Plasma Resistin Concentrations Research Articles

Adiponectin, Leptin and Resistin in Patients with Psoriasis.

Psoriasis is a common chronic, inflammatory skin disease characterised by keratinocyte hyperproliferation, parakeratosis, and T-cell infiltration. Adipose tissue has an endocrine function, producing an abundance of cytokines and adipokines. It has also been described that the major adipokines, leptin, resistin, and adiponectin, may be involved in the pathogenesis of psoriasis. The aim of the study was to examine the plasma levels of adiponectin, leptin, and resistin in patients with psoriasis and their correlations with disease activity parameters: Psoriasis Activity Severity Index (PASI), Dermatology Life Quality Index (DLQI), and Body Surface Area (BSA) index, as well as selected clinical parameters. The study included 53 patients with the plaque type and 31 healthy controls. The plasma concentrations of adiponectin were significantly lower in patients with psoriasis (p < 0.001) than in the control group. The plasma concentrations of leptin were higher in patients with psoriasis, however, due to high intra-patient variability of leptin plasma concentrations these differences did not reach statistical significance (p = 0.2). The plasma concentrations of resistin were significantly increased in patients with psoriasis compared to healthy controls (p = 0.02). There were no statistically significant correlations between adiponectin and leptin plasma concentrations and values of PASI, DLQI, and BSA. The resistin plasma concentrations correlated significantly with DLQI values. Additionally, we examined the correlations between adiponectin, leptin, and resistin plasma concentrations, and selected clinical parameters. Plasma concentrations of adiponectin correlated significantly with CRP values and ALT values. Leptin plasma concentrations correlated significantly with creatinine values. The results of our study confirm the role of adiponectin, leptin, and resistin in the pathogenesis of psoriasis.

Resistin Concentration in Early Sepsis and All-Cause Mortality at a Safety-Net Hospital in Riverside County.

BackgroundSepsis mortality has remained unchanged for greater than a decade, and early recognition continues to be the most important factor in mortality outcome. Plasma resistin concentration is increased in sepsis, but its mechanism and clinical relevance is unclear. As one function, resistin interacts with toll-like receptor 4 in competition with lipopolysaccharide, a main component of the gram-negative bacterial cell wall. It is not known if the type of infection leading to sepsis influences resistin production. The objective of this study was to investigate whether 1) early plasma resistin concentration can predict mortality, 2) elevated plasma resistin concentration is associated with clinical disease severity scores, such as SOFA, mSOFA and APACHE II, and 3) plasma resistin concentrations differ between gram negative versus other etiologies of sepsis.MethodsThis was an exploratory study in the framework of a prospective observational design. Peripheral venous blood samples were obtained from subjects admitted to the intensive care unit at clinical recognition of sepsis (0 hour) and at 6 and 24 hours. Vasopressor utilization was not a requirement for inclusion. Plasma was analyzed for resistin concentration by ELISA. Cytokine concentrations including IL-6, IL-8, and IL-10 were determined by cytokine bead array. Cytokine data were evaluated against publicly available sepsis RNA expression datasets to compare protein versus RNA expression levels in predicting clinical disease state. Clinical data were collected from electronic health records for clinical severity index calculations and context for interpretation of resistin and cytokine concentrations. Subjects were followed up to 60 days, or until death, whichever came first. Statistical analysis was completed with R package and SPSS software.ResultsResistin levels were elevated in subjects admitted to the intensive care unit with sepsis. Four-hundred subjects were screened with 45 subjects included in the final analysis. Thirteen of 45 patients were non-survivors. Mortality within 60 days correlated with significantly higher resistin concentrations than in survivors. A resistin concentration of >126 ng/mL at clinical recognition of sepsis and >197 ng/mL within the first 24 hours were associated with mortality within 60 days with an area under the curve of 0.82 and 0.88, respectively. Most subjects with resistin concentration greater than these threshold values were deceased prior to 30 days. Resistin concentrations correlated with SOFA, mSOFA, and APACHE II scores in addition to having association with increases in inflammatory and sepsis biomarkers. These associations were validated with analysis of RNA expression datasets.ConclusionPlasma resistin concentrations of >126 ng/mL at clinical recognition of sepsis and >197 ng/mL within the first 24 hours of clinical sepsis recognition are associated with all-cause mortality. Resistin concentration within this timeframe also has comparable mortality association to well-validated clinical severity indices of SOFA, mSOFA, and APACHE II scores.

