High-fructose Group Research Articles

YÜKSEK FRUKTOZLA BESLENEN SIÇANLARDA QUERCETİN’İN PERİRENAL YAĞ DOKUSUNDAKİ ADİPONEKTİN VE REZİSTİN DÜZEYLERİNE ETKİSİ

Obesity is defined as the accumulation of adipose tissue to excess and to an extent that impairs both physical and psychosocial health and well-being. The increase in adipose tissue observed in obesity causes proinflammatory and anti-inflammatory cytokine imbalance. Accumulating evidence on quercetin, one of the antioxidants frequently used in obesity treatment, suggests that quercetin has significant anti-obesity and lipid-lowering effects simultaneously. We hypothesized that quercetin supplementation could improve obesity parameters and restore adipokine balance in obese mice. Sprague Dawley rats, 8-10 weeks of age, were divided into 4 groups, including a control group (C), high fructose (HF) group, quercetine (Q) group, and high fructose+quercetin (HF+Q) group. Fructose was administered to HF groups as a 20% solution in drinking water for 6 weeks. The rats in the Q groups were given 50 mg quercetin per kg BW by gavage for the next 4 weeks. The body weight, lee index, TG, HDL, fasting insülin, fasting glucose, and HOMA-IR were determined in rats. ADP and resistin levels were determined by ELISA assay from perirenal adipose tissue homogenates. We showed that quercetin acts to improve TG, fasting glucose and insulin resistance in high fructose-fed rats. In this study, we found no effect of quercetin on perirenal adipose tissue ADP and resistin levels. These results showed that high fructose could induce obesity in rats, while quercetin could favorably affect these parameters.

Insulin Resistance through High-sugar Diets and its Effects on the Endometrium in Swiss Albino Mice: An Experimental Study to Elicit the Beneficial Effects of Coconut Sugar

Introduction: Insulin resistance (IR) has an insidious onset and is mainly due to the consumption of high-energy diets. Refined sugars contain high fructose which predisposes to IR and affects the endometrium since endometrium exhibits high-affinity insulin receptors, and the natural unrefined sugars such as coconut sugar are proved to be beneficial, but scientific studies are scarce to validate the findings. Subjects and Methods: A cross-sectional study was carried out, in which 36 female Swiss albino mice were divided into control and high-fructose and high-coconut sugar diet groups. The respective diets were prepared daily and fed for a period of 12 weeks, and the animals were sacrificed by the administration of ether. Biochemical parameters were assessed, and the uterus was removed and processed for histopathological analysis. Results: Glucose, insulin, and homeostasis model assessment-IR were assessed, in which there was an increase in the levels in the high-fructose group than the control and coconut sugar groups. The values were statistically significant in the Kruskal–Wallis analysis (P < 0.001) and post hoc test showed a significant difference between the control and fructose diet groups. Hormonal assay showed elevated testosterone levels in the fructose group (Kruskal–Wallis test, P < 0.001), which showed significance in post hoc test when compared with the control group (P < 0.030). Histopathological examination revealed complex hyperplasia with nuclear atypia in the fructose group, whereas the findings were normal in the coconut sugar and control groups. Discussion: The present study proved coconut sugar to be beneficial, and there is a strong correlation of high-energy diets on the endometrium due to IR. Conclusion: The present study concludes that the intake of natural sugars does not cause damage to the endometrium which is sensitive to insulin resistance.

The Acute Effect of Fructose on Cardiac Hemodynamic Responses and Infarcted Area in Isolated Rat Heart During Ischemia-Reperfusion

