We examined an association between ghrelin, including its major isoforms, interleukin-6 (IL-6), body mass index (BMI), and mean arterial pressure (MAP) in male overweight patients with essential ...hypertension. Twenty hypertensive male patients with newly diagnosed essential hypertension (EH) before starting drug treatment and 22 age-matched healthy controls were enrolled in the study. Fasting total plasma ghrelin (TGhr), acyl ghrelin (AGhr), des-acyl ghrelin (DGhr) and IL-6 were determined and correlations between studied parameters were calculated. We found significantly lower total plasma ghrelin and higher plasma IL-6 in hypertensives when compared with the control. In patients with hypertension the negative correlations were found: between TGhr and BMI, DGhr and BMI, TGhr and MAP, and between DGhr and MAP. IL-6 positively correlated with BMI and MAP in hypertensive subjects. No correlations between all forms of ghrelin and IL-6 were noted. The changes in plasma ghrelin and IL-6 contribute independently to the elevated blood pressure in essential hypertension. Negative correlation of DGhr and MAP may suggest its hemodynamic involvement in regulation of blood pressure.
Background:
Elevated plasminogen activator inhibitor type 1 (PAI 1) plays an important role in the pathogenesis of excess blood coagulability in obese patients. L-arginine supplementation has shown ...to be associated with enhanced cardiovascular and metabolic health. The aim of the study was to assess the effect of L-arginine supplementation on PAI 1 concentration and to evaluate the relation to changes in nitric oxide (NO) plasma level, insulin sensitivity (M value), and total antioxidant status (TAS) in obese patients.
Material/subjects and methods:
A randomized, double-blind, placebo-controlled study was conducted from March 2010 to June 2011. Eighty-eight obese patients were randomly assigned to receive either 9 g of L-arginine or placebo daily for 6 months. At baseline and after 6 months, selected anthropometrical measurements and blood biochemical analyses were performed, and PAI 1, NO, TAS levels were assessed. Insulin sensitivity was evaluated using the hyperinsulinemic euglycemic clamp technique.
Results:
We found that 6-month L-arginine supplementation resulted in significant decrease of PAI 1. Significant increase of NO, TAS, and insulin sensitivity level were noticed. In a group of patients treated with L-arginine, negative correlation between a change of insulin sensitivity value and a change of PAI 1 concentration was found.
Conclusions:
The present findings demonstrate favorable influence of L-arginine supplementation on PAI 1 concentration in obese patients. Beneficial influence is related to insulin sensitivity improvement. The potential therapeutic role of L-arginine administration in patients with obesity needs further investigation.
Although obesity may be linked to resistin, the role of resistin in humans is still controversial. Conflicting results of the associations between resistin and BMI and measures of insulin resistance ...were reported. In view of the yet unexplained role of resistin in human obesity, the aim of this study was to examine correlations between serum resistin concentrations and the degree of human obesity and insulin sensitivity. For this purpose, we investigated 2 homogenous groups of obese and non obese humans, in whom the presence of obesity was the solely differentiating factor. The WHO definition of obesity was used. Study group consisted of 136 obese subjects (75 women and 61 men) and 48 non-obese controls (31 women, 17 men) aged 48.0 ± 10.1, and 48.8 ± 13.4 yrs, respectively.
Obese subjects showed higher resistin concentrations than non obese controls (24.89 ± 9.73 ng/mL, median 26.61 vs. 15.34 ± 4.68 ng/mL, median 14.76, P < 0.0001). Resistin concentrations correlated with BMI in the whole cohort (r = 0.4296, P < 0.0001), but not in obese and non-obese subjects separately (r = 0.1418, P = 0.0997; r = 0.2712, P = 0.0623, respectively). Moreover, serum resistin was not influenced by insulin resistance in either group examined.
Although concentrations of resistin differ between obese and non-obese humans, no relationship between resistin concentration and insulin resistance has been found. Correlations between resistin and BMI are present only in a mixed population but disappear in non obese and obese subjects when analyzed separately.
