BackgroundThe aim of this study was to estimate associations between inflammatory markers and obesity indices in normo- and hypertensive subjects.Methods65 obese adult subjects were divided into two groups: (A) of hypertensives (n = 54) and (B) of normotensives (n = 11). Waist circumference (WC), body mass index (BMI), waist-to-hip ratio (WHR), waist-to-height ratio (WHtR), visceral adiposity index (VAI), body adiposity index (BAI) and tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and high sensitivity C-reactive protein (hsCRP) serum concentrations were estimated.ResultsIn group A WHtR was higher (0.69 ± 0.07 vs 0.63 ± 0.06; p < 0.01), hsCRP correlated with BMI and WHtR (r = 0.343; p = 0.011 and r = 0.363; p < 0.01, respectively). BAI correlated with hsCRP in group A and B (r = 0.329; p < 0.05 and r = 0.642; p < 0.05; respectively) and in females and males (r = 0.305; p = 0.05 and r = 0.44; p < 0.05, respectively). In females hsCRP was higher (3.2 ± 2.2 mg/l vs 2.1 ± 1.5 mg/l; p < 0.05). In patients without lipid lowering treatment hsCRP and IL-6 were higher (3.2 ± 1.7 mg/l vs 2.4 ±2.2 mg/l; p = 0.01 and 15.9 ± 7.2 pg/ml vs 13.6 ± 9.9 pg/ml; p < 0.01, respectively).ConclusionsWHtR is a sensitive index associated with chronic inflammation in obese hypertensive subjects. BAI correlates with hsCRP independently of hypertension and sex. hsCRP is more sensitive marker associated with obesity than IL-6 and TNF-α. Lipid lowering treatment influence chronic inflammation.
We compared adipokines and inflammatory markers in obese insulin-sensitive (group A, n = 16) and insulin-resistant (group B, n = 48) patients divided according to homeostasis model assessment of insulin resistance (HOMA-IR). Serum levels of adiponectin, leptin, resistin, high-sensitivity C-reactive protein, interleukin 6, and tumor necrosis factor α were measured. Weight, height, waist (WC) and hip circumferences, waist to hip ratio , weight to height ratio, visceral adiposity index (VAI), and body adiposity index (BAI) were measured. The WC and VAI were significantly higher in group B (113.9 ± 11.1 vs 105.3 ± 9.8 cm; P < .01 and 2.3 ± 1.1 vs 1.6 ± 0.9; P < .05, respectively), while serum adiponectin levels were higher in group A (24.5 ± 14.6 vs 15.1 ± 9.6 ng/mL; P < .005). The BAI strongly correlated with adiponectin and leptin in group B (r = .479; P < .001 and r = .705; P < .001). Insulin resistance is associated with visceral adiposity described by VAI and WC. The BAI may be a useful index in obese patients, especially with insulin resistance.
A b s t r a c tIntroduction: Hypertension often coexists with obesity. Adipokines, ghrelin and insulin play important roles in the pathogenesis of both diseases. The aim of this study was to compare adiponectin, leptin, resistin, insulin and ghrelin mean serum concentrations and insulin resistance (HOMA-IR) in normo-and hypertensive patients with obesity. Material and methods: All included patients were divided on the following groups: non-diabetic hypertensive patients with class I obesity (group A, n = 21) and class II/III obesity (group B, n = 10), and normotensive obese (class I)patients (group C, n = 7). Correlations between obesity indices (body mass index [BMI], waist-tohip ratio [WHR], waist circumference [WC]), HOMA-IR, and hormone and adipokine serum levels were also analyzed. Results: Leptin level and HOMA-IR were significantly higher in group B compared to group C (9.74 ±3.88 ng/ml vs. 4.53 ±3.00 ng/ml; p < 0.02 and 3.30 ±1.59 vs. 1.65 ±0.41; p < 0.02, respectively). A negative correlation between WC and adiponectin level (R = -0.6275; p < 0.01) and a positive correlation between WC and insulin concentration (R = 0.5122; p < 0.05) as well as with HOMA-IR (R = 0.5228; p < 0.02) were found in group A. Negative correlations between BMI and ghrelin level (R = -0.7052; p < 0.05), WHR and adiponectin level (R = -0.6912; p < 0.05) and WHR and leptin level (R = -0.6728; p < 0.05) were observed in group B. Conclusions: Insulin resistance and leptin may be important pathogenic factors in hypertensive patients with severe obesity. Indices of abdominal obesity (WC, WHR) correlate better than BMI with HOMA-IR, insulin, adiponectin and leptin serum levels in hypertensive obese patients.
