Oral supplementation with glycine reduces oxidative stress in patients with metabolic syndrome, improving their systolic blood pressure

2013 ◽  
Vol 91 (10) ◽  
pp. 855-860 ◽  
Author(s):  
Margarita Díaz-Flores ◽  
Miguel Cruz ◽  
Genoveva Duran-Reyes ◽  
Catarina Munguia-Miranda ◽  
Hilda Loza-Rodríguez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Systolic Blood Pressure ◽  
Specific Activity ◽  
Thiobarbituric Acid ◽  
Treated Group ◽  
Contributing Factors ◽  
Oral Supplementation ◽  
Glucose 6 Phosphate Dehydrogenase

Reactive oxygen species derived from abdominal fat and uncontrolled glucose metabolism are contributing factors to both oxidative stress and the development of metabolic syndrome (MetS). This study was designed to evaluate the effects of daily administration of an oral glycine supplement on antioxidant enzymes and lipid peroxidation in MetS patients. The study included 60 volunteers: 30 individuals that were supplemented with glycine (15 g/day) and 30 that were given a placebo for 3 months. We analysed thiobarbituric acid reactive substances (TBARS) and S-nitrosohemoglobin (SNO-Hb) in plasma; the enzymatic activities of glucose-6-phosphate dehydrogenase (G6PD), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) in erythrocytes; and the expression of CAT, GPX, and SOD2 in leukocytes. Individuals treated with glycine showed a 25% decrease in TBARS compared with the placebo-treated group. Furthermore, there was a 20% reduction in SOD-specific activity in the glycine-treated group, which correlated with SOD2 expression. G6PD activity and SNO-Hb levels increased in the glycine-treated male group. Systolic blood pressure (SBP) also showed a significant decrease in the glycine-treated men (p = 0.043). Glycine plays an important role in balancing the redox reactions in the human body, thus protecting against oxidative damage in MetS patients.

Empagliflozin treatment does not affect the hypertensive response to Ang II administration to rats but decreases oxidative stress in the arterial wall, and endothelial and cardiac dysfunction

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C Bruckert ◽  
L Remila ◽  
K Matsushita ◽  
C Auger ◽  
U Houngue ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Angiotensin Ii ◽  
Left Ventricle ◽  
Cardiac Function ◽  
Systolic Blood Pressure ◽  
Sglt2 Inhibitor ◽  
Treated Group ◽  
Funding Source ◽  
Ang Ii

Abstract Background Selective sodium-glucose cotransporter 2 (SGLT2) inhibitors have shown cardiovascular protection in type 2 diabetes patients with established cardiovascular disease independently of glycemic control. Angiotensin II (Ang II) and H2O2 have been shown to be strong inducers of the expression of SGLT2 and 1 in endothelial cells promoting oxidative stress and endothelial dysfunction. Purpose This study examined the cardiovascular protective effect of empagliflozin (empa) in a normoglycemic experimental model of hypertension in the rat. Methods Male Wistar rats received empa (30 mg/kg/day) provided in the diet for 5 weeks. After 1 week, rats underwent sham surgery (sham rats) or surgery with implantation of an osmotic mini-pump infusing Ang II (0.4 mg/kg/d) for 4 weeks. Systolic blood pressure (SBP) was assessed by sphygmomanometry, the cardiac function using echocardiography, the expression level of target proteins by immunofluorescence staining, and the level of oxidative stress using dihydroethidium staining. Results Angiotensin II administration increased systolic blood pressure from about 130 to 180 mmHg, which was not affected by the empa treatment. The 4-week Ang II treatment did not significantly affect the systolic cardiac function (cardiac output, left ventricle ejection fraction) but impaired the diastolic function as indicated by a reduced E' and IVRT values, and an increased E/E' value. The Ang II treatment increased significantly the heart and right ventricle weight whereas the left ventricle + septum weight was slightly but not significantly increased. No such functional and structural changes were observed in the Ang II + empa treatment group. An increased immunofluorescence eNOS signal in the endothelium, and a higher level of ROS throughout the aorta wall were observed in the Ang II-treated group, both of which were significantly reduced in the empa + Ang II-treated group. In the Ang II-treated group, the high level of oxidative stress in the aorta was significantly reduced by the AT1 receptor antagonist losartan, the NADPH oxidase inhibitor VAS-2871, the eNOS inhibitor NG-nitro-L-arginine and also to a greater extent by the selective SGLT2 inhibitor empa compared to the dual SGLT1/2 inhibitor sotagliflozin. Conclusion(s) The present findings indicate that although the empa treatment did not affect the hypertensive response of rats to Ang II, the SGLT2 inhibitor prevented the deleterious impact of Ang II on the diastolic cardiac function and remodeling, and the upregulation of eNOS expression and oxidative stress in the aorta wall. Thus, these findings highlight the protective potential of empa on the cardiovascular system in a normoglycemic hypertensive experimental model. Funding Acknowledgement Type of funding source: Private company. Main funding source(s): Boehringer Ingelheim Pharma GmbH & Co KG (Biberach an der Riss, Germany)

