Fructose Group Research Articles

Acute metabolic and endocrine responses induced by glucose and fructose in healthy young subjects: A double-blinded, randomized, crossover trial

A rise in fructose consumption has been implicated in the etiology of obesity, diabetes and cardiovascular disease. Serum uric acid (UA) elevates after fructose ingestion, increasing the risk of cardiovascular disease. However, the impact of fructose ingestion on nitric oxide (NO) has not yet been confirmed. The aim of this study was to investigate the postprandial metabolic and endocrine responses following an acute ingestion of fructose and glucose in healthy subjects. This was a double-blinded, randomized, crossover postprandial trial. Eighteen healthy young subjects (9 males and 9 females) with a mean age of 23.6±2.3 years and mean BMI of 20.2±1.5kg/m2 completed the experiment that was conducted in Hangzhou, China. Volunteers were randomized to two groups (A and B): after an 8-h overnight fast, volunteers either ingested 300mL of 25% glucose (group A) or fructose (group B) solution at 0830 within 5min. After a one-week washout period, volunteers were crossed over to receive the alternate test solution. Blood pressure was measured at 0h, 1h, 2h and 3h and venous blood was drawn at 0h, 0.5h, 1h, 2h and 3h after ingestion of the test solution. Eighteen subjects completed the study. Serum NO level tended to be lower at 1h (59.40±3.10μmol/L and 68.1±3.40μmol/L, respectively, p≤0.05) and 2h (62.70±3.10μmol/L and 70.10±3.50μmol/L, respectively, p≤0.05) after fructose ingestion than after glucose. The 3-h AUC (area under curve) of NO was significantly lower after fructose ingestion than after glucose (p≤0.05). UA level was higher at 1h (512.17±17.74μmol/L and 372.11±17.41μmol/L, respectively, p≤0.01) and 2h (440.22±16.07μmol/L and 357.39±14.80μmol/L, respectively, p≤0.05) after fructose ingestion than after glucose. The 3-h AUC of UA was significantly higher after fructose ingestion than after glucose (p≤0.01). Correlation analyses revealed that NO was negatively associated with UA at T0.5h (r=-0.62, p≤0.01), T1.0h (r=-0.69, p≤0.001), T2.0h (r=-0.86, p≤0.001) and T3.0h (r=-0.85, p≤0.001) after fructose ingestion. SBP (systolic blood pressure) tended to be higher at 1h (125.33±1.95mmHg and 112.06±1.77mmHg, respectively, p≤0.05) after fructose ingestion than after glucose. The 3-h AUC of SBP was significantly higher after fructose ingestion than after glucose (p≤0.05). The 3h-AUC of TG, TC, HDL-C and LDL-C showed no differences between fructose and glucose. LDH (lactate dehydrogenase) level was higher at 1h (195.00±5.6U/L and 177.67±6.8U/L, respectively, p≤0.05) and 2h (197.01±6.32U/L and 185.50±7.37U/L, respectively, p≤0.05) after fructose ingestion than after glucose. The 3-h AUC of LDH was significantly higher after fructose ingestion than after glucose (p≤0.05). AR was significantly higher at 1h (19.86±0.52ng/mg Hb and 16.98±0.29ng/mg Hb, respectively, p≤0.05) after fructose ingestion than after glucose. The 3-h AUC of AR (p≤0.05) was significantly higher after fructose ingestion than after glucose (p≤0.05). Ingestion of a 75g fructose load led to acute but unfavorable changes in certain metabolic and endocrine responses including increased serum concentrations and 3h-AUC of UA, AR and LDH, increased SBP, and decreased endothelial NO production when compared with the same amount of ingested glucose.

Effect of high fructose administration on histopathology of kidney, heart and aorta of rats

Objective: This study was conducted to assess the hazardous effects of high fructose administration on kidney, heart and aorta in rats. Materials and methods: Twenty adult healthy male albino rats weighing about 200-220 gm each were used in this study. The rats were divided into 2 duplicate groups; control group and fructose group. Fructose was administered to rats in fresh drinking water daily for 8 weeks (the whole experimental period). Serum urea, creatinine and sodium concentration were determined by using ready-made kits. Spectrophotometric and colorimetric methods were also used for the detection of other serum components. Histopathological examination of the tissues was done by staining with H&E, PAS and Masson trichrome stains. Results : Nephropathy was achieved in fructose group after one month as indicated by biochemical assay. Pathological observation showed that high fructose administration decreased size of cardio-myocytes, increased cardiac interstitial fibrosis score and aortic wall thickness. In kidneys, high fructose administration decreased glomerular tuft area and corpuscular area, increased percentage in the rats affected with interstitial renal fibrosis score 1 and percentage of rats had glomerular sclerosis score 2. Conclusion : High fructose in diet should be avoided because it can damage kidney, heart and aorta in rats. http://doi.org/10.5455/javar.2017.d193

Impact of Fish Oil Supplementation and Interruption of Fructose Ingestion on Glucose and Lipid Homeostasis of Rats Drinking Different Concentrations of Fructose.

