Katarzyna Musialik

Background: Resistin is a proinflammatory adipokine involved in metabolic disorders. Its interplay with hypertriglyceridemia remains to be elucidated. We aimed to evaluate the relationship between resistin (−420C/G) single nucleotide variant (SNV) and metabolic parameters and preference for fried food consumption in hypertriglyceridemia. Methods: The study enrolled 179 hypertriglyceridemic (HTG) and 182 normotriglyceridemic (NTG) patients. Anthropometric measurements, serum resistin, insulin and fasting glucose concentration, a homeostatic model assessment—insulin resistance (HOMA-IR), triglycerides (TG), cholesterol concentration, and fried food taste preference (FP) or other cooking methods preference (OP) were assessed in the study. Genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism. Results: HTG and NTG groups did not differ significantly in serum resistin concentration; HTG individuals demonstrated significantly increased serum levels of TG, glucose, total cholesterol (TCH), and HOMA-IR and decreased HDL cholesterol. Resistin, insulin, glucose, HOMA-IR, and cholesterol fractions were similar among particular resistin genotypes in HTG, NTG, FP, or OP groups. TG and TCH concentrations differ significantly among CG and CC genotypes in the FP group. Considering the FP group, GG and CG genotypes appeared more frequently in hyperlipidemic (OR 2.6 95% CI; 1.16–5.82; p = 0.01; significant after Bonferroni correction) than in NTG patients. Multivariable logistic regression models showed that the G allele and CG genotype of SNV (−420C/G), adjusted for selected confounders such as fried food preference, increased the odds of hypertriglyceridemia about twofold. Conclusions: Allele G and CG genotype of resistin SNV (−420C/G) are linked with the preference for fried food taste in hypertriglyceridemic patients.

Background: Resistin action links to conditions such as diabetes, obesity, but its role in hypertension is less well understood. This study aimed to estimate the relationship between resistin (−420G/C) single nucleotide variant (SNV) and markers associated with endothelial dysfunction in hypertension. Methods: The study enrolled 162 hypertensive patients (HT) and 165 non-hypertensive (NHT) patients. Resistin serum concentration was estimated with immuoenzymatic assay. Anthropometric measurements, blood pressure and arterial stiffness index (SI), uric acid (UA) serum concentration, and salty taste preference of normal (NS) or high (HS) were assessed in the study. Genotyping was achieved by polymerase chain reaction-restriction fragment length polymorphism. Results: Resistin concentration and SI do not differ significantly between HT and NHT individuals; UA significantly increased in HT subjects. Resistin, UA, and SI did not differ among particular resistin genotypes in HT, NHT, NS, or HS groups. GG and CG genotypes were more frequent (OR 1.57 (95% CI; 1.01–2.43); p = 0.04) in hypertensive individuals than the NHT group, but less frequent (OR 0.58 (95% CI; 0.37–0.91); p = 0.01) in HS patients compared to NS individuals. Concerning HT patients with different salt preferences, GG + CG genotypes were less frequent (OR 0.50 (95% CI; 0.26–0.97); p = 0.04) in the HS group than in NS individuals. HT carriers of GG and CG genotype have significantly increased UA concentrations compared to the respective NHT subjects. HS individuals carrying GG and CG genotypes have higher SI values than the NS group. Allele G of SNV (−420G/C) adjusted for age, BMI, serum resistin, UA concentration, salt taste preference, SI, and HR values increased the risk of developing hypertensive phenotype 1.8 fold. Conclusions: Resistin SNV (−420G/C) is related to several markers associated with endothelial dysfunction, including salt taste preference in hypertensive patients.

Adipocytes are hormonally active molecules modulating biochemical processes on-going in human organism. Visceral fat tissue is the source of many important substances, such as: adiponectin, TNF-α, resistin and many others. However, their role has not been fully elucidated. 1. To measure the concentrations of adiponectin, soluble receptors for TNF-α, and resistin in patients with metabolic syndrome (MetS). 2. To investigate the correlations between chosen adipocytokines and hypertension. The study included 85 patients with MetS, diagnosed according to the International Diabetes Federation (IDF) criteria from 2005, and 20 healthy volunteers as control subjects. In both groups, anthropological parameters (body mass index and waist circumference) and concentrations of adiponectin, soluble receptors for TNF-α and resistin were assessed. To measure adiponectin levels, radioimmunological and immunoenzymatic assays (sTNFR1, sTNFR2, and resistin) were employed. Concentration of adiponectin was markedly lower in patients with MetS compared to the control group (10.892 ± 10.440 vs. 19.307 ± 19.370 μg/mL, p 〈 0.001). In patients with MetS, sTNFR1 and sTNFR2 concentrations were significantly elevated and resistin level was significantly higher compared to control subjects (25.865 ± 25.8 vs. 9.60 ± 9.915 ng/mL, p 〈 0.001). Negative correlations between adiponectin and the values of systolic blood pressure (SBP) (Rp = 0.2898, p 〈 0.001) and diastolic blood pressure (DBP) (Rp = 0.2724, p 〈 0.001) were observed. Positive correlations between sTNFR2 and SBP (Rp = 0.450, p 〈 0.001) and DBP (Rp = 0.4695, p 〈 0.001) values were found. Resistin levels correlated positively with SBP (Rp = 0.5154, p 〈 0.001) and DBP (Rp = 0.5613, p 〈 0.001) values. In multiple regression model, the association of SBP with resistin level was observed in 32% of studied patients. 1. Patients with MetS are characterised by following disturbances: hypo-adiponectinaemia, elevated concentrations of soluble receptors for TNF-α, and hyperresistinaemia. 2. Elevated concentration of resistin may play a role in the development of high blood pressure.