CHRONIC AEROBIC EXERCISE PREVENTS HIGH-FRUCTOSE DIET-INDUCED IMPAIRMENT IN BLOOD PRESSURE IN HEALTHY YOUNG ADULTS: A DOUBLE-BLIND, RANDOMIZED CLINICAL TRIAL

Abstract The purpose of the study was to verify the effect of 4 weeks of a high-fructose diet associated with aerobic training on the risk factors for cardiometabolic diseases. Twenty-one young adults were randomized into three groups: high-fructose diet (HFD: 1 g/kg body weight of fructose/day), high-glucose diet (HGD: 1 g/kg body weight of glucose/day), and high-fructose diet and exercise (HFDE: 1 g/kg body weight of fructose/day + 3 weekly 60-minute sessions of aerobic exercise). Before and after the 4 weeks of the intervention, blood samples were taken and flow-mediated dilatation, insulin resistance index, pancreatic beta cell functional capacity index, insulin sensitivity index, and 24-hour blood pressure were evaluated. HFD showed an increase in uric acid concentrations (p = 0.040), and HGD and HFDE groups showed no changes in this outcome between pre- and post-intervention; however, the HFDE group showed increased uric acid concentrations from the middle to the end of the intervention (p = 0.013). In addition, the HFD group showed increases in nocturnal systolic blood pressure (SBP) (p = 0.022) and nocturnal diastolic blood pressure (DBP) (p = 0.009). The HGD group exhibited decreases in nocturnal SBP (p = 0.028) and nocturnal DBP (p = 0.031), and the HFDE group showed a decrease in 24-hour SBP (p = 0.018). The consumption of 1 g/kg of fructose per day can increase uric acid concentrations and blood pressure in adults. Additionally, aerobic exercises along with fructose consumption attenuate changes in uric acid concentrations and prevent impairment in nocturnal blood pressure.

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Investigation of the effect of coffee on body weight, serum glucose, uric acid and lipid profile levels in male albino Wistar rats feeding on high-fructose diet

Laboratory Animal Research ◽

10.1186/s42826-019-0024-y ◽

2019 ◽

Vol 35 (1) ◽

Cited By ~ 1

Author(s):

Teka Obsa Feyisa ◽

Daniel Seifu Melka ◽

Menakath Menon ◽

Wajana Lako Labisso ◽

Mezgebu Legesse Habte

Keyword(s):

Metabolic Syndrome ◽

Body Weight ◽

Uric Acid ◽

Lipid Profile ◽

Wistar Rats ◽

Serum Glucose ◽

Control Group ◽

Fasting Serum ◽

High Fructose Diet ◽

High Fructose

AbstractCoffee is one of the most commonly consumed beverages in the worldwide and is assumed to have protective effects against metabolic syndrome. The present study was aimed at investigating the effect of coffee on body weight, serum glucose, uric acid and lipid profile levels in male albino Wistar rats feeding on high fructose diet. A post-test experimental study was conducted on a total of 30 (9–10 weeks old) male albino Wistar rats. The rats were divided into 6 groups: group I (normal control)-fed on standard chow and plain tap water only; group II (fructose control)-fed on standard chow and 20% of fructose solution; group III–VI (treatment groups)-fed on standard chow, 20% of fructose solution and treated with 71, 142, 213 and 284 mg/kg body weight/day of coffee respectively for six weeks. At the end, body weight, serum glucose, uric acid and lipid profile levels were investigated. Data was entered and cleared by epi-data software version 3.1 and analyzed by one way ANOVA followed by Tukey post hoc multiple comparison tests using SPSS V. 23.00. Statistical significance was considered at p < 0.05. The results showed that body weight, fasting serum glucose and uric acid levels significantly lowered in rats treated with 213 (p = 0.047; 0.049; 0.026) and 284 (p = 0.035; 0.029; 0.010) mg/kg body weight/day of coffee compared to fructose control group. Fasting serum triglycide (TG) and low density lipoprotein (LDL-C) levels showed significant reduction in rats treated with 284 mg/kg body weight/day of coffee as compared to fructose control group (p = 0.031; 0.046) respectively. In conclusion, treating rats with coffee decreased body weight, fasting serum glucose, uric acid, TC, TG and LDL-C, and increased HDL-C in a dose dependent manner in rats feeding on high fructose diet, suggesting that coffee consumption may be helpful in ameliorating metabolic syndrome.