Leptin binds to the soluble form of its receptor (sOB-R). Leptin and sOB-R balance (free leptin index, FLI) reflect leptin activity. Leptin correlates with obesity and insulin resistance, but it ...remains uncertain whether sOB-R and FLI also do the same. Therefore, the aim of this study was to measure serum leptin, sOB-R, and FLI, and evaluate their associations with BMI and insulin resistance. We studied 145 obese and 49 nonobese humans. Obesity was defined according to WHO (BMI >30 kg/m (2)). Results are given as: median and interquartile range, obese vs. nonobese, respectively. Leptin (ng/ml): 30.83, 37.27 vs. 8.31, 10.04; sOB-R (ng/ml): 17.62, 17.05 vs. 27.25, 11.30; FLI: 231.2, 310.0 vs. 30.85, 27.77; HOMA: 5.99, 6.64 vs. 3.92, 4.52; p<0.001 for all. Serum leptin, sOB-R, and FLI did not correlate with insulin resistance separately in obese and nonobese humans. Leptin and FLI, but not sOB-R, were associated with insulin resistance in obese and nonobese subjects examined together. Leptin, sOB-R and FLI differed between obese and nonobese humans, and, except sOB-R, correlated with BMI. In piecewise linear regression, BMI threshold where leptin increased was 24.6 (r=0.5969, p=0.00016 and <0.00001). Leptin and its free index, but not sOB-R, correlate with BMI only in a mixed obese and nonobese human cohort, and not in isolated obese or nonobese groups. Moreover, BMI threshold where leptin starts to increase is 24.6 kg/m (2), which is lower than the cutoff for overweight. Under the conditions, metabolic abnormalities may occur in parallel to much lower BMI levels as expected so far.
Long-term therapy of hypertension may influence mineral status in patients. However, drug-micronutrient interactions are largely unexplored in practice. This study intended to evaluate the effect of ...hypotensive monotherapy on iron, zinc, and copper levels, as well as on selected biochemical parameters, in newly diagnosed patients with hypertension, and to assess the influence of diet with optimal mineral levels on the mineral balance in these subjects.
Forty-five patients, aged 18-65 years with diagnosed essential hypertension, beginning monotherapy treatment with diuretics, calcium antagonists, angiotensin-converting enzyme inhibitors, and β-blockers, were employed. Over three months, the patients underwent monotherapy (stage II). Next, patients were randomly divided into a diet group (of 27 subjects) and a control group (of 18 subjects). In this stage, which lasted one month, patients were given the same drug but also followed an optimal mineral-content diet (for the diet group), or else continued drug use without any change in diet (for control group) (stage III). Lipids, glucose, ceruloplasmin, and ferritin--along with superoxide dismutase and catalase activities--were assayed in serum. Iron, zinc, and copper concentrations in serum, erythrocytes, and urine were determined using flame atomic absorption spectrometry. Blood pressure was measured. Diet intake was monitored at each stage.
It was found that the zinc level in serum significantly decreased following treatment, and that the use of the optimal-mineral diet during antihypertensive treatment markedly increased zinc serum concentration. After treatment, a significant increase in zinc excretion in the urine was observed. Glucose levels in the serum of patients in stage II were significantly higher than in the baseline. In patients in the diet group, glucose levels markedly decreased. Moreover, a negative correlation was found between serum glucose and zinc levels in patients.
Antihypertensive treatments should include monitoring of mineral status. It seems that the zinc balance of patients on long-term therapy with hypotensive drugs may benefit from an optimal-mineral diet.
Widespread hypovitaminosis D and an increased incidence of metabolic syndrome (MetS) represent significant problems of contemporary medicine but link between them remain unresolved. We aimed to ...define relationship between vitamin D serum concentration and exponents of MetS.
The studies were conducted on 70 individuals (51 with and 19 without MetS). Concentrations of 25(OH)D (25-hydroxyergocalciferol and 25-hydroxycholecalciferol), calcium, cholesterol, HDL, cholesterol LDL, triglycerides, fasting glucose, blood pressure and anthropometric parameters were measured.
Median concentration of vitamin D in the research population amounted to 41.46 nmol/L. Concentration of 25(OH)D in MetS group was lower than in remainder participants (38.45 nmol/L vs. 58.50 nmol/L, p = 0.0104). An inverse correlation was demonstrated between 25(OH)D level on one hand and body weight, waist and hips circumference, adipose body weight, Body Mass Index, Waist to Height Ratio (WHtR), glycaemia and number of MetS components on the other in persons free of MetS. No such relationships could be documented in MetS group. In the entire population values of Waist to Hip Ratio (WHpR) and WHtR indices manifested correlation with hyperglycaemia, hypertriglyceridaemia, low HDL concentrations.
In persons without MetS a relationship was detected between vitamin D concentration and exponents of metabolic syndrome, although further studies on this problem are required.
