Fructose-induced Metabolic Syndrome Research Articles

Pregestational fructose-induced metabolic syndrome in Wistar rats causes sexually dimorphic behavioral changes in their offspring.

Metabolic syndrome (MetS), marked by enduring metabolic inflammation, has detrimental effects on cognitive performance and brain structure, influencing behavior. This study aimed to investigate whether maternal MetS could negatively impact the neurodevelopment and metabolism of offspring. To test this hypothesis, 2 months old female Wistar rats were subjected to a 10-week regimen of tap water alone or supplemented with 20% fructose to induce MetS. Dams were mated with healthy males to generate litters: OC (offspring from control dams) and OMetS (offspring from dams with MetS). To isolate prenatal effects, all pups were breastfed by control nurse dams, maintaining a standard diet and water ad libitum until weaning. Behavioral assessments were conducted between postnatal days (PN) 22 and 95, and metabolic parameters were analyzed post-sacrifice on PN100. Results from the elevated plus maze, the open field, and the marble burying tests revealed a heightened anxiety-like phenotype in OMetS females. The novel object recognition test showed that exclusively OMetS males had long-term memory impairment. In the reciprocal social interaction test, OMetS displayed a lower number of social interactions, with a notable increase in "socially inactive" behavior observed exclusively in females. Additionally, in the three-chamber test, social preference and social novelty indexes were found to be lower solely among OMetS females. An increase in visceral fat concomitantly with hypertriglyceridemia was the relevant postmortem metabolic finding in OMetS females. In summary, maternal MetS leads to enduring damage and adverse effects on offspring neurobehavior and metabolism, with notable sexual dimorphism.

Editorial Expression of Concern: Alterations in peripheral purinergic and muscarinic signaling of rat bladder after long-term fructose-induced metabolic syndrome.

Editorial Expression of Concern: Alterations in peripheral purinergic and muscarinic signaling of rat bladder after long-term fructose-induced metabolic syndrome.

Effect of Solanum melongena on Components and Kidney Damage of Fructose-Induced Metabolic Syndrome in Rats

: In traditional Mexican medicine, Solanum melongena is used to treat obesity, diabetes mellitus, hypertension, asthma, bronchitis, arthritis, and hypercholesterolemia. This study examined the effect of treatment with ethanolic extract (EE) from the fruit of S. melongena on kidney damage on metabolic syndrome (MS). Male Wistar rats were maintained for 12 weeks on a diet of 20% fructose in drinking water and chow to develop MS. After administering EE of S. melongena (100 and 200 mg/kg/day, orally) for 6 weeks, the histological study of the kidney cortex and determination by Western blot of the renal expression of angiotensin II AT1 receptor and cytokine transforming growth factor beta 1 (TGF-β1) were realized. The rats fed with high fructose developed MS and showed kidney damage characterized by proliferative glomerulonephritis and necrosis; this damage was reduced by S. melongena treatment and associated with decreased expression of AT1 receptor for angiotensin II and cytokine TGF-β1, controlling renal damage in this animal model. In rats affected by MS through high fructose feeding, the treatment with EE of S. melongena showed a renoprotective effect through decreased expression of AT1 receptor for angiotensin II and cytokine TGF-β1, causes of glomerulonephritis.

Manifestations of Liver Impairment and the Effects of MH-76, a Non-Quinazoline α1-Adrenoceptor Antagonist, and Prazosin on Liver Tissue in Fructose-Induced Metabolic Syndrome.

Excessive fructose consumption may lead to metabolic syndrome, metabolic dysfunction-associated fatty liver disease (MAFLD) and hypertension. α1-adrenoceptors antagonists are antihypertensive agents that exert mild beneficial effects on the metabolic profile in hypertensive patients. However, they are no longer used as a first-line therapy for hypertension based on Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) outcomes. Later studies have shown that quinazoline-based α1-adrenolytics (prazosin, doxazosin) induce apoptosis; however, this effect was independent of α1-adrenoceptor blockade and was associated with the presence of quinazoline moiety. Recent studies showed that α1-adrenoceptors antagonists may reduce mortality in COVID-19 patients due to anti-inflammatory properties. MH-76 (1-[3-(2,6-dimethylphenoxy)propyl]-4-(2-methoxyphenyl)piperazine hydrochloride)) is a non-quinazoline α1-adrenoceptor antagonist which, in fructose-fed rats, exerted anti-inflammatory, antihypertensive properties and reduced insulin resistance and visceral adiposity. In this study, we aimed to evaluate the effect of fructose consumption and treatment with α1-adrenoceptor antagonists of different classes (MH-76 and prazosin) on liver tissue of fructose-fed rats. Livers were collected from four groups (Control, Fructose, Fructose + MH-76 and Fructose + Prazosin) and subjected to biochemical and histopathological studies. Both α1-adrenolytics reduced macrovesicular steatosis and triglycerides content of liver tissue and improved its antioxidant capacity. Treatment with MH-76, contrary to prazosin, reduced leucocytes infiltration as well as decreased elevated IL-6 and leptin concentrations. Moreover, the MH-76 hepatotoxicity in hepatoma HepG2 cells was less than that of prazosin. The use of α1-adrenolytics with anti-inflammatory properties may be an interesting option for treatment of hypertension with metabolic complications.