Background. Continuous fructose consumption may cause elevation of circulating triacylglycerol. However, how much of this alteration is reverted after the removal of fructose intake is not known. We explored this question and compared the efficacy of this approach with fish oil supplementation. Methods. Male Wistar rats were divided into the following groups: control (C), fructose (F) (water intake with 10% or 30% fructose for 9 weeks), fish oil (FO), and fructose/fish oil (FFO). Fish oil was supplemented only for the last 33 days of fructose ingestion. Half of the F group remained for additional 8 weeks without fructose ingestion (FR). Results. Fructose ingestion reduced food intake to compensate for the increased energy obtained through water ingestion, independent of fructose concentration. Fish oil supplementation exerted no impact on these parameters, but the removal of fructose from water recovered both ingestion behaviors. Plasma triacylglycerol augmented significantly during the second and third weeks (both fructose groups). Fish oil supplementation did not attenuate the elevation in triacylglycerol caused by fructose intake, but the interruption of sugar consumption normalized this parameter. Conclusion. Elevation in triacylglyceridemia may be recovered by removing fructose from diet, suggesting that it is never too late to repair improper dietary habits.

BIOLOGICAL ACTIVITIES OF VITEX AGNUS-CASTUS (L.) LEAVES IN DIABETES CONTROL IN HIGH FAT/HIGH FRUCTOSE FED FEMALE RATS

AbstractThe aim of the current study is to investigate the effect Vitex agnus castus leaves on oxidative stress, glucose level and lipid profile in rats fed on high fat/ high fructose (HF/HFr) diet. The phenolic content as well as the antioxidant activity of the vitex leaves extract was analyzed. Rats were divided into four groups, group I received basal diet (control), group II received basal diet containing 20 g vitex leaves /kg., groups III received high fructose high fat diet and group IV received high fructose high fat diet containing 20 g vitex powder /kg diet. After 6 weeks, body weight, BMI, blood glucose, serum insulin, HOMA-index, lipid profile, leptin, resistin, TNF-α , total antioxidant capacity and total oxidant capacity were analyzed in the study male rats.Results showed high phenolic content as well as antioxidant activity of the vitex leaves extract. Vitex leaves showed significant decrease in blood glucose, serum insulin, HOMA-index, leptin, resistin, TNF-α, total oxidant capacity while increasing the total antioxidant capacity in addition to lipid profile normalization in group IV that received high fructose high fat diet containing 20 g vitex powder /kg diet as compared to high fructose high fat diet group (group III). It can be concluded that consumption of vitex leaves can improve the lipid profile, reduce insulin resistance, blood glucose level and inflammatory cytokines as well as it can protect the body from the oxidative stress, related to their phenolic compounds. Thus, vitex leaves consumption has a beneficial effect in control and management of diabetes and diabetes associated complications with no risk of hypoglycemic effect. Key words: Hypoglycemic- Vitex leaves - Hypolipidmic- Inflammatory Cytokines

English

This study aimed to evaluate the effect of supplementation of sucralose and fructose on the metabolism of adolescent rats. Eighteen male Wistar rats were divided into 3 groups: control group (GC), fructose group (GF) treated with 50 mg/kg of fructose, and sucralose group (GS) receiving 50 mg/kg of sucralose for 24 days. The weight and feed intake were measured weekly. At the end of the experiment, some biochemical parameters, histopathology of the liver and biodistribution of the radiotracer 99mTc-sodium phytate in liver and blood were analyzed. The GF showed higher body weight only in the first week compared with GS and GC (p<0.05). Histopathology and % ATI/g radiotracer 99mTc-sodium phytate in liver and blood were not different between the groups. The GF showed higher values ​​of aspartate aminotransferase activity, bilirubin, alkaline phosphatase activity and gamma glutamyl transferase activity, compared with the other groups (GC and GS) (p<0.05). Activity of alanine aminotransferase and albumin level of GF were higher than GS (p<0.05). For other parameters, no statistical difference was observed. It was concluded that the use of fructose during the experiment was able to alter hepatic enzymes, but on the other hands, the use of sucralose caused no change.   Key words: Sucralose, fructose, adolescent rats, radiopharmaceutical.