Measurement of Plasma Resistin Concentrations in Horses with Metabolic and Inflammatory Disorders.

Simple SummaryObesity and its associated complications, such as metabolic syndrome, are an increasing problem in both humans and horses in the developed world. Adipose tissue is a key endocrine organ that communicates with other organs by multiple endocrine substances called adipokines. There is evidence to suggest that adipokines may contribute to the regulation of biological processes, such as metabolism, immunity, and inflammation. The aim of this study was to investigate the usefulness of one of these adipokines in horses, resistin, and its relationship with insulin dysregulation (ID) and inflammation. Seventy-two horses, included in one of the four following groups, were studied: healthy controls, horses with inflammatory conditions, horses with mild, and horses with severe ID. Plasma resistin concentrations were significantly different between groups, and the highest values were recorded in the inflammatory and severe ID groups. The lack of correlation of resistin with basal insulin concentration and the significant correlation of resistin with the inflammatory marker serum amyloid A suggest that, as is the case in humans, plasma resistin concentrations in horses are predominantly related to inflammatory conditions and not to ID.Obesity and its associated complications, such as metabolic syndrome, are an increasing problem in both humans and horses in the developed world. The expression patterns of resistin differ considerably between species. In rodents, resistin is expressed by adipocytes and is related to obesity and ID. In humans, resistin is predominantly produced by inflammatory cells, and resistin concentrations do not reflect the degree of obesity, although they may predict cardiovascular outcomes. The aim of this study was to investigate the usefulness of resistin and its relationship with ID and selected indicators of inflammation in horses. Seventy-two horses, included in one of the four following groups, were studied: healthy controls (C, n = 14), horses with inflammatory conditions (I, n = 21), horses with mild ID (ID1, n = 18), and horses with severe ID (ID2, n = 19). Plasma resistin concentrations were significantly different between groups and the higher values were recorded in the I and ID2 groups (C: 2.38 ± 1.69 ng/mL; I: 6.85 ± 8.38 ng/mL; ID1: 2.41 ± 2.70 ng/mL; ID2: 4.49 ± 3.08 ng/mL). Plasma resistin was not correlated with basal insulin concentrations. A significant (r = 0.336, p = 0.002) correlation was found between resistin and serum amyloid A. Our results show that, as is the case in humans, plasma resistin concentrations in horses are predominantly related to inflammatory conditions and not to ID. Horses with severe ID showed an elevation in resistin that may be secondary to the inflammatory status associated with metabolic syndrome.

THE ROLE OF RESISTIN IN THE PROGRESSION OF NON-ALCOHOLIC FATTY LIVER DISEASE

The aim of the research was to study the relationship between plasma concentrations of resistin and indicators of enzyme and pigment metabolism in patients with non-alcoholic fatty liver disease (NAFLD) and its combination with type 2 diabetes mellitus (DM-2). Materials and methods. On the base of Kharkiv Regional Hospital a total of 90 patients were examined, including patients with NAFLD (n = 20) and its combination with DM-2 with normal body weight (n = 20) and obesity (n = 50), as well as 20 healthy volunteers. A complex of clinical, laboratory and instrumental (including liver biopsy in 9 patients) examinations of patients was performed. Results. A direct relationship was established between the level of resistin and indicators of enzyme and pigment exchange in groups of patients with combined pathology. A significant increase of resistin plasma level, as well as disorders of the liver function were determined in all groups of patients in comparison with the controls. The most marked changes were revealed in patients with combination of NAFLD, DM-2 and obesity. Conclusions. The established relationship between the level of resistin and the indicators of the liver functional state suggests that an increase of resistin level may reflect the presence of impaired liver function in patients with NAFLD in combination with DM-2, predicting the progression of NAFLD. In order to detect the disorders of liver function in patients with DM-2, it is recommended to determine the level of resistin in patients with NAFLD, especially when concomitant obesity is present. Patients with resistin level (> 8.06 ± 0.23 ng/ml) should be considered at risk of NAFLD progression.