scholarly journals Urinary sodium excretion and the risk of cardiovascular disease: A community-based cohort study in Taiwan

2021 ◽  
pp. 1-42
Author(s):  
Yi-Jie Wang ◽  
Kuo-Lioug Chien ◽  
Hsiu-Ching Hsu ◽  
Hung-Ju Lin ◽  
Ta-Chen Su ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Systolic Blood Pressure ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Salt Sensitivity ◽  
Urinary Sodium ◽  
Mediating Effect ◽  
Cvd Risk ◽  
Media Thickness

Abstract Urinary sodium excretion is a potential risk factor for cardiovascular diseases (CVD). However, the underlying biological mechanisms and effects of salt sensitivity are unclear. The purpose of this study was to characterize the relative contribution of biological factors to the sodium-CVD association. A total of 2112 participants were enrolled in this study. Structured questionnaires and blood and urine samples were obtained. Twenty-four-hour sodium excretion was estimated using a single overnight urine sample. Hypertension, metabolic syndrome, and overweight status were considered to indicate salt sensitivity. Cox proportional hazard models were used to investigate the effects of salt sensitivity on urinary sodium excretion and CVD risk. The traditional mediation approach was used to calculate the proportion of mediation. The mean age (standard deviation) of the 2112 participants was 54.5 (12.2) years, and they were followed up for a mean of 14.1 [8.1] years. Compared with those in the lowest quartile, the highest baseline urinary sodium excretion (>4.2g/24 hours) was associated with a 43% higher CVD risk (hazard ratio, 1.43; 95% confidence interval, 1.02-1.99). Participants with high urinary sodium excretion, hypertension, or metabolic syndrome had a significantly high risk of CVD. The carotid intima-media thickness had the largest mediating effect (accounting for 35% of the sodium-CVD association), followed by systolic blood pressure (33%), left ventricular mass (28%), and diastolic blood pressure (14%). Higher urinary sodium excretion increased the risk of CVD, which was explained largely by carotid media-thickness and systolic blood pressure.

Proximal tubule microvilli remodeling and albuminuria in the Ren2 transgenic rat

2007 ◽  
Vol 292 (2) ◽  
pp. F861-F867 ◽  
Author(s):  
Melvin R. Hayden ◽  
Nazif A. Chowdhury ◽  
Shawna A. Cooper ◽  
Adam Whaley-Connell ◽  
Javad Habibi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Proximal Tubule ◽  
Structural Damage ◽  
Kidney Tissue ◽  
Proximal Tubule Cell ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