Type of supplemented simple sugar, not merely calorie intake, determines adverse effects on metabolism and aortic function in female rats.

This is the first study comparing the effects of glucose and fructose consumption on metabolic factors and aortic function in female rats. Our results show that, although total caloric consumption was higher in glucose-supplemented rats, fructose ingestion had a greater impact in inducing metabolic and aortic dysfunction.

A diet of fructose-enrichedArtemiaimproves the response of juvenileLitopenaeus vannameishrimp to acute low-salinity challenge

The Pacific white shrimp (Litopenaeus vannamei), as an economically important species, has been reared in low-salinity water during the last decade. To investigate how juvenile L. vannamei shrimp fed with fructose-enriched Artemia respond to acute low-salinity stress, the shrimp were randomly divided into four treatment groups, three groups were fed with Artemia enriched with either 100, 200 and 300 mg L−1 of fructose and a control group fed with Artemia with no enrichment for 10 days. The results showed that the 300 mg L−1 fructose group demonstrated the maximum survival rate and glycogen content. Additionally, the 300 mg L−1 fructose group showed significantly higher Na+/K+-ATPase activity, total antioxidant capacity, and expression levels of Na+/K+-ATPase α-subunit, V-H ATPase α-subunit, hexokinase, phosphofructokinase, antioxidants (SOD, CAT, GPX) and Hsp70 mRNA when compared with the control group. Furthermore, after exposure to low salinity, the mRNA levels of phosphofructokinase, V-H ATPase α-subunit, GPX, p38, JNK and Rac1 stayed constant in shrimp fed with fructose-enriched Artemia but changed significantly in the control group. Thus, a diet of fructose-enriched Artemia can improve the osmoregulation and survival of juvenile L. vannamei shrimp exposed to low salinities.

Deep fried edible oils disturb hepatic redox equilibrium and heightens lipotoxicity and hepatosteatosis in male Wistar rats.

Hepatosteatosis is a complex disorder, in which insulin resistance and associated dyslipidemic and inflammatory conditions are fundamental. Dietary habit, especially regular consumption of fat and sugar-rich diet, is an important risk factor. Coconut and mustard oils (CO and MO) are medium-chain saturated and monounsaturated fats that are common dietary ingredients among the Indian populations. Present study analyzed the effect of prolonged consumption of the fresh and thermally oxidized forms of these oils on glucose tolerance and hepatosteatosis in male Wistar rats. Thermally oxidized CO (TCO) and MO (TMO) possessed higher amount of lipid peroxidation products and elevated p-anisidine values than their fresh forms. Dietary administration of TCO and TMO along with fructose altered glucose tolerance and increased hyperglycemia in rats. Dyslipidemia was evident by elevated levels of triglycerides and reduced high density lipoprotein cholesterol (HDLc) levels in fructose and edible oil-fed group ( p < 0.05). Additionally, hepatic antioxidant status was diminished and oxidative stress markers were elevated in TCO- and TMO-fed rats. Substantiating these, hike in liver function marker enzyme activities were also observed in these animals. Supporting this, histological analysis revealed higher incidence of microvesicles and hepatocellular ballooning. Results thus suggest that consumption of thermally oxidized fats may cause hepatic damage.

Abstract P164: The Role of the Adrenoreceptors Beta 3 on Metabolic Syndrome Induced by Fructose