The role of resistin and myeloperoxidase in severe sepsis and septic shock: Results from the ALBIOS trial.

Inflammatory biomarkers are useful in detecting patients with sepsis. The prognostic role of resistin and myeloperoxidase (MPO) has been investigated in sepsis. Plasma resistin and MPO were measured on days 1, 2 and 7 in 957 patients enrolled in the Albumin Italian Outcome Sepsis (ALBIOS) trial. The association between resistin and MPO levels on day 1, 2 and 7 and 90-day mortality was assessed. Plasma resistin and MPO concentrations were higher at day 1 and decreased until day 7. Both biomarkers were positively correlated with each other and with physiological parameters. Higher levels of resistin and MPO on day 1 were associated with the development of new organ failures. Patients experiencing death at 90days showed higher levels of resistin and MPO compared with survivors. At day 1, only MPO in the 4th quartile (Q4), but not resistin, was found to predict 90-day death (adjusted hazard ratio [aHR] 1.55 vs Q1). At day 2, resistin in the Q3 and Q4 predicted a>40% increase in mortality as also did MPO in the Q4. On day 7, Q4 resistin was able to predict 90-day mortality, while all quartiles of MPO were not. High levels of MPO, but not of resistin, on day 1 were able to predict 90-day mortality. These findings may either suggest that early hyper-activation of neutrophils is detrimental in patients with sepsis or reflect the burden of the inflammatory process caused by sepsis. Further studies are warranted to deepen these aspects (ALBIOS ClinicalTrials.gov Identifier: NCT00707122).

Impact of metabolic and inflammatory changes on glomerular function beyond conventional risk factors in an urban South Africa community with prevalent obesity

To determine the extent to which metabolic and inflammatory changes are associated with renal damage beyond conventional risk factors in a community sample with a high prevalence of obesity in urban South Africa. This was a cross-sectional, community-based study in 1 010 (n = 872 without diabetes mellitus, DM) randomly selected participants over 16 years of age in an urban, developing community (Soweto, Johannesburg) with a high prevalence of obesity (41.8%). We assessed estimated glomerular filtration rate (eGFR), conventional risk factors including adiposity indices, and metabolic changes and plasma resistin concentrations (ELISA) and the homeostasis model of insulin resistance (HOMA-IR). Relationships independent of haemodynamic loads were confirmed using ambulatory blood pressure and central arterial haemodynamics. In multivariate regression models conducted in those without DM, HOMA-IR (standardised β-coefficient = -0.13 ± 0.03, p < 0.0001) and plasma resistin concentrations (β-coefficient = -0.10 ± 0.02, p < 0.0001) were second only to age, and at least as strong as systolic blood pressure (β -coefficient = -0.04 ± 0.03, p = 0.19) in the impact on eGFR, while alternative conventional risk factors including adiposity indices and the metabolic syndrome features contributed little to eGFR. Similar results were obtained in relationships with chronic kidney disease (CKD) and in the whole group including those with DM. Adjustments for ambulatory blood pressure or central arterial loads did not influence these relationships. The impact on glomerular function of insulin resistance and inflammatory changes is well beyond modifiable conventional risk factors, including the metabolic syndrome. Targeting conventional risk factors alone is likely to result in a marked residual risk of renal damage produced by insulin resistance and inflammation.

Blood Plasma Resistin and Atrial Fibrillation in Patients With Cardiovascular Disease.