Background: The aim of this study was to estimate associations between inflammatory markers and obesity indices in normo-and hypertensive subjects. Methods: 65 obese adult subjects were divided into two groups: (A) of hypertensives (n = 54) and (B) of normotensives (n = 11). Waist circumference (WC), body mass index (BMI), waist-to-hip ratio (WHR), waist-to-height ratio (WHtR), visceral adiposity index (VAI), body adiposity index (BAI) and tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and high sensitivity C-reactive protein (hsCRP) serum concentrations were estimated.
(r = 0.27, p < 0.001) and highsensitivity Creactive protein (r = 0.20, p < 0.05 (Cardiol J 2013; 20, 6: 577-582)
We compared the obesity parameters and selected adipokines-leptin, adiponectin, and resistin-in obese patients with hypertension and normotensive patients. A total of 67 nondiabetic obese outpatients were divided into 2 groups: A-hypertensive and B-normotensive. Serum levels of leptin, adiponectin, resistin, and insulin were measured. Weight, height, waist circumference, and hip circumference were measured to calculate waist-to-hip ratio (WHR), weight-to-height ratio, visceral adiposity index, and body adiposity index (BAI). Among patients with hypertension, significant positive correlations were observed between leptin and body mass index and BAI (r = .31 and r = .63, respectively). In normotensive patients, leptin positively correlated with BAI (r = .73, P < .01) and negatively with WHR (r = -.55, P < .0001); adiponectin negatively correlated with WHR (r = .38, P < .01) and BAI (r = .52; P < .0001), and resistin negatively correlated with WHR (r = -.36, P < .05). In conclusion, visceral obesity and leptin are associated with hypertension in obese patients.
BackgroundThe aim of this study was to estimate obesity parameters: waist circumference (WC), waist-to-hip ratio (WHR), weight-to-height ratio (WHtR), visceral adiposity index (VAI), body adiposity index (BAI), and serum adipokines (leptin, adiponectin, resistin) and their associations with estimated glomerular filtration rate (eGFR), serum creatinine, and microalbuminuria (MA) in patients with early stages of CKD and in non-CKD obese patients.Material/Methods67 non-diabetic obese (BMI ≥30 mg/kg2) out-clinic patients (25 males, 42 females), aged from 36.5 to 64 years were divided into 2 groups: Group A (n=15) – patients with early stages of CKD (eGFR between 30 and 60 ml/min/1.73 m2 or with MA >20 mg/l in morning urine sample independently from GFR) and Group B – patients without chronic CKD (n=52).ResultsIn Group A compared to Group B, BAI and leptin were higher (42.2±7.1 vs. 37.5±7.0; p<0.05 and 51.8±26.7 ng/mL vs. 35.3±24.9 ng/mL; p<0.05; respectively) and negative correlations occurred between eGFR and BAI (r=−0.709; p=0.003), leptin (r=−0.68; p=0.005), and resistin (r=−0.528; p<0.05). In Group B, negative correlations occurred between creatinine and VAI (r=−0.332; p<0.05), BAI (r=−0.619; p<0.0001), leptin (r=−0.676; p<0.0001), and adiponectin (r=−0.423; p=0.002), and between eGFR and resistin (r=−0.276; p<0.05).ConclusionsBAI may be a valuable obesity parameter as a predictor of early stages of CKD in patients with obesity. Leptin may be an important pathogenic factor in obese patients with early stages of CKD. Resistin is associated with eGFR in obese patients, independently of CKD.
PurposeConsidering its prognostic usefulness and the relationship with chronic kidney disease, we analyzed the clinical utility of soluble urokinase plasminogen activator receptor (suPAR) in end-stage renal disease patients undergoing hemodialysis treatment. We focused on the association between suPAR levels and clinical outcomes, especially those related to cardiovascular events and mortality as well as the effect of hemodialysis on the protein levels.MethodsWe enrolled 64 patients. Blood samples for laboratory tests were collected before and after the midweek hemodialysis. The concentration of suPAR was assessed using suPARNostic ELISA, ViroGates.ResultsSpearman rank analyses showed a positive association between suPAR and creatinine, cystatin C, galectin 3, N-terminal prohormone of brain natriuretic peptide and troponin T (p < 0.05). In ROC analysis, the suPAR concentration equal to 11.5 ng/mL was established to be the cutoff value for the prediction of mortality in the analyzed patients. Simultaneous analysis of creatinine and suPAR increased the predictive value of the latter—the area under curve increased to 0.84 (95% CI 0.70–0.94, p < 0.0001). Logistic regression analysis revealed that increase in the suPAR level was associated with the increase in odds ratio for death by 1.3 (95% CI 1.1–1.6, χ2 = 8.2, p = 0.004). In multivariable analysis, the prediction power of suPAR appeared to be stronger after including creatinine (p = 0.0005).ConclusionsElevated suPAR levels provide independent information on mortality risk in patients undergoing hemodialysis. The protein appears not to cross the dialysis membrane; thus, blood collection before the second hemodialysis session seems to give reliable information on the suPAR level for clinical interpretation.
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