Introduction: This study aimed to investigate the effects of fructose on cardiac hemodynamics and infarct size and the role of the antioxidant mechanism in these effects in isolated rat hearts undergoing ischemiareperfusion. Patients and Methods: Isolated hearts obtained from female Wistar rats were perfused with Krebs-Henseleit solution containing 12 mM glucose or solution containing 12 mM fructose or 48 mM fructose and underwent lowflow ischemia followed by reperfusion on the Langendorff apparatus. Left ventricular developed pressure (LVDP), timedependent pressure changes (dp/dt max, dp/dt min) and heart rates were recorded at the 1st, 15th and 120th minutes of reperfusion following ischemia, and the percentage of the infarct area and the size of the risk area were determined. At the end of the reperfusion, total oxidant capacity (TOS), malondialdehyde (MDA) and glutathione (GSH) levels were examined in perfusion fluid samples. Results: Basal dp/dt max values were lower in the high fructose group compared to the glucose group (p= 0.032). When the hearts were perfused with 12 mM fructose, a significant increase was observed in the percentage of the ischemic area and risk area compared to equivalent glucose and high fructose (p< 0.001 and p< 0.001, respectively). MDA, GSH and TOS values were comparable in all groups. Conclusion: The present study shows that fructose perfusion plays a role in reduced ventricular contractile function relative to glucose in isolated rat hearts. This reduction triggered by fructose appears to be independent of antioxidant mechanisms. Furthermore, fructose perfusion at glucose-equivalent concentration causes a greater increase in infarct area in ischemic hearts, whereas an increase in fructose concentration appears to prevent this effect.

Fasting serum fructose is associated with metabolic dysfunction-associated fatty liver disease: A prospective study.

The association between sugar-sweetened beverages and metabolic disorders has been well studied. However, it has not been determined whether fasting serum fructose is associated with metabolic dysfunction-associated fatty liver disease (MAFLD). Participants were enrolled from 2011 to 2012 in Shanghai. Fasting serum fructose concentration was measured with a validated liquid chromatography-tandem mass spectrometry method. A total of 954 participants without diabetes were included. They were followed for an average of 3.5years. A total of 320 (33.5%) participants had MAFLD at baseline. With the increase in fasting serum fructose level by quartile, the MAFLD prevalence was increased by 27.0%, 25.0%, 37.4%, and 44.5%, respectively (p<0.001). Each SD increase in fasting serum fructose level was associated with a 60% increased risk of MAFLD (odds ratio 1.60; 95% confidence interval [CI], 1.36-1.88; p<0.001). Fasting serum fructose levels were more closely associated with four components of MAFLD (hepatic steatosis, prediabetes, insulin resistance, and low high-density lipoprotein). We built a diagnostic model named the fructose fat index (FFI). The area under the receiver operating characteristic curve of the FFI was 0.879 (95% CI, 0.850-0.908) in the derivation cohort and 0.827 (95% CI, 0.776-0.878) in the validation cohort. Subsequent prospective studies found that the incidence risk of MAFLD was 2.26 times higher in the high-fructose group than in the low-fructose group among female participants (95% CI, 1.46-3.49; p<0.001). Fasting serum fructose concentration, which mostly reflects endogenous fructose, was associated with a higher risk of MAFLD. The FFI derived from fasting serum fructose could be used to predict MAFLD.

Investigation of fructose consumption on hippocampal insulin and glucagon-like peptide-1 receptors, and metabolic effects in rats.

The detrimental effects of high fructose consumption on metabolic health have been extensively studied. However, limited research has focused on the impact of fructose intake on neuroprotective mechanisms, specifically the expression of insulin receptor (INSR) and glucagon-like peptide-1 receptor (GLP-1R) in the hippocampus. Understanding the effects of fructose on these neuroprotective molecules can provide valuable insights into the potential role of fructose in hippocampal dysfunction. The goal of this study is to aim at the basal plasma levels of lipid profile, insulin, GLP-1, and HOMA-IR, as well as the mRNA and protein expression of neuroprotective molecules such as INSR and GLP-1R in Wistar rats fed a high fructose diet. Rats were separated into control (C) and high fructose (HF) groups. The HF group was given 20% fructose water to drink for 16 weeks. Fructose ingestion significantly increased abdominal fat (C=1.24±0.08 g, HF=1.79±0.19 g, P<0.05) and plasma triglyceride levels (C=179.22±22.85 µg/ml, HF=242.45±14.45 µg/ml, P<0.05), but had no statistically significant effect on body weight and plasma HDL, LDL, total cholesterol, insulin, and GLP-1 levels (P>0.05). Although INSR mRNA expression in the hippocampus was significantly lower in the HF group compared to the control group (P<0.05), GLP-1R mRNA expression did not differ significantly across the groups (P>0.05). Furthermore, whereas INSR and GLP-1R protein levels in the experimental group were on a declining trend, this trend was not substantially different (P>0.05). These data suggest that fructose consumption may be harmful to the hippocampus by lowering the expression of INSR.