The aim of this study was to evaluate the role of the adrenoreceptor beta 3 (ARβ3) in the cardiovascular function on Metabolic Syndrome (MS) induced by fructose overload. Male mice after weaning (8-10g) were divided into 4 groups (n=7/group): FVB Control (C) and ARβ3 Knockout Control (Kβ3C), with free access to food and water for 8 weeks; FVB fructose (F) and ARβ3 Knockout fructose (Kβ3F), with free access to food and fructose added to the drinking water (10%) for 8 weeks. At the end of the protocol, intraperitoneal glucose tolerance test was performed. Triglycerides and HDL fractions were evaluated by colorimetric methods. The animals were submitted to catheterization of carotid artery. This catheter was connected to a transducer and continuous signals of blood pressure (BP) was recorded. The variability of the resultant signal was evaluated in frequency domain. Visceral fat deposits were collected, weighted and normalized as fat (mg)/body weight (g). Results: fructose increased the fasting glycemia in the knockout group (Kβ3C=93±3 vs. Kβ3F=122±7 mg/dL) and decreased the glucose tolerance in both fructose groups. Fructose increased the triglycerides and decreased HDL cholesterol. The uric acid increased in the knockout animals. There was an increase on visceral fat deposits only in FVB animals (C=10±2 vs. F=16±1 mg/g), as well as on blood pressure (C=123±4 vs. 136±2 mmHg) There was an increase on blood pressure variability for all experimental groups compared to Control (C=10.7±1 vs. F=36±11; Kβ3C=50±7; Kβ3F=24±4 mmHg 2 ) as well as on peripheral sympathetic modulation (C=3.3±0.4 vs. F=8.1±0.1; Kβ3C=22.9±3; Kβ3F=9.2±2 mmHg 2 ). Furthermore, Kβ3F showed a decrease on blood pressure variability and peripheral sympathetic modulation. Our data suggest that the hypertension induced by fructose is related with adiposity. Moreover, the blood pressure variability and its sympathetic modulation are dependent of the ARB3. The association between fructose and ARβ3 knockout leads to the loss of the sympathetic modulation.

Abstract P286: Modulation Way Classical and Alternatives of Renin Angiotensin System (RAS) in Mesangial Cells After Exposure to Fructose

Background: Our group demonstrated previously that rats subjected to a high fructose diet showed increased activity of kidney ACE.In order to understand the effect of fructose in the forming process of angiotensin II (AngII) and angiotensin 1-7 (Ang1-7) affecting the levels of these effectors, the aim of this study was to evaluate the activities of the RAS enzymes responsible for the formation of Ang1-7 and AngIIof immortalized human mesangial cells (IMCH)exposed to low and high concentration of fructose. Methods: IMCH were divided into control (low glucose medium), Fructose 5 mM(medium + 5 mM Fructose) and Fructose 30mM(medium + 30 mM Fructose) groups. The enzymatic activity of ACE, chymase, cathepsin D, Neutral Endopeptidase (NEP) and ACE2 were evaluated using Z-Phe-His-Leu,Abz-AIKFFSAQ-EDDnp, Abz-AIAFFSRQ-EDDnp,Abz(d)-Arg-Gly-Leu,Mca-APK (DNP) as substrates respectively. Data were analyzed using ANOVA one way. Results: Among the AngIIforming enzymes, fructose decreased ACE activity in cell lysate.Both fructose concentrations increased chymase in the culture medium. No effect was observed on the activity of cathepsin D. When evaluating the activities of peptidases forming Ang-1-7,NEP activity was increasedin culture medium.We did not detected differences in ACE2 activity. Conclusion: The results suggest fructose modulates renal and systemic RAS in IMCH acting in the classical andalternative pathways of AngII formation. Additionally this sugar was able to increase NEP activity, forming Ang-1-7. Quantitation of angiotensin remains necessary to better understand how the end effector is available in IMCH and evaluate possible effects on glomerular physiology.

The effects of genistein supplementation on fructose induced insulin resistance, oxidative stress and inflammation

AimsThis experimental study was designed to investigate the effects of 10weeks genistein administration on oxidative stress and inflammation in serum and liver of rats fed with fructose. Main methods6–8weeks old, 40 male Sprague-Dawley rats were included. Group 1 (control) was fed with standard chow food and 100μl/kg/day/rat dimethyl sulfoxide (DMSO) administered subcutaneously; group 2 (genistein) with standard chow food and 0.25mg/kg/day/rat genistein; group 3 (fructose) with standard chow food and drinking water 20% fructose, group 4 (fructose+genistein) with standard chow food, drinking water with 20% fructose and 0.25mg/kg/day/rat genistein. TNF-α, IL-6, visfatin as inflammatory markers and 8-isoprostane as a oxidative stress marker were measured by ELISA, glucose, triglyceride, total cholesterol, LDL-cholesterol and HDL-cholesterol by enzymatic colorimetric method, AST and ALT by kinetic UV method. Key findingsSignificantly high 8-isoprostane levels in serum (p<0.001) and liver (p<0.05) in group 3 compared to control group indicate that presence of oxidative stress. Significantly high TNF-α and IL-6 levels in serum (p<0.05) and liver (p<0.01) and visfatin levels in serum (p<0.001) of group 3 indicate inflammation accompanying insulin resistance and oxidative stress. Genistein administration to fructose group causes a significant decrease in HOMA-IR (p<0.001) and LDLC (p<0.05) level. Significantly lower serum 8-isoprostane (p<0.01) level indicates the antioxidant effect of genistein and significantly lower liver TNF-α (p<0.01), serum, liver IL-6(p<0.01) and serum visfatin (p<0.01) levels reflect the antiinflammatory effects of genistein. SignificanceGenistein administration to rats fed with fructose causes an ameliorating effect on HOMA-IR values and lipid status markers in addition to its antioxidant and antiinflammatory effects.