Effect of curcumin on plasma TBARS and IL-6, adipose tissue AFABP-4 and liver FGF-21 in fructose-induced metabolic syndrome rats

Effect of curcumin on plasma TBARS and IL-6, adipose tissue AFABP-4 and liver FGF-21 in fructose-induced metabolic syndrome rats

The effect of exenatide (a GLP-1 analogue) and sitagliptin (a DPP-4 inhibitor) on asymmetric dimethylarginine (ADMA) metabolism and selected biomarkers of cardiac fibrosis in rats with fructose-induced metabolic syndrome

Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide (NO) synthesis, is a risk factor for endothelial dysfunction, a common pathophysiological denominator for both atherogenesis and cardiac fibrosis.We aimed to investigate whether the cardioprotective and antifibrotic effects of incretin drugs, exenatide and sitagliptin, may be associated with their ability to affect circulating and cardiac ADMA metabolism.Normal and fructose-fed rats were treated with sitagliptin (5.0/10 mg/kg) or exenatide (5/10 µg/kg) for 4 weeks. The following methods were used: LC-MS/MS, ELISA, Real-Time-PCR, colorimetry, IHC and H&E staining, PCA and OPLS-DA projections.Eight-week fructose feeding resulted in an increase in plasma ADMA and a decrease in NO concentration. Exenatide administration into fructose-fed rats reduced the plasma ADMA level and increased NO level. In the heart of these animals exenatide administration increased NO and PRMT1 level, reduced TGF-ß1, α-SMA levels and COL1A1 expression. In the exenatide treated rats renal DDAH activity positively correlated with plasma NO level and negatively with plasma ADMA level and cardiac α-SMA concentration. Sitagliptin treatment of fructose-fed rats increased plasma NO concentration, reduced circulating SDMA level, increased renal DDAH activity and reduced myocardial DDAH activity. Both drugs attenuated the myocardial immunoexpression of Smad2/3/P and perivascular fibrosis.In the metabolic syndrome condition both sitagliptin and exenatide positively modulated cardiac fibrotic remodeling and circulating level of endogenous NOS inhibitors but had no effects on ADMA levels in the myocardium.

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.

Effect of Phosphatidylcholine on Dyslipidemia and Atherogenic Index in High Fructose Exposed Rats


 
 
 
 The purpose of this research was to investigate the beneficial effects of phosphatidylcholine in reducing changes in both lipid and protein profiles in addition to atherogenic index in adult rats with fructose-induced metabolic syndrome. Thirty-six mature Wistar Albino female rats (Rattus norvegicus) (aged 12-15 weeks and weighing 200±10 g) were divided randomly into four groups (G1, G2, G3, and G4); then variable treatments were orally administered for 62 days as follows: G1 (Control group), received distilled water; G2, treated with phosphatidylcholine (PC) orally (1 g/kg BW); G3 (Fr), orally dosed with 40% fructose and 25% fructose mixed with drinking water; G4 (Fr+PC), were also intubated with 40% fructose and 25% fructose in drinking water, and received PC at 1 g/kg BW by oral tube. At the end of the research, specimens were taken by cardio puncture approach after fasting for 8-12 h. Serum was obtained to measure lipid criteria (total serum cholesterol, triacylglycerol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, very low-density lipoprotein-cholesterol, non-high-density lipoprotein-cholesterol, and Atherogenic index) and protein profile (total protein, albumin, and globulins). The results showed that the occurrence of dyslipidaemia (hypercholesterolemia, triacyleglycerolemia) increase in low density of lipoprotein-cholesterol, very low-density lipoprotein-cholesterol, no-high density lipoprotein-cholesterol concentrations and atherogenic index and reduce the concentration of high-density lipoprotein-cholesterol) in fructose treated animals in addition to disturbance in protein profile (lowered in total protein and globulins level).PC treatment resulted in decreased changes in lipid profile, protein profile, and atherogenic index in rats, whereas fructose induced metabolic syndrome. In conclusion, using Phosphatidylcholine treatment in rats may reduce the changes of lipid and protein profiles and atherogenic index while fructose may lead to metabolic syndrome.
 