Effect of Creatine Supplementation on the Muscular Inflammation and Muscle Atrophy in High-Fat High-Fructose Fed Obese Growing Rats

Objective: This study aimed to investigate effects of creatine supplementation on high-fat high-fructose fed obese rats. Twenty-four six-week-old male Sprague-Dawley rats were randomly divided into three groups (n=8 each): control sedentary group (CD), high-fat high-fructose diet group (HD), and creatine-supplemented high-fat high-fructose diet group (CHD). Methodology: The CD group was supplemented with AIN-76G diet, and a high-fat high-fructose diet for HD and CHD groups was substituted with 5% corn oil fat to 35% lard. The CHD group was supplemented with 2% creatine. The total soleus muscle protein was extracted and prepared according to the procedure mentioned by Baghirova et al. for muscle cytokine assay and western blotting. Result: After eight weeks of the experimental period, weights of the soleus muscle in the HD and CHD groups were significantly lower than that in the CD group. In addition, levels of proinflammatory cytokines interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α in the HD groups were significantly higher than those in the CD group. In contrast, IL-1β, IL-6 concentrations in the CHD group were significantly lower than those in the HD group and irisin levels of HD and CHD group were significantly lower than those in the CD group. Moreover, levels of muscle protein degradation factors [Muscle RING-finger protein-1 (MuRF1) and atrogin-1] were significantly higher in the HD and CHD groups than those in the CD group. Conclusion: From these results, it was concluded that creatine supplementation attenuates the inflammation of skeletal muscle via pro-inflammatory cytokines; however, it has no significant role in preventing muscular atrophy in high-fat high-fructose fed obese rats.

Low Dietary n6/n3 Ratio Attenuates Changes in the NRF 2 Gene Expression, Lipid Peroxidation, and Inflammatory Markers Induced by Fructose Overconsumption in the Rat Abdominal Adipose Tissue.

The objective of this study was to examine the benefits of different n6/n3 polyunsaturated fatty acid ratios on the lipid metabolism, insulin resistance, and oxidative stress in the adipose tissue of rats fed a high-fructose diet. Male and female rats were divided into four groups: a control group (CON) (n6/n3 ratio ~7), a high-fructose group (HF) (n6/n3 ratio ~7), an N6-HF group (n6/n3 ratio ~50), and the DHA-HF group (n6/n3 ratio ~1, with the addition of docosahexaenoic (DHA) and eicosapentaenoic (EPA) acid). The CON group received plain water and the HF group received 15% fructose in their drinking water. Fructose induced an increase in the content of serum triglycerides, serum cholesterol, and HOMA-IR index. Among the fatty acids, elevated proportions of C18:1n9 and C16:1n7, as well as an increase in total monounsaturated fatty acid (MUFA), were found in the adipose tissue of the HF group. Fructose treatment also changed oxidative parameters, including a marked increase in the serum malondialdehyde (MDA) content. Meanwhile, DHA supplementation caused a significant decrease in the serum MDA concentration in comparison with the HF group. In addition, DHA/EPA supplementation attenuated oxidative stress by increasing NRF 2 gene expression. Fructose treatment also significantly decreased the adiponectin level, while DHA supplementation ameliorated it. The changes observed in this trial, including the decrease in the content of DHA and EPA, the decreased EPA/ARA ratio, and the increase in the expression of inflammatory genes, are characteristics of the low-grade inflammation caused by fructose treatment. These changes in the rat adipose tissue could be prevented by dietary intervention consisting of DHA supplementation and a low n6/n3 ratio.

Clerodendrum trichotomum extract improves metabolic derangements in high fructose diet-fed rats

ABSTRACT Clerodendrum trichotomum has been reported to possess beneficial properties for human health, but its effects on metabolic syndrome have not been reported. In this study, we investigated the effect of C. trichotomum leaf extract (CT) on the metabolic derangements induced by a high-fructose (HF) diet. Sprague–Dawley rats were fed with a 46% carbohydrate diet (HC group), 60% high-fructose diet (HF group), or HF diet supplemented with CT (500 mg/kg of body weight/day, CT group) via drinking water for 16 weeks. Results showed that CT alleviated HF diet-induced insulin resistance, dyslipidemia, and hepatic steatosis In liver tissues, CT affected the signaling pathways of AMP-activated protein kinase, peroxisome proliferator-activated receptor α (PPARα), and sterol regulatory element binding protein 1. CT enriched the genes that were mainly involved in cytokine-cytokine receptor interaction, PPAR, PI3K-Akt signaling pathways, and fatty acid metabolism pathway. These results suggest that CT is a promising therapeutic against metabolic disorders.