Fermented Red Ginseng Potentiates Improvement of Metabolic Dysfunction in Metabolic Syndrome Rat Models.

Metabolic syndrome including obesity, dyslipidemia and hypertension is a cluster of risk factors of cardiovascular disease. Fermentation of medicinal herbs improves their pharmacological efficacy. Red ginseng (RG), a widely used traditional herbal medicine, was reported with anti-inflammatory and anti-oxidant activity. Aim in the present study was to investigate that the effects of fermented red ginseng (FRG) on a high-fructose (HF) diet induced metabolic disorders, and those effects were compared to RG and losartan. Animals were divided into four groups: a control group fed a regular diet and tap water, and fructose groups that were fed a 60% high-fructose (HF) diet with/without RG 250 mg/kg/day or FRG 250 mg/kg/day for eight weeks, respectively. Treatment with FRG significantly suppressed the increments of body weight, liver weight, epididymal fat weight and adipocyte size. Moreover, FRG significantly prevented the development of metabolic disturbances such as hyperlipidemia and hypertension. Staining with Oil-red-o demonstrated a marked increase of hepatic accumulation of triglycerides, and this increase was prevented by FRG. FRG ameliorated endothelial dysfunction by downregulation of endothelin-1 (ET-1) and adhesion molecules in the aorta. In addition, FRG induced markedly upregulation of Insulin receptor substrate 1 (IRS-1) and glucose transporter type 4 (Glut4) in the muscle. These results indicate that FRG ameliorates obesity, dyslipidemia, hypertension and fatty liver in HF diet rats. More favorable pharmacological effects on HF diet induced metabolic disorders were observed with FRG, compared to an equal dose of RG. These results showed that the pharmacological activity of RG was enhanced by fermentation. Taken together, fermentated red ginseng might be a beneficial therapeutic approach for metabolic syndrome.

Aerobic training prevents oxidative profile and improves nitric oxide and vascular reactivity in rats with cardiometabolic alteration.

Cardiovascular disease is the major cause of death worldwide; therefore it is important to understand the natural history of the pathophysiologic process and develop strategies to halt its progression. Thus this study investigated the protective effect of aerobic training on pathophysiological mechanisms involved in subclinical cardiometabolic alterations in a model with constant exposure to a prejudicial agent. Male Wistar rats were divided into a control group (C), which received drinking water, fructose group (F), which was fed 10% fructose in drinking water for 10 wk, and control training (CT) and fructose training groups (FT), in which moderate aerobic training was added in the last 8 wk of the study. Insulin, triacylglycerol, and isoprostane were higher and superoxide dismutase (SOD) was lower in the F group. There was no difference in thoracic aorta histology, but a decreased vascularization was seen in the F group, avoided by training in left ventricle. Regarding vascular function, the F group exhibited increased vasoconstrictory reactivity to phenylephrine. The F group presented impaired vasodilation to acetylcholine. Regarding endothelial nitric oxide synthase (eNOS), the F group presented a lower expression, and phosphorylated eNOS was higher in the trained groups than in their respective control groups. This same pattern was observed for nitric oxide bioavailability, antioxidant protein expression in aorta, left ventricle, and muscle (catalase, SOD, and glutathione peroxidase), serum SOD activity, and muscle mass. These results suggest that exercise training enhanced the antioxidant pathway and, as a consequence, the eNOS pathway, preventing an impairment in vascular vasodilatory capacity.

Anti-nociceptive and anti-inflammatory effects of Withania somnifera root in fructose fed male rats.