 
 

Evaluation of the activity of trans-Resveratrol alone and in combination with Amlodipine and Pioglitazone against Fructose induced metabolic syndrome rats

Metabolic syndrome (MS) is a cluster of conditions that cause an increase in the risk of diabetes, heart disorders, and stroke.The present research was completed in Wistar rats, in which Metabolic Syndrome (MS) was induced with a High Fructose Diet. Animals were randomly divided into 7 gatherings and the test group animals received Resveratrol (RSVT), Amlodipine (AML), Pioglitazone (PIO), Resveratrol+Amoldipine, and Resveratrol+Pioglitazone at different doses for 5 weeks. Various behavioral, biochemical, and histopathological parameters were estimated.AML alone and along with RSVT was found to reduce diastolic and systolic pressures, there was the reduction in BP in the remaining groups. There was a significant reduction in serum insulin and Fasting glucose level (FGL) in all the treatment groups. And there was a noticeable reduction in the levels of total glycerides (TG), total cholesterol (TC) along with LDL, HDL, and VLDL when compared to the control group and HFD group. Histopathological study revealed that there was a reduction in the deposition of lipids in liver cells and aorta as compared to HFD group.The outcomes showed the defensive mechanism of Resveratrol against fructose-induced Metabolic Syndrome. The mechanism of protection may be due to an escalation of cellular antioxidants. The activity was found to increase in combination with amlodipine and pioglitazone.

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.

Pumpkin seed proteins (Cucurbita pepo L.) protect against diet-induced metabolic syndrome by improving insulin resistance and markers of oxidative stress and inflammation in rats

Pumpkin (Cucurbita pepo L.) seeds are enriched in bioactive compounds having functional properties. The aim of this study was to analyze the pumpkin seed proteins (PSP) effects on insulin resistance, oxidative stress damage and inflammation in rats with high fructose-induced metabolic syndrome.Twenty four male Wistar rats, fed isoenergetic diets supplemented with: (1) 20% casein (C); (2) 20% casein and 1 g/kg/day PSP (P); (3) 20% casein and 64% D-fructose (C-HF); (4) 20% casein, 1 g/kg/day PSP and 64% D-fructose (P-HF). After 8 weeks of treatment, fructose supply impaired white adipose tissue (WAT) weight, deteriorated glucose tolerance and tAUC, plasma glucose, insulin, insulinogenic index, HOMA-IR and HOMA-β, antioxidant status, lipid and protein oxidation, plasma TNF-α and IL-6 as compared to control diets. Interestingly, rats assigned to the PSPs diet with or without fructose displayed lower plasma glucose, insulin and fructose, improved tolerance of glucose, tAUC, HOMA-IR and HOMA-β and increased insulinogenic index as compared to C diets. PSPs consumption lowered thiobarbituric acid reactive substances, hydroperoxides and carbonyls in WAT and carbonyls in muscle. Superoxide dismutase and glutathione peroxidase in WAT were significantly diminished in P-HF but increased in P as compared to C-HF and C. Rats fed P-HF diet had low catalase in WAT and high in muscle than those fed C-HF. Moreover, catalase activity increased in muscle but decreased in WAT in P group than in C group. In conclusion, pumpkin seed proteins exhibit favorable effects on metabolic disorders of fructose-induced metabolic syndrome, suggesting a key role in disease therapy.

Histological and molecular study of N-acetyl cysteine’s effects on salivary glands in fructose-induced metabolic syndrome in albino rats

Histological and molecular study of N-acetyl cysteine’s effects on salivary glands in fructose-induced metabolic syndrome in albino rats

High-Fructose Diet Increases Renal ChREBPβ Expression, Leading to Intrarenal Fat Accumulation in a Rat Model with Metabolic Syndrome.