BackgroundAtrial fibrillation (AF) affects quality of life and prognosis of patients with cardiovascular disease. Resistin plays an important role in inflammatory response to internal and external factors. The aim of this study is to evaluate the association between resistin and permanent AF (PAF) in patients with cardiovascular disease.MethodsIn our study, we included 146 patients with cardiovascular disease. Plasma resistin concentrations and demographic characteristics of patients were recorded. The patients were divided in two groups: 118 patients without a history of PAF (NonAF group), and 28 patients with a history of PAF (AF group). Association of resistin with PAF and other variables was examined by parametric and non-parametric tests, and multivariable linear and univariable logistic regression analysis.ResultsNo differences of demographic characteristics (gender, age and body mass index (BMI)) between two groups were observed (P > 0.05). Higher median levels of resistin were observed in group AF than in group NonAF (6.90 ng/mL vs. 5.83 ng/mL, P = 0.03). Multivariate linear regression analysis (adjusted to gender, age, BMI, hypertension, diabetes mellitus, coronary artery disease, and mitral valve disease) showed that resistin was associated with PAF (β = 0.79, 95% confidence interval (CI): 0.08 to 1.51, P = 0.03).ConclusionsOur analysis showed that plasma resistin was associated with PAF, and resistin concentration was higher in patients with AF compared to those without AF.

Association among resistin, adenylate cyclase-associated protein 1 and high-density lipoprotein cholesterol in patients with colorectal cancer: a multi-marker approach, as a hallmark of innovative predictive, preventive, and personalized medicine

Elevated concentrations of resistin have been reported in colorectal cancer (CRC), but its interactions with adenylate cyclase-associated protein 1 (CAP-1) are largely unexplored. We investigated resistin plasma concentration, peripheral blood mononuclear cells (PBMCs) resistin messenger ribonucleic acid (mRNA), and CAP-1 mRNA levels in CRC patients, as well as the impact of resistin gene polymorphism rs1862513 on the examined markers. We also explored associations of resistin with high-density lipoprotein cholesterol (HDL-C) and predictive potential of our parameters for CRC. Eighty-six patients with CRC and 75 healthy adults were included. Commercial ELISA kit was used for obtaining resistin's concentrations, while polymerase chain reaction (PCR) method was applied for evaluation of resistin and CAP-1 mRNA levels and rs1862513 polymorphism. Plasma resistin and CAP-1 mRNA levels were higher in CRC patients (p < 0.001 and p < 0.05, respectively), while resistin mRNA levels were lower (p < 0.001). Negative association existed among plasma resistin and HDL-C concentrations (ρ = - 0.280; p < 0.05). A model including age, body-mass index, HDL-C, low-density lipoprotein cholesterol (LDL-C), and plasma resistin concentrations as independent predictors of CRC showed very good diagnostic accuracy (AUC = 0.898). We found no associations of rs1862513 with the examined markers. Our study demonstrated increased plasma resistin and CAP-1 mRNA levels, implying their possible interaction in CRC. The association among plasma resistin and HDL-C might indicate that HDL-C is involved in alterations of resistin's secretion process. As a hallmark of personalized medicine, multi-marker approach in determination of resistin-related parameters might be useful for prediction and prevention of CRC development.

The effects of quercetin supplementation on metabolic and hormonal parameters as well as plasma concentration and gene expression of resistin in overweight or obese women with polycystic ovary syndrome.

The aim of this study was to investigate the effect of quercetin on metabolic and hormonal parameters as well as plasma concentration and gene expression of resistin in overweight or obese women with polycystic ovary syndrome (PCOS). In this randomized, double-blind, placebo-controlled trial, 78 overweight or obese women (25≤BMI≤40kg/m2 , 20-40years) with PCOS were recruited. Patients were randomized to receive 1,000mg/day quercetin or placebo for 12weeks. Resistin plasma concentration and gene expression in peripheral blood mononuclear cells, parameters of glucose homeostasis, circulatory testosterone, luteinizing hormone (LH), and sex hormone-binding globulin, and anthropometries were assessed at baseline and at the end of the study. Following supplementation, quercetin significantly decreased resistin concentration (2.07±0.23 vs. 2.88±0.40ng/ml, p<0.001) and mRNA level (0.64±0.58 vs. 1±0.56 fold change, p=0.008), compared with placebo group. Moreover, testosterone (0.72±0.15 vs. 0.76±0.12ng/ml, p=0.001) and LH (8.05±2.88 vs. 8.77±1.99 mIU/ml, p=0.035) concentrations were significantly lower in quercetin compared with placebo group. Fasting blood glucose (p<0.001), insulin (p=0.02), and homeostatic model assessment of insulin resistance (p=0.009) decreased within the quercetin group; however, no significant differences were observed compared with the placebo group (p=0.074, p=0.226, p=0.22, respectively). Quercetin supplementation decreased resistin plasma levels and gene expression, and testosterone and LH concentration in overweight or obese women with PCOS.

