Acute ingestion of a high-fructose drink impairs vascular autonomic modulation and reflex control of blood pressure in first-degree relatives of diabetic patients.

First-degree relatives of diabetes patients, despite being euglycemic, presented impaired BRS and exacerbation of sympathetic modulation after ingestion of a high fructose drink when challenged to orthostatic stress. This finding alerts the importance of early autonomic dysfunction even in clinically healthy people, especially in face of a stressful situation.

Associations of multiple unhealthy lifestyle behaviors with overweight/obesity and abdominal obesity among Brazilian adolescents: A country-wide survey.

BACKGROUND AND AIMS: Physical inactivity, unhealthy diet, smoking and heavy drinking are four key unhealthy lifestyle behaviors (ULB) that may influence body weight and obesity development. More recently, sedentary time has been recognized as another potentially emerging ULB related to obesity. We therefore investigated the association of multiple ULB with overweight/obesity and abdominal obesity among Brazilian adolescents. METHODS AND RESULTS: This cross-sectional study involved 62,063 students (12-17 years). Physical inactivity, high screen time, low fiber intake, binge drinking and smoking were self-reported and combined to a ULB risk score, ranging from zero to five. Participants were classified as overweight/obese or with abdominal obesity using sex and age-specific cut-off points for BMI and waist circumference, respectively. Poisson regression models were used to examine the associations between ULB with overweight/obesity and abdominal obesity, adjusted for socio-demographic variables. Overall, 2.3%, 18.9%, 43.9%, 32.3% and 2.6% of participants reported zero, one, two, three and four/five ULB, respectively. Higher ULB risk score was associated with overweight/obesity and abdominal obesity in a dose-response gradient. Among 32 possible combinations of ULB, the three most prevalent combinations (physical inactivity + low fiber intake; high screen time + low fiber intake; physical inactivity + high screen time + low fiber intake) were positively associated with general and abdominal obesity. CONCLUSIONS: Our findings suggest a synergistic relationship between ULB and general and abdominal obesity. Preventive efforts targeting combined ULB should be sought to reduce the prevalence of general and abdominal obesity in Brazilian youth.

C-reactive protein in Brazilian adolescents: distribution and association with metabolic syndrome in ERICA survey.

BACKGROUND/OBJECTIVES: C-reactive protein (CRP) is a marker of inflammation that has been shown to be predictive of cardiovascular diseases in adults. To evaluate the distribution of CRP as well as its association with metabolic syndrome and its components. SUBJECTS/METHODS: This is a cross-sectional study on adolescents aged 12-17, participants in the Study of Cardiovascular Risk in Adolescents (ERICA). Anthropometric, biochemical and blood pressure data were collected from 6316 adolescents, selected from a random sample of students in the cities of Brasilia, Fortaleza, João Pessoa, Manaus, Porto Alegre and Rio de Janeiro. Metabolic syndrome was defined by the criteria proposed by International Diabetes Federation for adolescent. Poisson regression model with robust variance, taking into consideration the study's complex sampling design, was used to determine multivariate-adjusted prevalence rate ratios expressing the relationship of metabolic syndrome with CRP. RESULTS: In adolescents with metabolic syndrome, CRP concentrations were five times higher (1.01 mg/l; interquartile range (IQR): 0.54-3.47) compared with those without metabolic syndrome (0.19 mg/l; IQR: 0.10-0.78). In multivariate Poisson regression analysis adjusted by sex, age and skin color, the prevalence of elevated CRP (>3.0 mg/l) was almost three times higher in adolescents with metabolic syndrome than in those without this condition (prevalence ratio (PR): 2.9; 95%CI: 2.0-4.3; P<0.001). Of the metabolic syndrome components, elevated waist circumference, low high-density lipoprotein-cholesterol and high triglycerides were significantly related to CRP in a graded (dose-response) manner. CONCLUSIONS: The association of CRP with metabolic syndrome and its components suggests that inflammation may be useful in assessing cardiovascular risk in adolescents.