Simple SummaryFructose consumption leads to the development of metabolic syndrome. Fatty liver and chronic kidney disease are closely related to metabolic syndrome. Lately, a transcription factor that regulates fructose metabolism in the liver, named ChREBPβ, which is responsible for de-novo lipogenesis and intra-hepatic fat accumulation (“fatty liver”), was described. In this study, we demonstrate that the effect of fructose consumption on the kidneys resembles its liver effect. Rats fed with a high-fructose diet exhibit bigger kidneys with higher triglycerides content, compared to control rats. The expression of ChREBPβ and its downstream genes was upregulated as well. Treating kidney-origin cells with fructose increased the expression of this factor as well, showing the direct effect of fructose on this factor. Thus, the appearance of fatty kidney in response to high-fructose consumption revealed a new mechanism linking metabolic syndrome to chronic kidney disease.Fructose consumption is associated with metabolic syndrome (MeS). Dysregulated lipid metabolism and ectopic lipid accumulation, such as in “fatty liver’’, are pivotal components of the syndrome. MeS is also associated with chronic kidney disease (CKD). The aim of this study was to evaluate kidney fructose metabolism and whether the addition of fructose leads to intrarenal fat accumulation. Sprague Dawley rats were fed either normal chow (Ctrl) or a high-fructose diet (HFrD). MeS features such as blood pressure and metabolic parameters in blood were measured. The kidneys were harvested for ChREBPβ and de novo lipogenesis (DNL) gene expression, triglyceride content and histopathology staining. HK2 (human kidney) cells were treated with fructose for 48 h and gene expression for ChREBPβ and DNL were determined. The HFrD rats exhibited higher blood pressure, glucose and triglyceride levels. The kidney weight of the HFrD rats was significantly higher than Ctrl rats. The difference can be explained by the higher triglyceride content in the HFrD kidneys. Oil red staining revealed lipid droplet formation in the HFrD kidneys, which was also supported by increased adipophilin mRNA expression. For ChREBPβ and its downstream genes, scd and fasn, mRNA expression was elevated in the HFrD kidneys. Treating HK2 cells with 40 mM fructose increased the expression of ChREBPβ. This study demonstrates that fructose consumption leads to intrarenal lipid accumulation and to the formation of a “fatty kidney”. This suggests a potential mechanism that can at least partially explain CKD development in fructose-induced MeS.

Does fructose have a protective role on migraine?-experimental evidence in a rat model of metabolic syndrome under omega-3 supplementation.

BackgroundMigraine is a highly disabling disease, for which current therapies are limited to symptom alleviation. There is compelling evidence linking migraine with metabolic disorders, but the causal relationship is not clear. Omega-3 (n-3) fatty acids have anti-inflammatory properties, with clear benefits in metabolic disorders, but its effects on migraine remains to be tested. We hypothesized that fructose-induced metabolic syndrome could aggravate migraine by increasing neuroinflammation and that n-3 treatment could mitigate it.MethodsMale Wistar rats were used. Animals that received 10% high fructose diet (HFD) or tap water were subdivided into two additional groups: with or without n-3 supplementation. Fifteen days before euthanasia, each group was subdivided into two additional groups: with or without nitroglycerin (NTG)-induced migraine.ResultsHFD lessened the migraine-like painful symptoms, as indicated by decreased grimace scores, which paralleled with reduced CGRP and leptin serum levels, increased hypothalamic CGRP, and decreased hypothalamic adiponectin and IL-6. There was a recovery of body and adipose tissue weight, besides a reduction of crown-like structures (CLS) in the inguinal adipose tissue. N-3 supplementation had no effect on NTG-related pain, but it decreased body and adipose tissue weight of HFD and tap water NTG-injected rats. N-3 improved NTG-related affective behavior and inflammatory parameters in tap water NTG-injected rats, with decreased hypothalamic TNF, serum CGRP and inguinal adipose-tissue CLS.ConclusionsHFD relieved NTG-induced pain, possibly due to decreased energy expenditure, minimizing migraine energy needs. N-3 exhibited favorable effects regarding affective behavior and central and peripheral inflammation, irrespective of HFD.