The Interplay between Hyperresistinemia, Elevated ROS, and Hyperglycemia in Diabetic Rats and Their Roles in Diabetes‐Associated Neutrophil Dysfunction

Resistin originally was found as an adipocyte‐derived polypeptide leading to insulin resistanis. Emerging evidence suggests that it plays important roles in various inflammatory diseases. The levels of hyperresistinemia has been associated with immunosuppression and serves as biomarker for the severity of the diseases. Neutrophils play a key role in host defenses against invading microorganisms by releasing large quantities of Reactive Oxygen Species (ROS) via respiratory burst, which are essential for killing bacteria. Diabetic patients have an increased risk of infections mainly as a result of impaired neutrophil functions. Our recent study found that reduced Nrf2 (NF‐E2‐related factor 2), a master transcription factor regulating antioxidant defenses, contributes to elevated ROS levels and increased microvessel permeability in diabetic rats. Diabetes‐associated microvessel dysfunction is highly associated with inflammation. However, the inter‐relationship between the plasma resistin levels, elevated ROS, and their effect on neutrophil function under Diabetic conditions remains unclear and even contradictory. This study aims to examine the interplay between the plasma resistin levels, increased oxidant stress caused by downregulation of Nrf2‐dependent antioxidant defenses, and the neutrophils function in Diabetic rats. Plasma resistin concentrations were determined with a sandwich enzyme immunoassay kit from Wide‐type (WT) Rat, Nrf2 Knock out (Nrf2−/−) out rats and streptozotocin (STZ)‐induced Nrf2−/− diabetic rat. Diabetic rat had experienced elevated blood glucose and A1C level at 404 ± 10 mg/dl and 10.20% ± 0.14% for 14–21 days before the experiments. Neutrophils were isolated from normal and diabetic rats and neutrophil released ROS upon formyl‐Met‐Leu‐OH (fMLP) stimulation was quantified by measuring chemiluminescence (CL). The resistin concentration in WT rats was 6.16 ± 0.97 ng/ml. Nrf2−/− rats significantly increases the resistin level to 15.88 ± 0.45 ng/ml. The resistin levels in diabetic Nrf2−/− rats was markedly increased to 31.67 ± 2.62 ng/ml. Meanwhile, we found neutrophil killing power was significantly reduced in diabetic rats. The peak CL of diabetic neutrophils upon fMLP stimulation was reduced from 826 ± 202 RLU (normal neutrophils) to 259 ± 51 RLU. The CL area under curve, a measure of total ROS production, in normal and diabetic neutrophils was 77614 ± 5509 and 43327 ± 3561 RLU, respectively. When the normal neutrophils were incubated with high glucose solution, a reduced fMLP‐stimulated CL response was also observed, but that couldn't match the reduction of the ROS production in Diabetic rats. These results indicate that increased plasma ROS levels may play a role in increased resistin levels. Further, both increased ROS, hyperresistinemia and hyperglycemia may synergistically contribute to neutrophil dysfunction in diabetes.Support or Funding InformationSupported by HL130363 and DK097391This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Type 2 diabetes mellitus risk and exercise: is resistin involved?