Weight-loss interventions and gut microbiota changes in overweight and obese patients: a systematic review.

Imbalances in the gut microbiota, the bacteria that inhabit the intestines, are central to the pathogenesis of obesity. This systematic review assesses the association between the gut microbiota and weight loss in overweight/obese adults and its potential manipulation as a target for treating obesity. This review identified 43 studies using the keywords 'overweight' or 'obesity' and 'microbiota' and related terms; among these studies, 17 used dietary interventions, 11 used bariatric surgery and 15 used microbiota manipulation. The studies differed in their methodologies as well as their intervention lengths. Restrictive diets decreased the microbiota abundance, correlated with nutrient deficiency rather than weight loss and generally reduced the butyrate producers Firmicutes, Lactobacillus sp. and Bifidobacterium sp. The impact of surgical intervention depended on the given technique and showed a similar effect on butyrate producers, in addition to increasing the presence of the Proteobacteria phylum, which is related to changes in the intestinal absorptive surface, pH and digestion time. Probiotics differed in strain and duration with diverse effects on the microbiota, and they tended to reduce body fat. Prebiotics had a bifidogenic effect and increased butyrate producers, likely due to cross-feeding interactions, contributing to the gut barrier and improving metabolic outcomes. All of the interventions under consideration had impacts on the gut microbiota, although they did not always correlate with weight loss. These results show that restrictive diets and bariatric surgery reduce microbial abundance and promote changes in microbial composition that could have long-term detrimental effects on the colon. In contrast, prebiotics might restore a healthy microbiome and reduce body fat.

Does body mass index modify the association between physical activity and screen time with cardiometabolic risk factors in adolescents? Findings from a country-wide survey.

BACKGROUND: Moderate and vigorous physical activity (MVPA) and screen time (ST) have been associated with cardiometabolic health in youth. However, previous studies are conflicting whether these associations are independent of each other and it is unknown if they are modified by adiposity. We aimed to examine the independent and joint associations between MVPA and ST with cardiometabolic risk across body mass index (BMI) categories. METHODS: A total of 36 956 Brazilian adolescents (12-17 years) from the Study of Cardiovascular Risks in Adolescents were included. Information on time spent in MVPA and ST were assessed by self-reports. Blood pressure, Homeostasis Model Assessment of Insulin Resistance, triglycerides, high-density lipoprotein-cholesterol and waist circumference were used to calculate a cardiometabolic risk score (sex-age-specific top-risk quintile for each biomarker). Ordered logistic regression was used to examine the associations. RESULTS: In final adjusted models, both higher MVPA (proportional odds ratio (POR)=0.80; 95% confidence interval (CI): 0.67-0.95) and ST (POR=1.23; 95% CI: 1.10-1.37) were independently associated with cardiometabolic risk. After stratification by normal weight vs overweight/obese, the inverse independent association for MVPA remained unchanged, whereas ST was positively associated with cardiometabolic risk only in overweight/obese adolescents (POR=1.62; 95% CI: 1.18-2.22). Participants who met the recommendations for both MVPA and ST had lower odds for cardiometabolic risk, especially if they were overweight/obese (POR=0.46; 95% CI: 0.31-0.68). CONCLUSIONS: MVPA and ST are independently associated with cardiometabolic risk; the association with ST, however, appears modified by BMI. Normal-weight adolescents should be encouraged to increase MVPA, whereas a combination of increasing MVPA and decreasing ST is recommended in those who are overweight or obese.

Changes in renal glucose transporters in an animal model of metabolic syndrome.