Effects of Pumpkin (Cucurbita pepo L.) Seed Protein on Blood Pressure, Plasma Lipids, Leptin, Adiponectin, and Oxidative Stress in Rats with Fructose-Induced Metabolic Syndrome

This study evaluates the potential effects of pumpkin seeds protein on blood pressure (BP), plasma adiponectin, leptin levels, and oxidative stress in rats with fructose-induced metabolic syndrome. Twenty four male Wistar albino rats were divided into four groups and fed a 20% casein diet, 20% casein diet supplemented with pumpkin protein, 20% casein diet with 64% D-fructose, or 20% casein diet with pumpkin protein and 64% D-fructose for 8 weeks. Contin-uous fructose feeding induced an increase in plasma insulin/glucose ratio, BP, insulin and glucose, aspartate aminotrans-ferase, alanine aminotransferase (ALT), alkaline phosphatase (ALP), creatinine, urea, and uric acid levels, and a decrease in the liver and muscle glycogen stores. In addition, elevated levels of total cholesterol (TC), triglycerides (TG), and leptin and lowered adiponectin levels were observed in rats fed a fructose-enriched diet. These groups also exhibited lower plasma levels of ascorbic acid and glutathione, higher thiobarbituric acid-reactive substances, hydroperoxide, carbonyl, and nitric oxide in both the liver and kidneys than rats fed the control diet. Interestingly, pumpkin seed protein treatment significantly counteracted alterations induced by fructose improving glucose, insulin, BP, TG, TC, ALT, and ALP levels, increasing liver and muscle glycogen stores, adiponectin level, and adiponectin/leptin ratio, and reducing plasma leptin lev-els. In addition, rats fed pumpkin protein with a high-fructose diet improved oxidative stress in the liver and kidneys. In conclusion, proteins from Cucurbita pepo L. seeds effectively improve metabolic parameters and protect against oxidative stress induced by a high-fructose diet.

An Investigation of the Effect of Curcumin on Fructose-Induced Metabolic Syndrome Rat Models

Aim: This study aimed to evaluate the potential effect of curcumin on glucose homeostasis, insulin resistance, inflammation, and oxidative stress in a fructose-induced metabolic syndrome rat model. Material and Methods: 24 male adult Wistar albino rats were randomly separated in to 4 groups: control (Group 1), 20% fructose (Group 2), 20% fructose and 100 mg/kg curcumin (Group 3), and 20% fructose, and 200 mg/kg curcumin (Group 4). Serum glucose, insulin, and plasma lipoprotein levels were determined by an auto-analyzer. Other parameters were determined by the Elisa Assay Method. Mann-Whitney U test was performed using the Bonferroni Correction to determine the significance of the difference between the two group (p≤0.008). Spearman Correlation Analysis was performed among parameters. Results: Metabolic Syndrome (MetS) was successfully created by observing increased serum glucose, high blood pressure, insulin resistance, and dyslipidemia in Group 2 compared to Group 1 (p≤0.008). The significance of serum total antioxidant capacity (TAC) levels among the groups could not be determined. While serum total oxidant status (TOS) and oxidative stress index (OSI) levels of Group 2 increased significantly compared to Group 1, and the levels of these parameters were significantly decreased in Group 3 and Group 4 compared to Group 2 (p≤0.008). The serum tumor necrosis factor-α (TNF-α) level of Group 2 increased significantly compared to Group 1 (p≤0.008). It was determined that the serum TNF-α level of Group 3 and Group 4 decreased significantly compared to Group 2 (p≤0.008). There was a positive correlation between serum OSI and TNF-α levels and serum HOMA-IR and TNF-α levels (p≤0.01). Conclusion: Our findings indicated that curcumin has a healing effect against MetS in the rat experimental animal model.

Amelioration of the Abnormalities Associated with Metabolic Syndrome by L-Norvaline in Hyperlipidemic Diabetic Rats

Abstract The present study was designed to assess the treatment effect of arginase inhibitor, L-Norvaline in abnormalities associated with high fat diet (HFD) and fructose-induced metabolic syndrome. The HFD and fructose was fed to the rats for a period of 45 days. Animals having body weight of 350 g and fasting blood sugar level of more than 250 mg/dl were considered as hyperlipidemic diabetic rats (HDR) and selected for the study. The HDR were divided into three groups having six animals each. The HDR received L–Norvaline (10 mg/kg/day, i.p.) and standard drug, gemfibrozil (60 mg/kg/day, p.o.), for a period of 30 days. Various hormonal, biochemical and tissue parameters were evaluated at the end of the study. Both treatments significantly decreased body weight, BMI, fasting blood sugar and insulin level and improved insulin resistance in HDR as compared to the toxicant control group. A significant improvement was observed in the lipid profile, levels of nitrate, leptin, C-reactive protein and adiponectin in HDR. L-Norvaline also caused slight decrease in the malondialdehyde level, though, no prominent effect was observed on the level of superoxide dismutase and reduced glutathione in the pancreas of HDR, as compared to the toxicant control group. L-Norvaline treatment also improved the histo-architecture of pancreatic cells. Results of the present study concludes that L-Norvaline caused significant alleviation of the abnormalities of MetS indicating that it can be used as potential treatment strategy for managing the symptoms of metabolic syndrome.

