficial against changes in cardiovascular hemodynamics caused by MS.

Effects of resveratrol nanocapsules on the quantitative insulin sensitivity check index in insulin resistance: a study on metabolic syndrome induce mice

The aim of this study is to evaluate the effect of resveratrol nanocapsules (RV-NCs) by quantitative insulin sensitivity check index (QUICKI) for insulin resistance diagnosis on metabolic syndrome induction in mice. Next, the applicability of these nanocapsules (NCs) was evaluated in metabolic syndrome induced in 40 mice. RV-NCs were synthesized by interfacial deposition method and was analyzed by various methods including Zetasizer, high-performance liquid chromatograph, potentiometer and scanning electron microscopy. The analysis results show a zeta potential of − 7.15, loading efficiency of 99.54 ± 1.02% and particle size of 207 nm for RV-NC production. Collected data from mice examination were analyzed by ANOVA and Tukey criteria. The validity and the reproducibility of the QUICKI index in a population of mice were determined and found that is a significant difference between high fat diet group and the control group (p < 0.05). In addition, the result obtained by the Tukey test indicated the difference in insuline and glucose levels of these group. Also, it probably is associated with the increase in the in vivo stability, which is obtained by the effective formulation of nanocapsules for resveratrol delivery.

Metabolic syndrome accentuates post-traumatic stress disorder-like symptoms and glial activation

The relationship between individuals with post-traumatic stress disorder (PTSD) and the development of metabolic syndrome (MS) is well understood, but the relationship between individuals with preexisting MS and the development of PTSD is not yet known. Therefore, we evaluated the course of PTSD development in preexisting MS rats and we quantified the glial fibrillary acidic protein (GFAP) and ionized the calcium binding adaptor molecule 1 (Iba-1) in the cortex and hippocampus of the experimental animals. Male Wistar rats were divided into two groups: control or 10 % fructose for 5 weeks. After 5 weeks of MS induction, a group of animals was used to characterize MS. In another group, after 5 weeks of MS induction, animals were exposed to or not exposed to inescapable footshocks, followed by social isolation. After 14 days of a retention interval, the animals were re-exposed to the inescapable footshocks box, and the freezing time was evaluated. Over the following days, the animals were tested using the open field, social interaction and forced swimming tests, respectively. In another group of animals, after induction of MS and PTSD as previously described, elevated plus maze and object recognition tests were performed. Our results demonstrate that fructose solution for 5 weeks was able to induce MS, and animals with MS had more pronounced PTSD-like symptoms and a greater increase in GFAP and Iba-1 in the hippocampus and prefrontal cortex. In conclusion, MS accentuated PTSD-like symptoms that may be related to increased glial activation. This study helps reveal factors that may predispose individuals to the development of PTSD, such as metabolic disorders.