Considering the similarity between structural, hemodynamic, and functional changes of obesity-related renal disease and diabetic nephropathy, we hypothesized that renal glucose transporter changes occur in obesity as in diabetes. The aim of the work was to evaluate GLUT1 and GLUT2 in kidneys of an animal model of metabolic syndrome. Neonate spontaneously hypertensive rats (SHR), n=15/group, were treated with monosodium glutamate (5 mg/g) (MetS) for 9 days and compared with saline-treated Wistar-Kyoto (C) and SHR (H) rats. Lee index, systolic arterial pressure (SAP), glycemia, insulin resistance, triglycerides, and HDL cholesterol were evaluated at 3 and 6 months. Medullar GLUT1 and cortical GLUT2 were analyzed by Western blot. MetS vs. C and H rats had the highest Lee index (p<0.001) and insulin resistance (3-months C: 4.3±0.7, H: 3.9±0.9, MetS: 2.7±0.6; 6-months C: 4.2±0.6, H: 3.8±0.5, MetS: 2.4±0.6% · min⁻¹, p<0.001), similar glycemia, and the lowest HDL-cholesterol at 6-months (p<0.001). In the MetS and H rats, SAP was higher vs. C at 3-months (p<0.001) and 6-months (C: 151±15, H: 190±11, MetS: 185±13 mm Hg, p<0.001) of age. GLUT1 was Ì´ 13× lower (p<0.001) at 3-months, reestablishing its content at 6-months in MetS group, while GLUT2 was 2× higher (p<0.001) in this group at 6-months of age. Renal GLUT1 and GLUT2 are modulated in kidney of rats with metabolic syndrome, where obesity, insulin resistance and hypertension coexist, despite normoglycemia. Like in diabetes, cortical GLUT2 overexpression may contribute to the development of kidney disease.

Perception of uncontrolled blood pressure and non-adherence to anti-hypertensive agents in diabetic hypertensive patients.

We assessed the association between adherence to antihypertensive drug treatment and patient's perception of uncontrolled blood pressure (BP) in diabetic hypertensive subjects. This was a cross-sectional study that evaluated adherence to antihypertensives (Morisky questionnaire), patients' perception of abnormal BP, office BP, and ambulatory BP monitoring in diabetic hypertensive subjects. We evaluated 323 patients, 65.2% women, aged 56.5 ± 7 years, glycosylated hemoglobin (HbA1c) 8.0% (range, 6.9%-9.6%), diabetes duration of 10 years (range, 5-17 years). Adherence to drug treatment was 51.4%. Patients who reported hypertension-related symptoms (60.4%) had a lower level of adherence (P < .001). Non-adherence occurred four times more frequently in patients who reported hypertension-related symptoms (P < .001, adjusted for use of three or more anti-hypertensives, age, and duration of diabetes). Non-adherents had higher office diastolic BP (83.6 ± 11.9 vs. 79.8 ± 9.9; P = .003), but no difference between groups was observed considering systolic, diastolic, and mean BP evaluated by ambulatory BP monitoring. Low rates of adherence to antihypertensive drug treatment were observed in outpatient hypertensive diabetic subjects. Perception of uncontrolled BP levels was strongly and independently associated with non-adherence. Non-adherence determined repercussion on office BP that may have clinical implications in cardiovascular risk.

Progressive cardiovascular autonomic dysfunction in rats with evolving metabolic syndrome.