Effects of antioxidant diet on the RBC indices in fructose-induced obesity rat model

Abstract The oxidative stress is one of the known and discussed culprits for development and progression of the disturbances in Metabolic syndrome (MetS). In our study, we are investigating the effects of antioxidant additives as additional treatment and prophylaxis in a model of MetS. We are using a fructose-induced metabolic syndrome rat model to examine the effects of antioxidant preparation ZellSchutz. Four experimental groups were formed using male Wistar rats (n = 60). The control group received standard rat chow, the other groups received either ZellSchutz (Z), fructose (F), or fructose and ZellSchutz (ZF). Our results showed an unexpected increase in the RBC indices in rats with dual treatment. There was a significant increase in hemoglobin concentration, MCHC, and MCV in those animals (p<0.001). The preliminary data shows the important role of antioxidants as supplementary therapy in metabolic syndrome. Further investigations will be carried on to reveal the molecular mechanisms of the observed changes.

Melatonin ameliorates cardiac remodelling in fructose-induced metabolic syndrome rat model by using genes encoding cardiac potassium ion channels.

Metabolic syndrome comprises a group of disorders, including cardiac abnormalities. Ventricular arrhythmias observed in metabolic syndrome are due to the impaired ventricular repolarization. This study aims to determine the effects of melatonin on cardiac ventricular repolarization in metabolic syndrome rat model. Sprague-Dawley rats were divided into control (n = 8), melatonin (n = 8), metabolic syndrome (n = 8) and metabolic syndrome + melatonin (n = 8) groups. Fructose (200g/lt/day) was added into the drinking water during 8weeks of rats to induce metabolic syndrome model. In the last two weeks, melatonin (20mg/kg/day) was administered via oral gavage. Blood pressure measurements and ECG recordings were taken at three different times. Blood and left ventricular tissue samples were harvested and the KCNQ1,3 and KCNH2 gene expressions were analysed by qRT-PCR method. We observed insulin resistance, hyperglycemia, dyslipidemia and higher systolic blood pressure in metabolic syndrome group (p < 0.01, for all). Prolonged QT interval was observed in metabolic syndrome group (p < 0.001). The expression levels of the KCNQ genes encoding the Kv7 channel was significantly reduced, however KCNH2 gene which encodes Kv11.1 channel was increased in metabolic syndrome group compared to control group (p < 0.05, p < 0.001, respectively). Melatonin significantly normalised the prolongation on QT interval in metabolic syndrome group (p < 0.001) and the expressions of the KCNQ (p < 0.002) and KCNH2 genes (p = 0.003). The present study revealed that melatonin had ameliorative effects on ventricular repolarization by improving the prolonged QT duration in rats with metabolic syndrome and this effect was generated by the KCNQ and KCNH2 gene families.

Nigella Sativa and Ginger Increase GLUT4 and PPARγ in Metabolic Syndrome‐Induced Rats

Increased fructose intake has been linked to the epidemiology of insulin resistance, type 2 diabetes mellitus, renal damage, and metabolic syndrome (MS). As oxidative stress plays a pivotal role in the pathology of insulin resistance, the present study was conducted to investigate the effects of Nigella Sativa (NS) and ginger as potent antioxidants on fructose-induced MS in rats. Male rats were fed with a high‐fructose high-fat-fed diet for 8 weeks. By the end of the 8th week, rats were divided into four groups; one was left untreated (normal control) and MS control group was treated with saline. MS groups were given Nigella sativa (4 ml/kg) and ginger (500 mg/kg) daily for 4 weeks. Markers chosen for assessment included the effect on body weight gain, glucose, insulin, adiponectin levels, and lipid profile. Also, protein expressions were estimated by glucose transporter 4 (GLUT4) content and peroxisome proliferator‐activated receptor‐gamma (PPARγ). Nigella sativa and ginger ameliorated some manifestations of MS, including an increase in body weight, glucose, insulin level, and resistance. Besides, both drugs lowered insulin resistance, induced hyperlipidemia and increased adiponectin level. Drugs also increased GLUT4 and PPARγ protein expression compared with MS control group. Nigella sativa and ginger ameliorated parameters of MS via increased GLUT4 and PPARγ expression.