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P0964EFFECTS OF XANTHINE OXIDASE INHIBITORS AND DAPAGLIFLOZIN ON RENAL GLUCOSE AND URATE TRANSPORTERS IN METABOLIC SYNDROME

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfaa144.p0964 ◽

2020 ◽

Vol 35 (Supplement_3) ◽

Author(s):

Hwee-Yeong Ng ◽

Chien-Te Lee ◽

Foong-Fah Leung ◽

Yuai-Ting Lee

Keyword(s):

Insulin Resistance ◽

Metabolic Syndrome ◽

Uric Acid ◽

Xanthine Oxidase ◽

Resistance Index ◽

High Fructose Diet ◽

Insulin Resistance Index ◽

Xanthine Oxidase Inhibitors ◽

High Fructose ◽

Uric Acid Transporters

Abstract Background and Aims Metabolic syndrome consists of several medical conditions that collectively predict the risk for cardiovascular disease. Hyperglycemia and hyperuricemia are the major disorders of metabolic syndrome. Kidney reabsorbs almost all filtrated glucose by active transport at normal concentrations of plasma glucose via members of the sodium glucose transport (SGLT) family. Besides, the kidney plays a pivotal role in handling uric acid homeostasis. Uric acid is mainly controlled by urate transporter (UAT), urate anion exchanger 1 (URAT1) and glucose transporter 9 (GLUT9). The aims of the study were to determine the alteration of renal glucose and uric acid transporters in animals with metabolic syndrome after treatment of xanthine oxidase inhibitors and SGLT2 inhibitor. Method Sprague-Dawley rats were fed with normal chow (Control) or high fructose diet (60%) for totally 6 months. For those animals fed with high fructose diet for 3 months, they were divided into 4 groups including high fructose diet without treatment (FR), treatment with allopurinol (150 mg/L in drinking water), with febuxostat (30 mg/L in drinking water) or with dapagliflozin (1mg/kg/day intraperitoneal injection). Blood, urine and blood pressure were collected and measured at the end of study. Gene and protein expression of renal glucose and uric acid transporters were determined by reverse transcriptase polymerase chain reaction. The changes of transporters were then confirmed by immunohistochemical staining. Results High-fructose diet induced higher levels of fasting glucose, insulin resistance index, uric acid, triglyceride and blood pressure in FR group (all p <0.05 vs. control). Treatment of allopurinol, febuxostat and dapagliflozin reduced body weight significantly. Fasting glucose, insulin resistance index and hyperuricemia were improved in all drug treatment groups (all p <0.05). In the kidney, high fructose diet significantly upregulated SGLT1, SGLT2 and GLUT2 but downregulated GLUT1 expression. Urate transporters, including GLUT9, UAT and URAT1 were also increased (p <0.05). The improvement of insulin resistance by xanthine oxidase inhibitors was associated with suppression of renal SGLT1, SGLT2 and GLUT2 expression. Dapagliflozin alleviated hyperuricemia and induced uricosuria without affecting serum xanthine oxidase activity. Compared to FR, dapagliflozin significantly inhibited fructose-induced overexpression of GLUT9, UAT and URAT1 in the kidney. Conclusion Long term high fructose diet induced metabolic syndrome in rats. Treatment of xanthine oxidase inhibitors and dapagliflozin ameliorated components of metabolic syndrome. Both allopurinol and febuxostat improved insulin resistance in association with suppression of renal SGLT1, SGLT2 and GLUT2 expression. Although dapagliflozin and xanthine oxidase inhibitors reduced uric acid in different mechanisms, they shared a similar molecular changes in the kidney by downregulating GLUT9, UAT and URAT1 expression.

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High-Fructose Diet Increases Inflammatory Cytokines and Alters Gut Microbiota Composition in Rats

Mediators of Inflammation ◽

10.1155/2020/6672636 ◽

2020 ◽

Vol 2020 ◽

pp. 1-10 ◽

Cited By ~ 1

Author(s):

Yong Wang ◽

Wentao Qi ◽

Ge Song ◽

Shaojie Pang ◽

Zhenzhen Peng ◽

...