Metabolic syndrome is linked to increased cardiovascular mortality, which may be partially attributed to cardiac sympatho-vagal imbalance. However, autonomic changes were not evaluated during the metabolic syndrome development in a monosodium glutamate-induced animal model. We evaluate temporal changes in cardiovascular autonomic modulation in an animal model of metabolic syndrome. Eighteen neonate male spontaneously hypertensive rats (SHR) were treated with monosodium glutamate (MetS), and compared with Wistar-Kyoto (C) and saline-treated SHR (H). Lee index, insulin resistance and autonomic control (spectral analysis) were evaluated at 3 (3-mo), 6 (6-mo) and 9 (9-mo) months of age (compared by two-way ANOVA, p<0.05). Weight of visceral fat, Lee index and arterial pressure were higher in the MetS vs. C and H groups (p<0.001) at all ages. Heart rate variability (HRV) was decreased in the MetS and H groups at 3-mo and 9-mo vs. C. The LF component of HRV was reduced in the MetS group at 3-mo vs. C (p=0.032), and higher vs. C and H at 9-mo (p<0.001, all comparisons). H and MetS rats had a higher LF/HF index vs. C at 9-mo (p=0.001, all comparisons). The VLF component of systolic arterial pressure variability of the MetS was higher earlier (6-mo) than that of the H group. A reduction of 70%, 98% and 54% in αLF index of H and MetS rats vs. C, was observed at 3, 6 and 9 months, respectively. Metabolic syndrome and hypertension in rats evolve with progressive autonomic dysfunction (worst at 9 months), with specific derangements occurring very early.

Volume of supervised exercise training impacts glycaemic control in patients with type 2 diabetes: a systematic review with meta-regression analysis.

AIMS/HYPOTHESIS: Supervised exercise programmes improve glycaemic control in type 2 diabetes, but training characteristics associated with reduction in HbA(1c) remain unclear. We conducted a systematic review with meta-regression analysis of randomised clinical trials (RCTs) assessing the association between intensity and volume of exercise training (aerobic, resistance or combined) and HbA(1c) changes in patients with type 2 diabetes. METHODS: Five electronic databases were searched (1980-2012) to retrieve RCTs of at least 12 weeks' duration, consisting of supervised exercise training vs no intervention, that reported HbA(1c) changes and exercise characteristics. Two independent reviewers conducted study selection and data extraction. RESULTS: Twenty-six RCTs (2,253 patients) met the inclusion criteria. In multivariate analysis, baseline HbA(1c) and exercise frequency explained nearly 58% of between-study variance. Baseline HbA(1c) was inversely correlated with HbA(1c) reductions after the three types of exercise training. In aerobic training, exercise volume (represented by frequency of sessions) was associated with changes in HbA(1c) (weighted r = -0.64), while no variables were correlated with glycaemic control induced by resistance training. In combined training, weekly volume of resistance exercise explained heterogeneity in multivariate analysis and was associated with changes in HbA(1c) levels (weighted r = -0.70). CONCLUSIONS/INTERPRETATION: Reduction in HbA(1c) is associated with exercise frequency in supervised aerobic training, and with weekly volume of resistance exercise in supervised combined training. Therefore, exercise volume is a major determinant of glycaemic control in patients with type 2 diabetes.

Neuromuscular electrical stimulation improves GLUT-4 and morphological characteristics of skeletal muscle in rats with heart failure.

AIM: Changes in skeletal muscle morphology and metabolism are associated with limited functional capacity in heart failure, which can be attenuated by neuromuscular electrical stimulation (ES). The purpose of the present study was to analyse the effects of ES upon GLUT-4 protein content, fibre structure and vessel density of the skeletal muscle in a rat model of HF subsequent to myocardial infarction. METHODS: Forty-four male Wistar rats were assigned to one of four groups: sham (S), sham submitted to ES (S+ES), heart failure (HF) and heart failure submitted to ES (HF+ES). The rats in the ES groups were submitted to ES of the left leg during 20 days (2.5 kHz, once a day, 30 min, duty cycle 50%- 15 s contraction/15 s rest). After this period, the left tibialis anterior muscle was collected from all the rats for analysis. RESULTS: HF+ES rats showed lower values of lung congestion when compared with HF rats (P = 0.0001). Although muscle weight was lower in HF rats than in the S group, thus indicating hypotrophy, 20 days of ES led to their recovery (P < 0.0001). In both groups submitted to ES, there was an increase in muscle vessel density (P < 0.04). Additionally, heart failure determined a 49% reduction in GLUT-4 protein content (P < 0.03), which was recovered by ES (P < 0.01). CONCLUSION: In heart failure, ES improves morphological changes and raises GLUT-4 content in skeletal muscle.