TG(mRen2)27 (Ren2) transgenic rats overexpress the mouse renin gene, with subsequent elevated tissue ANG II, hypertension, and nephropathy. The proximal tubule cell (PTC) is responsible for the reabsorption of 5–8 g of glomerular filtered albumin each day. Excess filtered albumin may contribute to PTC damage and tubulointerstitial disease. This investigation examined the role of ANG II-induced oxidative stress in PTC structural remodeling: whether such changes could be modified with in vivo treatment with ANG type 1 receptor (AT1R) blockade (valsartan) or SOD/catalase mimetic (tempol). Male Ren2 (6–7 wk old) and age-matched Sprague-Dawley rats were treated with valsartan (30 mg/kg), tempol (1 mmol/l), or placebo for 3 wk. Systolic blood pressure, albuminuria, N-acetyl-β-d-glucosaminidase, and kidney tissue malondialdehyde (MDA) were measured, and ×60,000 transmission electron microscopy images were used to assess PTC microvilli structure. There were significant differences in systolic blood pressure, albuminuria, lipid peroxidation (MDA and nitrotyrosine staining), and PTC structure in Ren2 vs. Sprague-Dawley rats (each P < 0.05). Increased mean diameter of PTC microvilli in the placebo-treated Ren2 rats ( P < 0.05) correlated strongly with albuminuria ( r2 = 0.83) and moderately with MDA ( r2 = 0.49), and there was an increase in the ratio of abnormal forms of microvilli in placebo-treated Ren2 rats compared with Sprague-Dawley control rats ( P < 0.05). AT1R blockade, but not tempol treatment, abrogated albuminuria and N-acetyl-β-d-glucosaminidase; both therapies corrected abnormalities in oxidative stress and PTC microvilli remodeling. These data indicate that PTC structural damage in the Ren2 rat is related to the oxidative stress response to ANG II and/or albuminuria.

scholarly journals Osobennosti funktsional'nogo sostoyaniyakory nadpochechnikov i shchitovidnoy zhelezypri metabolicheskom sindrome

2011 ◽  
Vol 8 (3) ◽  
pp. 46-50 ◽  
Author(s):  
I V Madyanov ◽  
V A Kichigin ◽  
T N Markova ◽  
S M Semakina ◽  
I B Bashkova
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Thyroid Gland ◽  
Systolic Blood Pressure ◽  
Adrenal Cortex ◽  
Functional State ◽  
Thyroid Stimulating Hormone ◽  
Blood Levels ◽  
Dehydroepiandrosterone Sulphate ◽  
Total Triiodothyronine

The aim. To study the functional state of adrenal cortex and thyroid gland in metabolic syndrome (MS). 186 women and 65 men were included. Blood levels of cortisol, dehydroepiandrosterone sulphate, total thyroxin, total triiodothyronine, thyroid stimulating hormone were studied in subjects with and without metabolic syndrome (IDF test) and their relation with MS components. The results. 75 (29,9%) of the 251 examined patients had MS. In the group with MS the levels of total thyroxin and dehydroepiandrosterone sulphate were decreased to 1,90±0,18 microgram/milliliter vs. 2,37±0,12 microgram/milliliter (р=0,033) in patients without MS and 2,19±0,26 nmol/l vs. 2,59±0,15 nmol/l (р=0,040), respectively. The levels of dehydroepiandrosterone sulphate were inversely correlated with the systolic blood pressure (r=-0,23, р

scholarly journals Sitagliptin-Dependent Differences in the Intensity of Oxidative Stress in Rat Livers Subjected to Ischemia and Reperfusion

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Małgorzata Trocha ◽  
Małgorzata Krzystek-Korpacka ◽  
Anna Merwid-Ląd ◽  
Beata Nowak ◽  
Małgorzata Pieśniewska ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Liver ◽  
Ischemia Reperfusion ◽  
Antioxidant Properties ◽  
Thiobarbituric Acid ◽  
Treated Group ◽  
Paraoxonase 1 ◽  
Pon1 Activity ◽  
Tbars Level ◽  
Rat Livers