The effects of high fructose fruits and honey on the serum level of metabolic factors and nonalcoholic fatty liver disease.

The effect of the natural sources of fructose such as high fructose fruits and honey on the risk of fatty liver is still challenging. This study aimed to compare the effect of fructose, high fructose fruits, and honey on the metabolic factors and non-alcoholic fatty liver disease (NAFLD). Forty-four rats were divided into four groups including normal diet group, high fructose group (HF), high fructose fruits group (HFF), and honey group (HO). After 120days of intervention, the levels of insulin resistance, hepatic enzyme, and lipid profile were measured. Also, the expression levels of the acetyl-coA carboxylase (ACC), sterol regulatory element-binding protein 1c (SREBP-1c), Interleukin 6 (IL-6), and transforming growth factor-beta (TGF-β) genes were assessed. In addition, a histopathologic assessment was performed on liver tissues. Insulin resistance (IR) increased significantly in the HF, HFF, and HO groups (All P < 0.05). The levels of liver enzymes was significantly increased only in the group receiving the HF regimen (P < 0.01). A significant decrease in total cholesterol and HDL-C (high density lipoprotein cholesterol) levels was found in HO group compared to the control group (P < 0.05). The expression levels of ACC and SREBP-1c genes in HF, HFF, and HO groups were significantly higher than the control group (All P < 0.05). The HF group had a greater increase in the level of gene expression of IL-6 and TGF-β (All P < 0.05). Histopathological assessment did not find any changes in fatty liver formation and inflammatory damage. Consumption of fructose-rich honey and fruits improved the status of inflammatory markers and liver enzymes compared with the industrial fructose-rich products.

The effect of 1,25-dihydroxyvitamin D3 on liver damage, oxidative stress, and advanced glycation end products in experimental nonalcoholic- and alcoholic- fatty liver disease

Background/aim Oxidative stress and advanced glycation end products (AGEs) formation are proposed as effective mechanisms in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD). 1,25(OH)2D3 was proposed to have antioxidant, antiinflammatory and antiglycation properties. In this study, the effect of 1,25(OH)2D3 treatment on oxidative stress parameters and AGEs levels together with hepatic histopathology was investigated in high fructose (HFr) or ethanol (EtOH)-treated rats. Materials and methods Rats were treated with fructose (30%) or ethanol (5-20%) in drinking water with and without 1,25(OH)2D3 treatment (5 µg/kg two times a week) for 8 weeks. Insulin resistance (IR), oxidative stress parameters, AGEs, triglyceride (TG), and hydroxyproline (Hyp) levels together with histopathology were investigated in the liver. Results1,25(OH)2D3 decreased hepatic reactive oxygen species, lipid and protein oxidation products together with histopathological improvements in HFr- and EtOH-treated rats. 1,25(OH)2D3 treatment was observed to decrease significantly serum and hepatic AGEs in HFr group, and hepatic AGEs in EtOH group.Conclusion Our results clearly show that 1,25(OH)2 D3 treatment may be useful in the alleviation of hepatic lesions by decreasing glycooxidant stress in both NAFLD and ALD models created by HFr- and EtOH-treated rats, respectively.

Association of Dietary Fructose With Serum Advanced Glycation End Products in a Controlled Feeding Study of Healthy Adults