Microalbuminuria is associated with impaired arterial and venous endothelium-dependent vasodilation in patients with Type 2 diabetes.

BACKGROUND: Microalbuminuria in Type 2 diabetes is associated with arterial endothelial dysfunction, but the venous bed was never evaluated. AIM: To study the endothelial function in the venous and arterial bed in patients with Type 2 diabetes with normoalbuminuria or microalbuminuria. MATERIAL AND METHODS: We evaluated 28 patients with Type 2 diabetes, glycated hemoglobin (HbA(1c)) <7.5%, who were classified as normo- (albuminuria <30 mg/24 h; no.=16) or microalbuminuric (albuminuria 30-300 mg/24 h; no.=12). Venous and arterial endothelial function were assessed by the dorsal hand vein technique (venodilation by acetylcholine) and brachial artery flow-mediated vasodilation, respectively. RESULTS: Patients were normotensive (systolic arterial pressure: 131.1±10.6 mmHg) and on good metabolic control (HbA(1c): 6.6±0.6%). Microalbuminuric patients presented impaired venous (32.9±17.4 vs 59.3±26.5%; p=0.004) and arterial vasodilation (1.8±0.9 vs 5.1±2.4; p<0.001), as compared to normoalbuminuric patients. There was a negative correlation between acetylcholine-induced venodilation and albuminuria (r=-0.62; p<0.001) and HbA(1c) (r=-0.41; p=0.032). The same was observed between flow mediated arterial vasodilation and albuminuria (r=-0.49; p=0.007) and HbA(1c) (r=-0.44; p=0.019). Venous and arterial vasodilation was positively correlated (r=0.50; p=0.007). CONCLUSIONS: Both venous and arterial endothelial function are impaired in Type 2 microalbuminuric diabetics, in spite of good metabolic control, suggesting that other factors are involved in its pathogenesis.

C-reactive protein in acute coronary syndrome: association with 3-year outcomes

Inflammatory markers have been associated with clinical outcome in patients with acute coronary syndrome (ACS). The present study evaluated the role of high-sensitivity C-reactive protein (CRP) measurements as a predictor of late cardiovascular outcomes after ACS. One hundred and ninety-nine ACS patients in a Coronary Care Unit from March to November 2002 were included and were reassessed clinically after ~3 years. Clinical variables and CRP levels were evaluated as predictors of major cardiovascular events (MACE, defined as the occurrence of cardiac death, ischemic stroke or myocardial infarction) and mortality. Statistical analyses included Cox multivariable analysis and survival curves (Kaplan-Meier). Of the 199 patients, 11 died within 1 month (5.5 percent). Of the 188 remaining patients, 22 died after a mean follow-up of 2.9 ± 0.5 years. Baseline CRP levels for patients with MACE (N = 57) were significantly higher than those of patients with no events (median = 0.67 mg/L; 25th-75th percentiles = 0.32 and 1.99 mg/L vs median = 0.45 mg/L; 25th-75th percentiles = 0.24 and 0.83 mg/L; P < 0.001). Patients with CRP levels >3 mg/L had a significantly lower survival than the other two groups (1-3 and <1 mg/L; P = 0.001, log-rank test). The odds ratio for MACE was 7.41 (2.03-27.09) for patients with CRP >3 mg/L compared with those with CRP <1 mg/L. For death by any cause, the hazard ratio was 4.58 (1.93-10.86). High CRP levels predicted worse long-term outcomes (MACE and death by any cause) in patients with ACS.

C-reactive protein in acute coronary syndrome: association with 3-year outcomes.