Purpose. Ischemia/reperfusion (IR) is the main cause of liver damage after transplantation. We evaluated the effect of sitagliptin (STG) on oxidative stress parameters in the rat liver under IR. Methods. Rats were treated with STG (5 mg/kg) (S and SIR) or saline solution (C and CIR). Livers from CIR and SIR were subjected to ischemia (60 min) and reperfusion (24 h). During reperfusion, aminotransferases (ALT and AST) were determined in blood samples. Thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase (CAT), paraoxonase-1 (PON1), glutathione peroxidase (GPx), and the mRNA expression of SOD1 were determined in liver homogenates after reperfusion. Different regions of livers were also histologically evaluated. Results. The PON1 activity was higher, and the TBARS level was lower in SIR than in CIR. There was an inverse relationship between TBARS and PON1 levels in the whole cohort. The GPx activity was lower in ischemic than in nonischemic groups regardless of the STG treatment. In SIR, the SOD1 activity was higher compared to that in CIR. In S, the expression of SOD1 mRNA was the highest of all examined groups and positively correlated with the SOD1 activity in the whole animal cohort. During IR aminotransferases, the activity in the drug-treated group was lower in all examined points of time. In drug-treated groups, the percentage of steatosis was higher than that in nontreated groups regardless of IR. Conclusions. The protective effect of STG on the rat liver, especially its antioxidant properties, was revealed under IR conditions.

scholarly journals Pattern of Metabolic Syndrome in Clinical Practice

1970 ◽  
Vol 10 (2) ◽  
pp. 48-51
Author(s):  
Quazi Tarikul Islam ◽  
Md Azizul Haque ◽  
ASM Shawkat Ali ◽  
ARM Saifuddin Ekram ◽  
Sultana Monira Hussain ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Body Weight ◽  
Clinical Practice ◽  
Waist Circumference ◽  
Prospective Study ◽  
Systolic Blood Pressure ◽  
Total Cholesterol ◽  
Age Group ◽  
Inclusion Criteria

1068 randomly sampled adult Bangladeshi people were studied during a period of six months from October 2004 to March 2005. It was a randomized, prospective study. Cases that fulfilled two criteria of metabolic syndrome (MetS) were evaluated to see pattern and types of MetS. Out of 1068 patients, 110 (10.3%) fulfilled the inclusion criteria. 101 (9.4%) cases were labeled as metabolic syndrome according to NCEP ATP III criteria, 09 cases had only two criteria. 40 cases were male & 70 cases were female (M:F= 1:1.8). Mean age of patients with was 44.88, ranging from the age of 20-68 years. Majority (55%) of the patients were in the age group of 30-49 years. Half of the cases had BMI 30-34.9. Mean body weight of male was 85.9 kg and of female was 78.2 kg. Mean waist circumference of male was 41.7 inches and of female 40 inches. Mean HDL for male was 38.3 mg/dL and for female is 40.2 mg/dL. Mean Triglyceride for male was 172.1 and for female was 169.3 mg/dL. Mean total cholesterol for male was 216.7 and for female was 207.6 mg/dL. Mean systolic blood pressure (SBP) for men is 162 mm Hg & diastolic blood pressure (DBP) 99 mm Hg and for female mean SBP 155 and DBP 96 mm Hg. Metabolic syndrome is more prevalent in the 3rd and 4th decade of life in both sexes. It is almost twice common in female than male. Combination of hypertension, obesity & dyslipidemia comprises nearly 40% of its presentation.    doi: 10.3329/jom.v10i2.2813 J MEDICINE 2009; 10 : 48-51

scholarly journals Enhanced expression of glucose-6-phosphate dehydrogenase in human cells sustaining oxidative stress

1997 ◽  
Vol 323 (3) ◽  
pp. 801-806 ◽  
Author(s):  
Matilde V. URSINI ◽  
Angelina PARRELLA ◽  
Graziella ROSA ◽  
Salvatore SALZANO ◽  
Giuseppe MARTINI
Keyword(s):  
Oxidative Stress ◽  
Mammalian Cells ◽  
Specific Activity ◽  
Redox Status ◽  
Enzyme Synthesis ◽  
Oxygen Intermediates ◽  
New Information ◽  
Enhanced Expression ◽  
A Minor ◽  
Glucose 6 Phosphate Dehydrogenase

Recent reports have demonstrated that glucose-6-phosphate dehydrogenase (G6PD) activity in mammalian cells is necessary in order to ensure cell survival when damage is produced by reactive oxygen intermediates. In this paper we demonstrate that oxidative stress, caused by agents acting at different steps in the biochemical pathway controlling the intracellular redox status, determines the increase in G6PD-specific activity in human cell lines of different tissue origins. The intracellular level of G6PD-specific mRNA also increases, with kinetics compatible with the induction of new enzyme synthesis. We carried out experiments in which cells were exposed to oxidative stress in the presence of inhibitors of protein or RNA synthesis. These demonstrated that increased G6PD expression is mainly due to an increased rate of transcription, with a minor but significant contribution of regulatory mechanisms acting at post-transcriptional levels. These results provide new information on the defence systems that eukaryotic cells possess in order to prevent damage caused by potentially harmful oxygen derivatives.