Insulin resistance is a metabolic disorder which affects the diabetes mellitus pathophysiology and alters the cell excitability. This study has been designed to evaluate the anti-nociceptive and anti-inflammatory effects of chronic administration of Withania somnifera root (WSR) in fructose drinking water rats. An experiment was carried out on 48 Wistar-Albino male rats, weighting 200±30 g, which were divided into six groups (n=8): control group (C), control morphine (CM), W. somnifera group (WS) which received WSR (62.5 mg/g diet), W. somnifera naloxone group (WSN) which received WSR and naloxone, fructose (F) group which received fructose drinking water and FWS group which received fructose-enriched drinking water and WSR during the trial period. A biphasic pain response was induced after intraplantar injection of formalin (50 μL, 1%). Pain behavior was measured using Dubuisson methods. The obtained data were analyzed by SPSS software V. 18, using ANOVA and Tukey test. Results were expressed as mean±SD. Statistical differences were considered significant at p<0.05. The results showed that the insulin resistance index, blood sugar, insulin, IL-6, TNF-α, and acute and chronic pain score in the F group were significantly increased in comparison with the control group, but these parameters in the FWS group were significantly decreased compared with the F group (p<0.001). Our findings indicated that chronic oral administration of WSR has analgesic and anti-inflammatory effects in fructose drinking water rats and causes improved insulin resistance index.

Cariogenicity features of Streptococcus mutans in presence of rubusoside.

BackgroundOne promising way of reducing caries is by using sucrose substitutes in food. rubusoside is a prototype sweet substance isolated from the leaves of the plant Rubrus suavissimus S. Lee. (Rosaceae), and is rated sweeter than sucrose. The purpose of this study was to investigate the effects of rubusoside on Streptococcus mutans growth, acidogenicity, and adherence to glass in vitro.MethodsThe effects of rubusoside on the growth and glass surface adhering of Streptococcus mutans were investigated by measuring the optical density of the culture at 540 nm with a spectrophotometer. Rubusoside influence on Streptococcus mutans acidogenicity was determined by measuring the pH of the culture. Sucrose, glucose, maltose, fructose and xylitol were designed to compare with rubusoside.ResultsS. mutans growth in the rubusoside-treated group was significantly lower than that in the sucrose, glucose, maltose and fructose groups (p < 0.05) except for xylitol group (p > 0.05). Sucrose-treated S. mutans exhibited the highest adherence to glass, and rubusoside-treated S. mutans exhibited the lowest. S. mutans adherence to a glass surface and acidogenicity with sucrose were significantly reduced by rubusoside.ConclusionsRubusoside may have some potential as a non-cariogenic, non-caloric sweetener.

High-fructose diet in pregnancy leads to fetal programming of hypertension, insulin resistance, and obesity in adult offspring

Consumption of fructose-rich diets in the United States is on the rise and thought to be associated with obesity and cardiometabolic diseases. We sought to determine the effects of antenatal exposure to high-fructose diet on offspring's development of metabolic syndrome-like phenotype and other cardiovascular disease risk factors later in life. Pregnant C57BL/6J dams were randomly allocated to fructose solution (10% wt/vol, n= 10) or water (n= 10) as the only drinking fluid from day 1 of pregnancy until delivery. After weaning, pups were started on regular chow, and evaluated at 1 year of life. We measured percent visceral adipose tissue and liver fat infiltrates using computed tomography, and blood pressure using CODA nonivasive monitor. Intraperitoneal glucose tolerance testing with corresponding insulin concentrations were obtained. Serum concentrations of glucose, insulin, triglycerides, total cholesterol, leptin, and adiponectin were measured in duplicate using standardized assays. Fasting homeostatic model assessment was also calculated to assess insulin resistance. P values <.05 were considered statistically significant. Maternal weight, pup number, and average weight at birth were similar between the 2 groups. Male and female fructose group offspring had higher peak glucose and area under the intraperitoneal glucose tolerance testing curve compared with control, and higher mean arterial pressure compared to control. Female fructose group offspring were heavier and had higher percent visceral adipose tissue, liver fat infiltrates, homeostatic model assessment of insulin resistance scores, insulin area under the intraperitoneal glucose tolerance testing curve, and serum concentrations of leptin, and lower concentrations of adiponectin compared to female control offspring. No significant differences in these parameters were noted in male offspring. Serum concentrations of triglycerides or total cholesterol were not different between the 2 groups for either gender. Maternal intake of high fructose leads to fetal programming of adult obesity, hypertension, and metabolic dysfunction, all risk factors for cardiovascular disease. This fetal programming is more pronounced in female offspring. Limiting intake of high fructose-enriched diets in pregnancy may have significant impact on long-term health.