Abstract Objectives Sugars form advanced glycation end products (AGEs) through natural metabolism and interactions with proteins, lipids, and nucleic acids, which accumulate in tissues and have been implicated in the etiology of chronic diseases. Due to the increased consumption of fructose and its high ability to form AGEs, a further understanding of this association is important to clarify the role of sugars in disease. Our objective was to explore the association between usual fructose intake and serum levels of AGEs in healthy adults. Methods This is a secondary analysis of a 15-d controlled feeding study (n = 100) consuming their usual diet conducted in the Phoenix metropolitan area. Participants completed two 7-d food diaries, and custom 15-d menu plans were created to replicate their habitual diet. Forty participants (mean age: 42.5y, BMI: 27.8, gender: 55% male) were selected based on their 15-d mean total fructose intake for this analysis [top and bottom 20% of the sample distribution; high fructose (HF) =20 (76.3 ± 12.5 g/day), low fructose (LF) = 20 (27.3 ± 5.4 g/day)]. Fasting serum collected five weeks after the feeding period were analyzed for carboxymethyl-lysine (CML), a major AGE, using ELISA kits. A database of 549 common foods with known CML amounts was used to calculate exogenous CML intake. A general linear model was fitted to investigate the difference in serum CML between LF and HF groups while adjusting for age, gender, BMI, and exogenous CML intake. Results Exogenous CML intake was not significantly different between the HF and LF groups (P = 0.925). Participants in the HF group had significantly higher serum CML levels compared to participants in the LF group (37.3 ± 8.4 ng/mL versus 30.5 ± 8.0 ng/mL; P = 0.013). This difference remained statistically significant after adjusting for covariates [LF vs. HF: β = −6.4 (SE = 2.9); P = 0.036; Log10(age): β = −12.0 (10.6), P = 0.267; BMI: β = 0.4 (0.4), P = 0.352), male vs. female: β = 1.2 (3.6), P = 0.753; and exogenous CML intake: β = −8.5 (10.2), P = 0.411]. Conclusions Our findings suggest that endogenous CML formation may be an explanation for the significant difference in serum CML between HF and LF groups. This is significant in further understanding mechanisms of sugar intake and disease etiology and could have implications for at-risk populations consuming a high fructose diet. Funding Sources NIH/NCI and ASU

Germinated millet flour (Pennisetum glaucum (L.) R. Br.) reduces inflammation, oxidative stress, and liver steatosis in rats fed with high-fat high-fructose diet

This study investigated the effects of germinated millet flour on inflammation, oxidative stress, adiposity, and liver steatosis in Wistar rats fed with a high-fat high-fructose diet. In phase 1 of the experiment (8 weeks) the animals were separated into a control group with an AIN-93M diet (n = 10) and a high-fat high-fructose group (HFHF) (n = 20) with a diet rich in saturated fat (31%) and fructose (20%). In phase 2 (10 weeks), the control group was maintained on the AIN-93M diet (n = 10) and the HFHF group was divided into HFHF group (HFHF diet, n = 10) and the Millet group (HFHF with germinated millet flour replacing 43.6% dietary fiber, 100% starch, 36% protein and 39% oil in the experimental diet, n = 10). The germinated millet flour reduced (p < 0.05), in comparison with HFHF group, the adiposity (24.18 ± 4.45g to millet and 32.89 ± 8.46g to HFHF), triglycerides (100.00 ± 17.93g to millet and 147.8 ± 21.57g to HFHF), uric acid, ALT, NF-κB (131.9 ± 97.14 pg/ml to millet and 346.3 ± 58.88 pg/ml to HFHF), TNF-α (98.80 ± 19.90 pg/ml to millet and 141.4 ± 25.12 pg/ml to HFHF), platelet/lymphocyte and neutrophil/lymphocyte ratio, liver steatosis, inflammatory infiltrate (0.1880 ± 0.07 pg/ml to millet and 1.269 ± 0.17 pg/ml to HFHF), MDA levels, and liver collagen deposition. Further, germinated millet increased (p < 0.05) IL-10 (1511 ± 528.50 pg/ml to millet and 483.8 ± 91.59 pg/ml to HFHF), PPARα protein, total antioxidant capacity of the liver (0.2825 ± 0.04 pg/ml to millet and 0.2075 ± 0.05 pg/ml to HFHF) and the activity of SOD and catalase, compared to HFHF group. Thus, germinated millet flour was able to reduce adiposity and liver steatosis and presented anti-inflammatory and antioxidant effects, which highlight its functional biological effects.