Inflammatory markers have been associated with clinical outcome in patients with acute coronary syndrome (ACS). The present study evaluated the role of high-sensitivity C-reactive protein (CRP) measurements as a predictor of late cardiovascular outcomes after ACS. One hundred and ninety-nine ACS patients in a Coronary Care Unit from March to November 2002 were included and were reassessed clinically after approximately 3 years. Clinical variables and CRP levels were evaluated as predictors of major cardiovascular events (MACE, defined as the occurrence of cardiac death, ischemic stroke or myocardial infarction) and mortality. Statistical analyses included Cox multivariable analysis and survival curves (Kaplan-Meier). Of the 199 patients, 11 died within 1 month (5.5%). Of the 188 remaining patients, 22 died after a mean follow-up of 2.9 +/- 0.5 years. Baseline CRP levels for patients with MACE (N = 57) were significantly higher than those of patients with no events (median = 0.67 mg/L; 25th-75th percentiles = 0.32 and 1.99 mg/L vs median = 0.45 mg/L; 25th-75th percentiles = 0.24 and 0.83 mg/L; P < 0.001). Patients with CRP levels >3 mg/L had a significantly lower survival than the other two groups (1-3 and <1 mg/L; P = 0.001, log-rank test). The odds ratio for MACE was 7.41 (2.03-27.09) for patients with CRP >3 mg/L compared with those with CRP <1 mg/L. For death by any cause, the hazard ratio was 4.58 (1.93-10.86). High CRP levels predicted worse long-term outcomes (MACE and death by any cause) in patients with ACS.

SLC2A2 gene expression in kidney of diabetic rats is regulated by HNF-1alpha and HNF-3beta.

We hypothesize that, in kidney of diabetic rats, hepatocyte nuclear factors (HNF-1alpha and HNF-3beta) play a critical role in the overexpression of solute carrier 2A2 (SLC2A2) gene. Diabetic rats submitted or not to rapid (up to 12h) and short-term (1, 4 and 6 days) insulin treatment were investigated. Twofold increase in GLUT2 mRNA was observed in diabetic, accompanied by significant increases in HNF-1alpha and HNF-3beta expression and binding activity. Additional 2-fold increase in GLUT2 mRNA and HNF-3beta expression/activity was observed in 12-h insulin-treated rats. Six-day insulin treatment decreased GLUT2 mRNA and HNF-1alpha expression and activity to levels of non-diabetic rats, whereas HNF-3beta decreased to levels of non-insulin-treated diabetic rats. Our results provide evidence for a link between the overexpression of SLC2A2 gene and the transcriptional activity of HNF-1alpha and HNF-3beta in kidney of diabetic rats. Furthermore, recovery of SLC2A2 gene after 6-day insulin treatment also involves HNF-1alpha and HNF-3beta activity.

Reduced cortical renal GLUT1 expression induced by angiotensin-converting enzyme inhibition in diabetic spontaneously hypertensive rats.

Diabetes in spontaneously hypertensive rats is associated with cortical renal GLUT1 and GLUT2 overexpression. Our objective was to evaluate the effect of the angiotensin-converting enzyme blockade on cortical renal GLUT1 and GLUT2 expression, urinary albumin and urinary TGF-beta1. Streptozotocin, 50 mg/kg, or citrate buffer (N = 16) was administered as a single injection into the tail vein in adult spontaneously hypertensive rats (approximately 260 g). Thirty days later, these diabetic spontaneously hypertensive rats received ramipril by gavage: 0.01 mg x kg(-1) x day(-1) (D0.01, N = 14), 1 mg x kg(-1) x day(-1) (D1, N = 9) or water (D, N = 11) for 15 days. Albumin and TGF-beta1 (24-h urine), direct arterial pressure, renal tissue angiotensin-converting enzyme activity (fluorometric assay), and GLUT1 and GLUT2 protein levels (Western blot, renal cortex) were determined. Glycemia and glycosuria were higher (P < 0.05) in the diabetic rats compared with controls, but similar between the diabetic groups. Diabetes in spontaneously hypertensive rats lowered renal tissue angiotensin-converting enzyme activity (40%), which was reduced further when higher ramipril doses were used. Diabetes associated with hypertension raised GLUT1 by 28% (P < 0.0001) and GLUT2 by 76% (P = 0.01), and both doses of ramipril equally reduced cortical GLUT1 (D vs D1 and vs D0.01, P < or = 0.001). GLUT2 levels were reduced in D0.01 (P < 0.05 vs D). Diabetes increased urinary albumin and TGF-beta1 urinary excretion, but the 15-day ramipril treatment (with either dose) did not reduce them. In conclusion, ramipril is effective in lowering renal tissue angiotensin-converting enzyme activity, as well as blocking cortical GLUT1 overexpression, which may be beneficial in arresting the development of diabetic nephropathy.