Obesity and associated disorders such as type 2 diabetes mellitus (T2DM) pose an increasing risk to the health of both individuals and society. Adipose tissue is an active endocrine organ, secreting many hormones, known as adipokines. Evidence suggests that one suggest adipokine, resistin, may be elevated in the plasma of individuals with T2DM, and early reports indicated that this may contribute to the impaired glucose tolerance and insulin resistance observed in T2DM, hence its name, resistin, however subsequent evidence suggests it may have a proinflammatory role. Performing regular exercise and dietary interventions improve insulin sensitivity and glucose tolerance in the majority of individuals with T2DM, and we hypothesized that plasma resistin levels may drop in individuals following a long term aerobic and/or resistance exercise intervention program. Articles analyzing the effects of exercise on serum resistin levels were therefore analyzed. Articles were selected and analyzed based on a minimum aerobic and/or resistance training program of 2 sessions per week for 12 weeks. Plasma resistin levels decreased following either endurance aerobic exercise and/or resistance training plans in individuals with obesity and/or insulin resistance, although this was not related to BMI change. Exercise intervention programs generally showed potentially beneficial changes in plasma resistin concentrations. It is possible these effects are mediated through exercise-induced decreases in inflammation via anti-inflammatory cytokine release rather than alterations in glucose metabolism and reductions in BMI per se. A possible link between resistin, exercise and T2DM is discussed.

Cardiovascular risk biomarkers and metabolically unhealthy status in prepubertal children: Comparison of definitions

Background and aimsThe early onset of cardio-metabolic abnormalities, known as metabolically unhealthy (MU) status, is highly associated with obesity and cardiovascular disease (CVD), as well as with increased morbidity and mortality later in life. Given the lack of a consensus MU classification for prepubertal children, we aimed to compare available MU definitions in terms of their association with CVD risk biomarkers. Methods and resultsA total of 930 prepubertal children (622 with overweight/obesity, 462 males) aged 5–10.9 years were recruited, anthropometric measures were taken and biomarkers were analyzed. Children were classified using eight MU definitions based on different cut-offs for blood pressure, triacylglycerides, high-density lipoprotein cholesterol, glucose and homeostasis model assessment for insulin resistance (HOMA-IR). MU prevalence in children with overweight/obesity ranged between 30% and 60% across definitions. Plasma concentrations of resistin, leptin, myeloperoxidase (MPO) and total plasminogen activator inhibitor 1 (tPAI-1) were higher, and those of adiponectin were lower, in MU compared to MH children with overweight/obesity. Linear regression analyses confirmed the contribution of MPO and tPAI-1 concentrations to MU status, with most significant results derived from definitions that use age and sex-specific criteria and that account for HOMA-IR. ConclusionPlasma concentrations of MPO and tPAI-1 are increased in prepubertal MU children irrespective of having normal-weight or overweight/obesity. Inclusion of age and sex-specific cut-offs for cardio-metabolic components as well as insulin resistance criteria increases the quality of MU definitions as seen by their stronger association with CVD biomarkers concentrations.

Effect of 6 months of aerobic training on adipokines as breast cancer risk factors in postmenopausal women: A randomized controlled trial.

Physical activity has been introduced as an inexpensive and effective behavior to reduce postmenopausal breast cancer risk. Decreased concentrations of adipokines such as leptin and resistin may be a possible mechanism. This study aimed to investigate the effects of 6 months of aerobic training on leptin and resistin levels in postmenopausal women. The study participants were 50-74 years old, sedentary and postmenopausal women. Forty-one women met the inclusion criteria and were randomly assigned to the training (n = 22) or the control group (n = 19). Participants in intervention group engaged in a moderate supervised aerobic training, 3 days per week for 6 months, while controls were asked not to change their physical activity levels for the duration of the trial. Plasma concentrations of leptin and resistin, aerobic fitness, and anthropometric measures were assessed at baseline and after 6 months. Twenty-seven out of 41 participants completed the study. Plasma leptin decreased by 0.6% in exercisers and increased by 8.2% in controls; however, the exercise effect was not statistically significant. Plasma concentrations of resistin also decreased by 16.1% and 15.1% in exercise and control group, respectively. Aerobic fitness increased, and body mass index (BMI) decreased significantly in the intervention group. The exercise intervention did not have a statistically significant impact on the concentrations of the adipokines in question; however, this long-term aerobic training reduced BMI and body fat percentage and enhanced aerobic fitness. Thus, exercise programs can be considered as an effective behavioral modification in breast cancer prevention.