Obesity and smoking are leading causes of morbidity and mortality worldwide. Cross-sectional studies indicate that heavy smoking may be associated with a greater risk of obesity. While there are ...important unresolved issues in relation to the effect of smoking on body weight, there is increasing evidence that smoking is conducive to a greater accumulation of visceral fat and greater insulin resistance.
of this study was to determine the potential influences of obesity and smoking on tumor necrosis factor alpha (TNF-α), total antioxidant status (TAS), and insulin resistance.
30 obese nonsmokers, 30 obese smokers, 30 normal-weight smokers, and 30 healthy volunteers (the control) were studied. In all subjects, assessments of TNF-α, TAS, and insulin were made. Insulin resistance was evaluated according to the homeostasis model assessment-insulin resistance (HOMA-IR) protocol.
TNF-α concentrations, as well as insulin resistance levels, in obese patients significantly exceeded those observed in the control. Compared to the control, obese patients presented significantly lower TAS levels. In the group of obese patients who actively smoked cigarettes, further increases in TNF-α and insulin resistance, as well as decreases in TAS level, were noticed. TNF-α concentration and insulin resistance levels were significantly higher, while TAS was lower in normal-weight smoking subjects, compared to the control. A positive correlation between TNF-α and HOMA-IR was found in the overall population.
Obesity may evoke inflammatory processes, oxidative stress, and insulin resistance, all of which are aggravated by cigarette smoking. TNF-α should be considered in the complex pathogenesis of insulin resistance in obese patients who actively smoke.
Potential role of L-arginine supplementation as a new effective strategy of improving endothelial function in patients with hypertension is recently under consideration.
To evaluate influence of ...28-day oral supplementation of L-arginine on plasma level of asymmetric dimethylarginine (ADMA), L-citrulline, L-arginine and total antioxidant status (TAS), in patients with mild arterial hypertension.
54 participants (24 women and 30 men) were studied. Ambulatory blood pressure monitoring (ABPM) was used for allotting patients to either healthy control group (19 subjects) or hypertensive treatment group (35 patients). Patients were later randomized to either L-arginine (2 g tid or 4 g tid) or placebo. During 28 days of study on 5 consecutive visits TAS, plasma level of ADMA, L-citrulline, and L-arginine were measured.
In patients with mild hypertension treated with L-arginine significant increase in TAS and plasma level of arginine and citrulline was observed. Additionally plasma ADMA concentrations after 28 days of L-arginine supplementation significantly exceeded initial concentrations.
L-arginine supplementation increases plasma arginine, citrulline and TAS in patients with mild arterial hypertension. It confirms the thesis that augmented concentrations of L-arginine stimulate NO biosynthesis which leads to reduction of oxidative stress. Increase of ADMA plasma level after L-arginine supplementation confirms correlation between ADMA and L-arginine.
Abstract Chronic sub-clinical inflammation observed in hypertension plays a prominent role in the progression of atherosclerosis. Accumulating evidence suggests that homocysteine (Hcy) can cause ...inflammation. The aim of this study was to compare the predictive utility of Hcy and lipid measures as determinants of inflammation in hypertensive patients. We studied a group of 100 patients (45.0 ± 12.2 years old) with essential hypertension and a control group of 40 healthy volunteers (44.0 ± 8.7 years old). We found that plasma total Hcy (tHcy), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), and C-reactive protein (CRP) were significantly higher in hypertensive patients compared with the control group. The subgroup of hypertensive patients with obesity had higher levels of TNF-α ( p < 0.001), IL-6 ( p < 0.01), and tHcy ( p = 0.063), compared with the subgroup of hypertensive patients without obesity. The subgroup of patients with a history of myocardial infarction or stroke had significantly higher levels of tHcy, TNF-α, IL-6, and CRP compared to patients with a negative history of vascular events. In the group of hypertensive patients, a strong positive correlation between tHcy and TNF-α was observed ( r = 0.48; p < 0.001). In contrast, no correlation was observed between TNF-α and any of the lipid measures. In multivariate regression analysis tHcy, but not lipids, was an independent predictor of TNF-α. In conclusion, our findings show that plasma tHcy is a determinant of TNF-α in hypertension and that obesity or a history of vascular events aggravates inflammation in patients with hypertension. A positive correlation between Hcy and TNF-α suggests a mechanism underlying the pro-atherogenic properties of Hcy.