Reduced cortical renal GLUT1 expression induced by angiotensin-converting enzyme inhibition in diabetic spontaneously hypertensive rats

Diabetes in spontaneously hypertensive rats is associated with cortical renal GLUT1 and GLUT2 overexpression. Our objective was to evaluate the effect of the angiotensin-converting enzyme blockade on cortical renal GLUT1 and GLUT2 expression, urinary albumin and urinary TGF-¦Â1. Streptozotocin, 50 mg/kg, or citrate buffer (N = 16) was administered as a single injection into the tail vein in adult spontaneously hypertensive rats (~260 g). Thirty days later, these diabetic spontaneously hypertensive rats received ramipril by gavage: 0.01 mg¡¤kg-1¡¤day-1 (D0.01, N = 14), 1 mg¡¤kg-1¡¤day-1 (D1, N = 9) or water (D, N = 11) for 15 days. Albumin and TGF-¦Â1 (24-h urine), direct arterial pressure, renal tissue angiotensin-converting enzyme activity (fluorometric assay), and GLUT1 and GLUT2 protein levels (Western blot, renal cortex) were determined. Glycemia and glycosuria were higher (P < 0.05) in the diabetic rats compared with controls, but similar between the diabetic groups. Diabetes in spontaneously hypertensive rats lowered renal tissue angiotensin-converting enzyme activity (40 percent), which was reduced further when higher ramipril doses were used. Diabetes associated with hypertension raised GLUT1 by 28 percent (P < 0.0001) and GLUT2 by 76 percent (P = 0.01), and both doses of ramipril equally reduced cortical GLUT1 (D vs D1 and vs D0.01, P ¡Ü 0.001). GLUT2 levels were reduced in D0.01 (P < 0.05 vs D). Diabetes increased urinary albumin and TGF-¦Â1 urinary excretion, but the 15-day ramipril treatment (with either dose) did not reduce them. In conclusion, ramipril is effective in lowering renal tissue angiotensin-converting enzyme activity, as well as blocking cortical GLUT1 overexpression, which may be beneficial in arresting the development of diabetic nephropathy.

Hemodialysis improves endothelial venous function in end-stage renal disease.

The objective of the present study was to determine the acute effect of hemodialysis on endothelial venous function and oxidative stress. We studied 9 patients with end-stage renal disease (ESRD), 36.8 +/- 3.0 years old, arterial pressure 133.8 +/- 6.8/80.0 +/- 5.0 mmHg, time on dialysis 55.0 +/- 16.6 months, immediately before and after a hemodialysis session, and 10 healthy controls matched for age and gender. Endothelial function was assessed by the dorsal hand vein technique using graded local infusion of acetylcholine (endothelium-dependent venodilation, EDV) and sodium nitroprusside (endothelium-independent venodilation). Oxidative stress was evaluated by measuring protein oxidative damage (carbonyls) and antioxidant defense (total radical trapping antioxidant potential - TRAP) in blood samples. All patients were receiving recombinant human erythropoietin for at least 3 months and were not taking nitrates or a-receptor antagonists. EDV was significantly lower in ESRD patients before hemodialysis (65.6 +/- 10.5) vs controls (109.6 +/- 10.8; P = 0.010) and after hemodialysis (106.6 +/- 15.7; P = 0.045). Endothelium-independent venodilation was similar in all comparisons performed. The hemodialysis session significantly decreased TRAP (402.0 +/- 53.5 vs 157.1 +/- 28.3 U Trolox/microL plasma; P = 0.001). There was no difference in protein damage comparing ESRD patients before and after hemodialysis. The magnitude of change in the EDV was correlated negatively with the magnitude of change in TRAP (r = -0.70; P = 0.037). These results suggest that a hemodialysis session improves endothelial venous function, in association with an antioxidant effect.