The protective effects of red beetroot (Beta vulgaris l.) against oxidative stress in rats induced by high fat and fructose diet

Background: One of consequence high-fat and fructose diet is oxidative stress. Consumption of antioxidants from red beetroot may increase antioxidant defense.&#x0D; Objectives: This study aimed to evaluate red beetroot administration on improving antioxidant defense in rats induced high fat and fructose diet.&#x0D; Methods: A total 20 male Wistar rats were divided into 4 groups: 1) normal control group (N), received standard diet; 2) High fat and fructose diet (HF), received high fat and fructose diet (HFFD); 8 weeks induction with HFFD and received 9g red beetroot (BA); and combination of HFFD and 9g of red beetroot from beginning of the study (HFBA). At the end of the study the levels of circulatory oxidized LDL (ox-LDL) were determined using enzyme-linked immunosorbent assay (ELISA) method. Superoxide dismutase 2 (SOD2) and catalase (CAT) gene expressions were determined by quantitative polymerase chain reaction (qPCR) method.&#x0D; Results: Induction HFFD increased the levels of circulatory ox-LDL levels compared to normal control (10.00±0.29 vs 12.69±0.57). Administration of red beetroot for 6 weeks and combination HFFD with red beetroot during the study significantly decreased ox-LDL levels compared to high fat and fructose group (12.69±0.57 vs 9.66±0.46) and (12.69±0.57 vs 8.59±0.18), respectively. The decreased circulatory ox-LDL levels were found negatively correlated with upregulation SOD2 (r=-0.548; P=0.012) and CAT (r=-0.460; P=0.041) gene expression in the liver tissues.&#x0D; Conclusion: Administration of red beetroot may ameliorate oxidative stress in rats induced high-fat and fructose diet through increasing antioxidant defense.

Preventive Role of Soy Protein in Fructose Induced Metabolic Dysfunction in Rats via Inhibition of Nuclear Factor kappa B Pathway

Soy protein is an important component of soybeans that has beneficial role in improving insulin resistance. Nuclear factor kappa B (NF-κB) is a crucial pathway that has been implicated in the development of metabolic syndrome. Our study aimed to examine the protective effect of soy protein isolate - as a natural NF-κB inhibitor - and its possible mechanism of action in amelioration of inflammatory and metabolic disorders induced in male albino rats by high fructose diet (10% w/v) via using synthetic NF-κB inhibitor (IMD-0354). Rats were randomized into normal control group, soy group, NF-κB inhibitor (IMD-0354) group, high fructose group, high fructose with soy group, high fructose with NF-κB inhibitor group, high fructose with soy and NF-κB inhibitor group. Serum glucose, serum insulin, serum free fatty acids, insulin resistance (HOMA-IR), NF-κB, phosphorylated insulin receptor (pISR), carbohydrate-responsive element-binding protein (ChREBP) were determined and histopathological examination of liver tissue was performed. The concurrent administration of IMD-0354 and/or soy protein with high fructose significantly increased pISR and decreased FFAs, NF-κB, glucose, insulin, HOMA-IR, and ChREBP as well as improved the pathological conditions of the livers. The metabolic and inflammatory disorders induced by chronic consumption of fructose could be inhibited by co-administration of soy protein through regulation of NF-κB signalling pathway.

Maternal high-fructose intake during pregnancy and lactation induces metabolic syndrome in adult offspring.

BACKGROUND/OBJECTIVESNutritional status and food intake during pregnancy and lactation can affect fetal programming. In the current metabolic syndrome epidemic, high-fructose diets have been strongly implicated. This study investigated the effect of maternal high-fructose intake during pregnancy and lactation on the development of metabolic syndrome in adult offspring.SUBJECTS/METHODSDrinking water with or without 20% fructose was administered to female C57BL/6J mice over the course of their pregnancy and lactation periods. After weaning, pups ate regular chow. Accu-Chek Performa was used to measure glucose levels, and a tail-cuff method was used to examine systolic blood pressure. Animals were sacrificed at 7 months, their livers were excised, and sections were stained with Oil Red O and hematoxylin and eosin (H&E) staining. Kidneys were collected for gene expression analysis using quantitative real-time Polymerase chain reaction.RESULTSAdult offspring exposed to maternal high-fructose intake during pregnancy and lactation presented with heavier body weights, fattier livers, and broader areas under the curve in glucose tolerance test values than control offspring. Serum levels of alanine aminotransferase, aspartate aminotransferase, glucose, triglycerides, and total cholesterol and systolic blood pressure in the maternal high-fructose group were higher than that in controls. However, there were no significant differences in mRNA expressions of renin-angiotensin-aldosterone system genes and sodium transporter genes.CONCLUSIONSThese results suggest that maternal high-fructose intake during pregnancy and lactation induces metabolic syndrome with hyperglycemia, hypertension, and dyslipidemia in adult offspring.