Keyword(s):

Uric Acid ◽

Inflammatory Response ◽

Gut Microbiota ◽

Inflammatory Cytokines ◽

Proinflammatory Cytokines ◽

Lipid Accumulation ◽

Fasting Blood Glucose ◽

High Fructose Diet ◽

Fructose Intake ◽

High Fructose

High-fructose diet induced changes in gut microbiota structure and function, which have been linked to inflammatory response. However, the effect of small or appropriate doses of fructose on gut microbiota and inflammatory cytokines is not fully understood. Hence, the abundance changes of gut microbiota in fructose-treated Sprague-Dawley rats were analyzed by 16S rRNA sequencing. The effects of fructose diet on metabolic disorders were evaluated by blood biochemical parameter test, histological analysis, short-chain fatty acid (SCFA) analysis, ELISA analysis, and Western blot. Rats were intragastrically administered with pure fructose at the dose of 0 (Con), 2.6 (Fru-L), 5.3 (Fru-M), and 10.5 g/kg/day (Fru-H) for 20 weeks. The results showed that there were 36.5% increase of uric acid level in the Fru-H group when compared with the Con group. The serum proinflammatory cytokines (IL-6, TNF-α, and MIP-2) were significantly increased ( P < 0.05 ), and the anti-inflammatory cytokine IL-10 was significantly decreased ( P < 0.05 ) with fructose treatment. A higher fructose intake induced lipid accumulation in the liver and inflammatory cell infiltration in the pancreas and colon and increased the abundances of Lachnospira, Parasutterella, Marvinbryantia, and Blantia in colonic contents. Fructose intake increased the expressions of lipid accumulation proteins including perilipin-1, ADRP, and Tip-47 in the colon. Moreover, the higher level intake of fructose impaired intestinal barrier function due to the decrease of the expression of tight junction proteins (ZO-1 and occludin). In summary, there were no negative effects on body weight, fasting blood glucose, gut microbiota, and SCFAs in colonic contents of rats when fructose intake is in small or appropriate doses. High intake of fructose can increase uric acid, proinflammatory cytokines, intestinal permeability, and lipid accumulation in the liver and induce inflammatory response in the pancreas and colon.

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Caffeine affects autonomic control of heart rate and blood pressure recovery after aerobic exercise in young adults: a crossover study

Scientific Reports ◽

10.1038/s41598-017-14540-4 ◽

2017 ◽

Vol 7 (1) ◽

Cited By ~ 16

Author(s):

Luana Almeida Gonzaga ◽

Luiz Carlos Marques Vanderlei ◽

Rayana Loch Gomes ◽

Vitor Engrácia Valenti

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Young Adults ◽

Aerobic Exercise ◽

Crossover Study ◽

Autonomic Control ◽

Pressure Recovery

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Abstract 608: Uric Acid Potentially Interacts With Parathyroid Hormone To Promote Left Ventricular Diastolic Dysfunction In Mice Fed A Western Diet

Hypertension ◽

10.1161/hyp.64.suppl_1.608 ◽

2014 ◽

Vol 64 (suppl_1) ◽

Author(s):

Guanghong Jia ◽

Brian P Bostick ◽

Javad Habibi ◽

Annayya R. Aroor ◽

Vincent G. DeMarco ◽

...

Keyword(s):