Hemodialysis improves endothelial venous function in end-stage renal disease

The objective of the present study was to determine the acute effect of hemodialysis on endothelial venous function and oxidative stress. We studied 9 patients with end-stage renal disease (ESRD), 36.8 ± 3.0 years old, arterial pressure 133.8 ± 6.8/80.0 ± 5.0 mmHg, time on dialysis 55.0 ± 16.6 months, immediately before and after a hemodialysis session, and 10 healthy controls matched for age and gender. Endothelial function was assessed by the dorsal hand vein technique using graded local infusion of acetylcholine (endothelium-dependent venodilation, EDV) and sodium nitroprusside (endothelium-independent venodilation). Oxidative stress was evaluated by measuring protein oxidative damage (carbonyls) and antioxidant defense (total radical trapping antioxidant potential - TRAP) in blood samples. All patients were receiving recombinant human erythropoietin for at least 3 months and were not taking nitrates or a-receptor antagonists. EDV was significantly lower in ESRD patients before hemodialysis (65.6 ± 10.5) vs controls (109.6 ± 10.8; P = 0.010) and after hemodialysis (106.6 ± 15.7; P = 0.045). Endothelium-independent venodilation was similar in all comparisons performed. The hemodialysis session significantly decreased TRAP (402.0 ± 53.5 vs 157.1 ± 28.3 U Trolox/µL plasma; P = 0.001). There was no difference in protein damage comparing ESRD patients before and after hemodialysis. The magnitude of change in the EDV was correlated negatively with the magnitude of change in TRAP (r = -0.70; P = 0.037). These results suggest that a hemodialysis session improves endothelial venous function, in association with an antioxidant effect.

Circuit weight training and cardiac morphology: a trial with magnetic resonance imaging.

BACKGROUND: Aerobic training (AT) and circuit weight training (CWT) improve peak oxygen uptake (VO(2)peak). During CWT the circulatory system is exposed to higher pressure, which could induce left ventricle morphological adaptations, possibly distinct from those derived from aerobic training. OBJECTIVE: To compare the effects of aerobic training and CWT upon morphological and functional cardiac adaptations detected by magnetic resonance imaging. METHODS: Twenty healthy sedentary individuals were randomly assigned to participate in a 12-week programme of aerobic training (n = 6), CWR (n = 7) or no intervention (n = 7, controls). Training programmes consisted of 36 sessions, 35 min each, 3 times per week, at 70% of maximal heart rate, and CWT included series of resistance exercises performed at 60% of 1 maximal repetition. Cardiopulmonary exercise testing and cardiac magnetic resonance imaging were performed before and after the intervention. RESULTS: There was a similar improvement in VO(2)peak following aerobic training (mean (SD) increment: 12 (4)%) and CWT (12 (4)%), while there was no change in the control group. Aerobic training (12 (6)%) and CWT (16 (5)%) improved strength in the lower limbs, and only CWT resulted in improvement of 13 (4)% in the strength of the upper limbs. However, there were no detectable changes in left ventricular mass, end-diastolic volume, stroke volume or ejection fraction. CONCLUSION: In previously sedentary individuals, short-term CWT and aerobic training induce similar improvement in functional capacity without any adaptation in cardiac morphology detectable by cardiac magnetic resonance imaging.