Favorable effects of Globularia alypum on cardiometabolic markers in high fructose-fed rats

PurposeThis study aims to examine whether Globularia alypum (Ga) lyophilized aqueous leaves extract treatment improves cardiometabolic syndromes such as hyperglycemia, lipid profiles and oxidative damage resulting from a high-fructose diet induced in hypertriglyceridemic rats.Design/methodology/approachA total of 24 male Wistar rats weighing 80 ± 5 g were first randomly divided into 2 groups. A total of 12 control rats (C) were fed a standard-diet (St-D) and 12 high fructose (HF) rats were fed a high-fructose diet (HF-D) containing St-D in which cornstarch was substituted by fructose (61.4%). After 15 weeks of feeding, body weight (BW) was about 320 ± 20 g and hypertriglyceridemia was noted in HF vs C group (2.69 ± 0.49 mmol/L) vs (1.25 ± 0.33 mmol/L). Each group of rats was then divided into two equal groups (n = 6) and fed during four weeks either a St-D or HF-D, treated or not with 1% of Ga extract (C-Ga) and (HF-Ga). After 28 days, fasting rats were anesthetized and blood and tissues were removed to measure biochemical parameters.FindingsThe results showed no significant differences in BW and insulinemia between all groups. Ga extract supplementation reduced glycemia (−36%), glycosylated hemoglobin (−37%), Homeostasis Model of Assessment-Insulin Resistance index (−34%) and triacylglycerol’s contents in plasma (−33%), very low density lipoproteins–low density lipoproteins (VLDL-LDL) (−48%), liver (−52%) and aorta (−39%); total cholesterol concentrations in aorta was 3.7-fold lower in HF-Ga vs HF group. Ga treatment reduced lipid peroxidation in plasma, VLDL-LDL, red blood cells (RBC), liver, muscle and kidney by improving superoxide dismutase (SOD) activity and glutathione peroxidase (GPx) in RBC and catalase (CAT) activity in kidney (p < 0.05). Moreover, Ga ameliorates glutathione (GSH) production in RBC (+41%) and kidney tissues (+35%).Originality/valueGa extract ameliorated cardiometabolic syndrome by its hypotriglyceridemic effect and prevented development of insulin resistance. It reduces lipid peroxidation by enhancing non-enzymatic (GSH) and enzymatic (SOD, GPx and CAT) antioxidant defense systems in high-fructose hypertriglyceridemic rats. Therefore, supplementation of Ga leaves extract as an adjuvant could be used for the treatment of hypertriglyceridemia and the prevention and/or the management of cardio-metabolic adverse effects.

Garlic ameliorates long-term pre-diabetes induced retinal abnormalities &lt;br /&gt; in high fructose fed rat model

Retinopathy is one of the micro vascular complications of diabetes and can also be observed in pre-diabetic state. However, there are only limited studies available on the pathophysiology of retinopathy in pre-diabetic state and its preventive strategies. In this study, we investigated the retinal functional, structural and molecular alterations using high fructose (HF) induced pre-diabetic rat model and also the protective role of garlic. Feeding of HF to Wistar NIN (WNIN) rats had developed insulin resistance (IR) and impaired glucose tolerance (IGT) by three months, while retinal functional abnormalities by ten months as evidenced by decrease of Electroretinogram (ERG) scotopic, photopic b-wave amplitudes, oscillatory potentials (OPs) when compared to controls. Supplementation of garlic (3%) to HF+G group rats had marginally protected these changes. Elevated expression of glial fibrillary acidic protein (GFAP), vascular endothelial growth factor (VEGF), aldose reductase (AR) and decreased rhodopsin (Rho) in HF group rats as evidenced by immunohistochemistry, immunoblot methods, which were further supported by gene expression studies, indicate the initiation of retinal abnormalities. Increased immune-fluorescence signal of carboxymethyl lysine (CML-KLH) and 4-hydroxynanoenol (4-HNE) in retina of HF group rats indicate the association of glycation and oxidative stress, respectively. Early intervention of garlic to HF+G group rats attenuated retinal functional, structural, and molecular abnormalities

Animal Models with Metabolic Syndrome Markers Induced by High Fat Diet and Fructose