Blood Pressure ◽

Body Weight ◽

Uric Acid ◽

Parathyroid Hormone ◽

Diastolic Dysfunction ◽

Cardiac Mri ◽

Left Ventricular ◽

Western Diet ◽

P Value ◽

Lv Diastolic Dysfunction

Hyperuricemia is frequently observed in obese people and rising obesity rates parallel increased consumption of a high-fat/high-fructose western diet (WD). Epidemiologic and clinical data suggest that serum uric acid (UA) is positively associated with serum parathyroid hormone (PTH) and may be linked with left ventricular (LV) hypertrophy and LV diastolic dysfunction. Accordingly, we hypothesized that allopurinol, a potent xanthine oxidase (XO) inhibitor, would prevent development of LV diastolic dysfunction, independent of blood pressure, by reducing the levels of UA and PTH. Four week-old C57BL6/J male mice were fed a WD and water with 125mg/L allopurinol. After 16 weeks, we assessed levels of UA, XO activity, PTH, as well as diastolic function by cardiac MRI and cardiac ultrastructure by transmission electron microscopy (TEM). Body weight and fat composition were obtained along with HOMA -IR testing for insulin resistance. Allopurinol has been show to exert no effect on blood pressure. High resolution cardiac MRI revealed diastolic dysfunction with WD feeding that was prevented by allopurinol (LV diastolic relaxation time 35.3 ms for WD, 25.4 ms for CD and 27.7 ms for WD+ allopurinol, p value <0.01; Initial filling rate 0. 28 μl/ms for WD, 0.43 μl/ms for CD and 0.42 μl/ms for WD+ allopurinol, p value <0.05). Body weight, fat mass, and HOMA-IR were increased by WD feeding but not significantly improved by allopurinol. However, allopurinol markedly decreased the WD-induced increase in heart weight associated with activation of translational S6 kinase. TEM examination of myocardial ultrastructure revealed that WD induced remodeling changes with large mitochondria with disordered cristae and increased lysosomes. The ultrastructural changes were improved with treatment by allopurinol. Furthermore, allopurinol significantly inhibited both of plasma and urine UA levels and cardiac XO activity caused by WD. Interestingly , WD increased PTH levels which were decreased in parallel with reductions in uric acid with allopurinol. These findings support the notion that increased plasma levels of UA, in concert with elevated PTH, may play a key role in LV hypertrophy and associated LV diastolic dysfunction that result from consuming a WD high in fructose and fat.

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Acute emotional stress and high fat/high fructose diet modulate brain oxidative damage through NrF2 and uric acid in rats

Nutrition Research ◽

10.1016/j.nutres.2020.05.009 ◽

2020 ◽

Vol 79 ◽

pp. 23-34

Author(s):

C. Batandier ◽

T. Poyot ◽

N. Marissal-Arvy ◽

K. Couturier ◽

F. Canini ◽

...

Keyword(s):

Uric Acid ◽

Oxidative Damage ◽

Emotional Stress ◽

High Fat ◽

High Fructose Diet ◽

Acute Emotional Stress ◽

High Fructose

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Augmented transcripts of kidney injury markers and renin angiotensin system in urine samples of overweight young adults

Scientific Reports ◽

10.1038/s41598-020-78382-3 ◽

2020 ◽

Vol 10 (1) ◽

Author(s):

Patricia Rivera ◽

Catalina Miranda ◽

Nicole Roldán ◽

Aaron Guerrero ◽

Javier Olave ◽

...

Keyword(s):

Blood Pressure ◽

Chronic Kidney Disease ◽

Young Adults ◽

Body Weight ◽

Kidney Disease ◽

Kidney Injury ◽

Tissue Growth ◽

Mrna Levels ◽

Simple Method ◽

Renin Angiotensin

AbstractObesity has been firmly established as a major risk factor for common disease states including hypertension, type 2 diabetes mellitus, and chronic kidney disease. Increased body mass index (BMI) contributes to the activation of both the systemic and intra-tubular renin angiotensin systems (RAS), which are in turn associated with increased blood pressure (BP) and kidney damage. In this cross-sectional study, 43 subjects of normal or increased body weight were examined in order to determine the correlation of BMI or body fat mass (BFM) with blood pressure, fasting blood glucose (FBG), and urinary kidney injury markers such as interleukin-18 (IL-18), connective tissue growth factor (CTGF), neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1 (KIM-1). Our results showed that: (1) subjects with increased body weight showed significantly higher BP, BFM, total body water and metabolic age; (2) BMI was positively correlated to both systolic (R2 = 0.1384, P = 0.01) and diastolic BP (R2 = 0.2437, P = 0.0008); (3) BFM was positively correlated to DBP (R2 = 0.1232, P = 0.02) and partially correlated to urine protein (R2 = 0.047, P = 0.12) and FBG (R2 = 0.07, P = 0.06); (4) overweight young adults had higher urinary mRNA levels of renin, angiotensinogen, IL-18 and CTGF. These suggest that BMI directly affects BP, kidney injury markers, and the activation of the intra-tubular RAS even in normotensive young adults. Given that BMI measurements and urine analyses are non-invasive, our findings may pave the way to developing a new and simple method of screening for the risk of chronic kidney disease in adults.

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