Enhanced Dietary Fructose Rapidly Induces Salt‐Sensitive Hypertension in Rats

Fructose consumption is associated with increased sodium reabsorption, increased formation of reactive oxygen species, and the development of hypertension. In normal rats, 20% dietary fructose supplementation induces hypertension within 8–12 weeks. We hypothesized a diet combining 20% fructose supplemented with high salt (4% NaCl) would induce abnormal sodium retention, increased oxidative stress, and accelerate the development of elevated blood pressure. Rats weighing 200–225 g were pre‐trained for 2 weeks for non‐invasive tail cuff blood pressure measurements and then placed in metabolic caging. Rats were pair‐fed for 2 weeks with one of 4 different diets: 1) control group (0.4% NaCl), 2) high salt chow group (4% NaCl), 3) 20% fructose group (in the drinking water), and 4) 20% fructose plus high salt group (n's = 9,5,9,18). Blood pressure, urinary sodium excretion and cumulative sodium balance were measured over 2 weeks and urinary 8‐Isoprostane excretion, as a marker for reactive oxygen species, during the final two days. High salt chow replaced normal chow at the beginning of the second week. By the end of the protocol, systolic blood pressure was unchanged in control group (121±2 to 122±2 mmHg) as well as the high salt group (122±2 to 122±1 mmHg). 20% fructose alone had no effect on blood pressure over the 2 weeks (121±1 to 125±1 mmHg). However, blood pressure significantly increased in the 20% fructose plus high salt group (125 to 140 mmHg p&lt;0.001). The increased blood pressure was concomitant with increased positive cumulative sodium balance. During the final week mean urinary sodium excretion in the high salt and 20% fructose plus high salt groups were 5–6 fold higher than normal salt controls (p&lt;0.001): 1.13±0.07, 7.67±0.31, 1.20±0.10, 5.33±0.21 μmol/24 hrs, respectively. Despite similar consumption, urinary sodium excretion in the 20% fructose plus high salt group was significantly lower than the high salt group (p&lt;0.0001). Urinary 8‐Isoprostane excretion was significantly higher in the high salt, 20% fructose, and 20% fructose plus high salt groups compared to control: 16.4±1.3, 29.5±2.5, 32.2±3.9, 31.2±2.5 ng/24 hrs, (p&lt;0.001). Our results suggests enhanced fructose and salt consumption increases sodium retention and oxidative stress. High salt can induce elevations in blood pressure in 20% fructose‐fed rats within just one week. Increased blood pressure appears to associate with increased sodium retention and positive cumulative sodium balance. Overall, fructose combined with high salt in the diet contributes to the accelerated development of salt‐sensitive hypertension.Support or Funding InformationNational Institutes of Health Grant 5P01HL090550‐05

Arginine and Aerobic Training Prevent Impairment in Endothelial Function in Rats Under High Risk to Develop Metabolic Syndrome

It is not elucidated if aerobic training and arginine supplementation can have similar protective effects in individuals with constant exposure to the triggering agent of the metabolic syndrome, with the presence of subclinical alterations, but without the presence of cardiovascular disease. So the purpose of this study was to investigate the effect of arginine supplementation and aerobic training on vascular reactivity of rats under high risk of metabolic syndrome development. Wistar rats, males, adults were, initially, divided in two groups Control group (C; drinking water) and Fructose group (F; water with 10% fructose), after two weeks the F group was divided into four others groups: Fructose group (F), that continued with the same treatment, Fructose Arginine group (FA), Fructose Training group (FT) and Fructose Training Arginine group (FTA) same as F group, adding aerobic training on a treadmill and/or arginine supplementation by gavage (800mg/kg BM/day), in the last 8 weeks. There were no differences in body mass gain and caloric intake between groups (P&gt;0.05). It was observed higher serum insulin in F group compared to control group after two (P=0.046) and ten weeks (P=0.014), while it was not observed any difference between the other groups compared to C group. In relation to serum triacylglycerol levels, after two weeks, there was no difference (P=0.154) between C and F groups. After ten weeks the F group presented higher triacylglycerol concentration (P&lt;0.01) compared to C group and the training normalized this increased, however arginine supplementation had no effect on this parameter. The malondialdehyde serum concentration, an oxidative stress marked, had the same pattern as the triacylglycerol. Concerning vascular reactivity, there was no difference after two weeks of treatment. While at the end of protocol, the F group exhibited increased vasoconstrictory reactivity (P&lt;0.01) to phenylephrine when compared to C and to trained groups (FT and FTA). The F group also presented an impaired endothelial vasodilator response to acetylcholine compared to other groups and the arginine supplementation and the aerobic training were able to prevent this impaired response. Thus aerobic training prevents the metabolic alterations, the hypereactivity to phenylephrine and the endothelial damage of rats with high risk to develop metabolic syndrome, while arginine supplementation was capable only to prevent the endothelial damage in this experimental model, with no potentiating effect.Support or Funding InformationCAPES, CNPq, FAPERJ e FINEP.