Metabolic syndrome is lipid and non-lipid metabolism disorder due to the association of several factors such as physiological, clinical, biochemical, and interrelated factors. People with metabolic syndrome can be diagnosed by fulfilling 3 of 5 criteria, including obesity and increased waist circumference, increased TG levels, increased blood pressure, hyperglycemia, and increased High-Density Lipoprotein (HDL) serum. The high-fat diet disrupts tissue lipid metabolism, so insulin resistance occurs due to lipotoxicity. Besides, some studies use a combination of mixtures (fructose, sucrose) and fat-rich food components to build metabolic characteristics in mice that affect human characteristics. The purpose of this study was to make an animal model with a metabolic syndrome marker induced by the High Fat Diet (HFD) consisting of pork oil and chicken egg yolk, as well as fructose from simple and economical ingredients. This study was an experimental study using experimental animals of male Rattus norvegicus strain wistar, which were grouped into three random treatment groups, namely the control group, HFD group, and High Fat Diet Fructose (HFDF) group. The number of samples used was 27 rats, with nine rats in each group. The animal was induced for four weeks, then measured levels of FPG, HD, and TG. From the research that has been done, it is found that there are significant differences in levels of Fasting Plasma Glucose (FPG), High-Density Lipoprotein (HDL), and Triglycerides (TG) (p

Prolonged overnutrition with fructose or fat induces metabolic derangements in rats by disrupting the crosstalk between the hypothalamus and periphery: Possible amelioration with fenofibrate

Metabolic Syndrome (MetS) increases the risk of developing type 2 diabetes mellitus and cardiovascular complications. The crosstalk between the hypothalamus and periphery is vital for regulating food intake and energy homeostasis. However, it is impaired during MetS. The present study aimed to compare the distinct central and peripheral metabolic derangements induced by a high-fructose drink or high-fat diet, as well as the possible intervention by fenofibrate. Rats were divided into five groups: standard chow diet (SCD) group, high-fructose group (FR), high-fat group (HF), FR plus fenofibrate group (FR-F), and HF plus fenofibrate group (HF-F). FR and HF groups showed hyperglycemia, hyperinsulinemia, hypertriglyceridemia, hyperleptinemia, steatosis, and adipocyte hypertrophy. This was associated with elevated circulating levels of proinflammatory cytokines and free fatty acids (FFAs). The latter mediators are involved in the hypothalamic inflammation and dysregulation of signaling cascades that control food intake and glucose homeostasis. The effects were more pronounced in the HF group than FR group, which were matched with the observed higher levels of plasma FFAs and cytokines. Fenofibrate administration improved not only the peripheral metabolic disturbances, but also the central disturbances associated with insulin resistance induced by FR or HF diet. This study sheds light on the pivotal role of the hypothalamus in diet-induced MetS. Furthermore, the study suggests the utmost importance of developing a standardized model of metabolic syndrome in place of the great diversity between available models, which can induce different effects and negatively impact the validity of prospective studies.

Effects of exercise on biological trace element concentrations and selenoprotein P expression in rats with fructose-induced glucose intolerance.

In the present study, we investigated the effects of exercise intended to prevent or treat lifestyle-related diseases on the glucose tolerance, insulin level, lactic acid utilization, muscle glycogen synthesis, hepatic and renal oxidative stress, hepatic selenoprotein P and biological trace element levels in organs of obese, glucose-intolerant rats. We fed normal, healthy rats a 20% casein diet while the glucose-intolerant, obese rats received a high-fructose diet. They were forced to run for one hour per day, six days per week, for ten weeks. Exercise reduced visceral fat and ameliorated glucose tolerance in the high-fructose group, lowered blood lactic acid levels, improved lactic acid usage efficiency, and increased oxidative stress and hepatic levels of Mn, Fe, Cu, and Zn in the normal and high-fructose groups. Additionally, exercise significantly upregulated hepatic selenoprotein P expression in both groups, however, its effect was remarkable in healthy group. On the other hand, muscle glycogen synthesis was not markedly enhanced in high-fructose-diet rats but in normal-diet rats in response to exercise. It is concluded that exercise conditions rather than exercise load must be customized and optimized for each health and disease states in advance before starting exercise training intended to prevent or treat lifestyle-related diseases.