Moderate zinc restriction during fetal and postnatal growth of rats: effects on adult arterial blood pressure and kidney

2008 ◽  
Vol 295 (2) ◽  
pp. R543-R549 ◽  
Author(s):  
Analía Lorena Tomat ◽  
Felipe Inserra ◽  
Luciana Veiras ◽  
María Constanza Vallone ◽  
Ana María Balaszczuk ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Lipid Peroxidation ◽  
Systolic Blood Pressure ◽  
Zinc Deficiency ◽  
Control Diet ◽  
Adult Life ◽  
Fetal Life ◽  
Arterial Blood ◽  
End Products

Intrauterine and postnatal zinc restriction may result in an adverse environment for the development of cardiovascular and renal systems. This study evaluated the effects of moderate zinc deficiency during fetal life, lactation, and/or postweaning growth on systolic blood pressure, renal function, and morphology in adult life. Female Wistar rats received low (8 ppm) or control (30 ppm) zinc diets from the beginning of pregnancy up to weaning. After weaning, male offspring of each group of mothers were fed low or control zinc diet. Systolic blood pressure, creatinine clearance, proteinuria, renal morphology, renal apoptosis. and renal oxidative stress state were evaluated after 60 days. Zinc deficiency during pre- and postweaning growth induced an increase in systolic blood pressure and a decrease in the glomerular filtration rate associated with a reduction in the number and size of nephrons. Activation of renal apoptosis, reduction in catalase activity, glutathione peroxidase activity, and glutathione levels and increase in lipid peroxidation end products could explain these morphometric changes. Zinc deficiency through pre- and postweaning growth induced more pronounced renal alteration than postweaning zinc deficiency. These animals showed signs of renal fibrosis, proteinuria, increased renal apoptosis, and higher lipid peroxidation end products. A control diet during postweaning growth did not totally overcome renal oxidative stress damage, apoptosis, and fibrosis induced by zinc deficiency before weaning. In conclusion, zinc deficiency during a critical period of renal development and maturation could induce functional and morphological alterations that result in elevated blood pressure and renal dysfunction in adult life.

Effects of aldosterone on blood pressure and glucose-6-phosphate dehydrogenase activity of heart muscle

1969 ◽  
Vol 47 (2) ◽  
pp. 193-197 ◽  
Author(s):  
C. C. Liew ◽  
A. G. Gornall
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Heart Muscle ◽  
Specific Activity ◽  
Systolic Pressure ◽  
Experimental Hypertension ◽  
Low Doses ◽  
Significant Elevation ◽  
Desoxycorticosterone Acetate ◽  
Glucose 6 Phosphate Dehydrogenase

A study was made of the effects of aldosterone on the activity of heart muscle glucose-6-phosphate dehydrogenase (G6PDH) in relation to the pathogenesis of experimental hypertension. In a 17-day experiment, with rats given daily 1-μg doses of aldosterone/100 g body weight, no change in systolic pressure occurred and the specific activity (s.a.) of heart muscle G6PDH declined. Rats receiving daily 100 μg of aldosterone, or 500 μg of desoxycorticosterone acetate (DOCA) per 100 g body weight, showed a significant elevation of systolic pressure by the 17th day. This effect was accompanied by increases in the s.a. of heart muscle G6PDH, apparently preceding the development of hypertension. Evidence for a homeostatic role for aldosterone was revealed by the ability of low doses to prevent a decline in s.a. of cardiac G6PDH during fasting, and to reverse the increase produced by DOCA.

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