The effect of high dietary fructose on the kidney of adult albino rats and the role of curcumin supplementation: A biochemical and histological study

Background Consumption of fructose, in the form of added sugars such as high fructose corn syrup (HFCS) or sucrose, has increased markedly in the last few years, which is strongly correlated with the prevalence of metabolic syndrome. It is widely used as a food ingredient and has potential to increase oxidative stress. Curcumin is a phenolic compound, and it exhibits protective effects against oxidative damage. Objective The aim of the study was to investigate the effects of curcumin on renal injury in fructose-fed rats and the possible underlying mechanism. Methods Eighty male rats were randomly divided into control group, fructose group, 200 mg/kg curcumin group and curcumin-fructose group. The histopathological changes in the kidney of rats were observed using hematoxylin and eosin and Masson's trichrome stains. The expressions of renal reduced glutathione (GSH) concentration, glutathione reductase (GR), super oxide dismutase (SOD), catalase activities, lipid peroxidation (LPO), DNA fragmentation %, inducible nitrous oxide (INOS) and homooxygenase 1 (HO-1) mRNA in renal tissue homogenates were assessed. Immunohistochemical detection of alpha-smooth muscle actin (α-SMA) and tumor necrosis factor alpha (TMF-α) were also investigated. Results Compared to the control group, GSH, GR, SOD and catalase activities were significantly decreased in the fructose group, while there was a significant increase in LPO, DNA fragmentation %, INOS and HO-1. These changes were accompanied by renal tubular injury, increased collagen deposition and lipid accumulation. Immunohistochemical results revealed increased expression of both α-SMA and TNF-α. Curcumin at 200 mg/kg evidently improved renal tubular injury, suppressed the expressions of renal LPO, DNA fragmentation %, INOS and HO-1, and decreased the expression of both α-SMA and TNF-α in kidney tissue. Conclusion Curcumin administration protected the kidney cells from fructose induced oxidative stress by increasing the antioxidant defence mechanism of the kidney cells and its ability to act as a free radical scavenger.

The effects of melatonin on brain nitrosative stress and energy balance in fructose-mediated metabolic syndrome model / Fruktoz-aracılı metabolik sendrom modelinde melatoninin beyinde nitrozatif stres ve enerji dengesi üzerine etkisi

Abstract Objective: Metabolic syndrome (MetS), one of the common health problems seen with increasing frequency in today’s modern societies, is also a important risk factor for neurological disorders such as stroke, depression, Alzheimer’s disease. On the other hand, melatonin is a neurohormone, has potent antioxidant and neuroprotective activities. In the present study, we aimed to investigate the possible protective effects of melatonin administration on brain tissue in fructose-mediated MetS model. Methods: Male adult Sprague-Dawley rats were randomly divided into four groups (n=8); control, fructose, melatonin and fructose plus melatonin. MetS was induced by fructose solution 20% in tap water, and melatonin was administered at the dose of 20 mg/kg bw/day by oral gavage. Systolic blood pressures (SBP) were measured by tail-cuff method. After the experimental period of 8 weeks, serum triglyceride, glucose, insulin, and tissue ATP/ADP ratio, nitric oxide (NOx) and 3-nitrotyrosine (3-NT) levels were measured. Also tissue endothelial and inducible nitric oxide synthase (eNOS and iNOS) protein levels were determined. Results: Fructose consumption increased SBP, serum triglyceride, insulin levels and induced insulin resistance significantly compared to control group and MetS model was successfully demonstrated. In comparison with control group, fructose administration did not cause significant changes in tissue ATP/ADP ratio and 3-NT levels. NOx levels did not change significantly among groups, and iNOS-eNOS proteins were not detected in any groups. Interestingly, tissue 3-NT levels were elevated significantly while ATP/ADP ratio was diminished in fructose plus melatonin group compare with both control and fructose groups. Conclusion: These results indicate that high fructose diet for 8 weeks does not influence nitric oxide production, energy metabolism and protein nitration in brain. Nevertheless melatonin acted as a pro-oxidant at that dose when administered with fructose.