Involvement of plasma adipokines in metabolic and reproductive parameters in Holstein dairy cows fed with diets with differing energy levels

This study aimed to investigate the association between plasma adipokine concentrations and metabolic and reproductive parameters in Holstein dairy cows fed diets with different energy levels during the peripartum period. The experiment started 1 mo before first calving and was maintained for 2 lactations. Dry matter intake and energy balance in animals fed a low-energy (LE) diet were significantly lower than that of animals fed a high-energy (HE) diet in the first lactation. Body weight, milk production, back fat thickness, and plasma concentrations of fatty acids, glucose, and insulin were not affected by diet, whereas plasma leptin and adiponectin concentrations were lower and plasma resistin concentrations higher in animals fed the LE diet. Unlike concentrations of adiponectin, plasma resistin concentrations were positively correlated with back fat thickness and plasma fatty acids concentrations and negatively correlated with dry matter intake and plasma leptin concentrations. No effect of diet was found on reproductive variables; that is, pregnancy rates at 35 or 90 d after artificial insemination (AI); numbers of small (3-5 mm), medium (>5 and ≤7 mm), and large (>7 mm) follicles; calving-to-AI and calving-to-calving intervals; and magnitude and duration of the LH surge. However, the commencement of luteal activity after first calving occurred sooner and the frequency of LH pulses was higher in the HE group than in the LE group. A significant positive correlation was found between the number of follicles (of any size) and the area under the curve of plasma resistin concentrations. The number of small follicles was also positively correlated with the nadir of plasma resistin concentrations. Taken together, these results suggest that dietary energy content in the range applied here can alter the resumption of ovarian activity and LH pulsatility without affecting fat mobilization. Plasma adipokine profiles (leptin, resistin, and adiponectin) were significantly altered by diet and negative energy balance but relationships with reproductive variables were limited to follicular growth characteristics and plasma resistin concentrations.

Association of adenylate cyclase‐associated protein 1 with coronary artery disease

Adenylate cyclase-associated protein 1 (CAP1) is a recently identified receptor for human resistin. As resistin has been related to CAD development and progression and CAP1 has never been evaluated in CAD, the aim of this study was to determine its peripheral blood mononuclear cells (PBMCs) mRNA in patients with CAD, and resistin plasma concentration, PBMCs resistin and CD36 mRNA, considering resistiǹs ability to stimulate CD36 expression invitro. This case-controlled study included 27 healthy subjects (CG) and 66 patients requiring coronary angiography. Of the latter, 42 had nonsignificant CAD whereas 24 had significant CAD. Circulating resistin was measured by ELISA; PBMCs CAP1, resistin and CD36 mRNA were determined by real-time PCR. Patients with significant as well as patients with nonsignificant CAD had significantly higher resistin concentrations compared to the CG (P<0·001; P=0·003). Resistin mRNA did not show significant difference between the investigated groups. CAP1 and CD36 mRNA were significantly higher in significant CAD (P<0·001; P<0·001, respectively) and nonsignificant CAD (P<0·001; P<0·001, respectively) compared to the CG; significant CAD showed significantly higher CD36 mRNA (P=0·040) compared to the nonsignificant CAD group. Multiple linear regression analysis identified Tg and CD36 mRNA as independent predictors of CAP1 (R2 =0·402; adjR2 =0·376). Significant up-regulation of PBMCs CAP1, CD36 mRNA and plasma resistin found in significant CAD, as well as in nonsignificant CAD compared to CG, indicates that resistin could be able to exert its effects stronger on cells with up-regulated CAP1 mRNA thus contributing atherosclerosis development.

Resistin is a predictor of asthma risk and resistin:adiponectin ratio is a negative predictor of lung function in asthma.

Adipokines, such as resistin and adiponectin, modify inflammation and may contribute to increased asthma risk and severity in obese people. To examine plasma resistin and resistin:adiponectin ratio (i) in asthmatics compared to healthy controls, (ii) according to asthma severity, obesity and gender (iii) following weight loss in obese asthmatics. In a cross-sectional observational study of asthmatic adults (n = 96) and healthy controls (n = 46), plasma resistin and adiponectin were measured. In a separate intervention study, obese asthmatic adults (n = 27) completed a 10-week weight loss intervention and plasma resistin and adiponectin concentrations were analysed. Plasma resistin and resistin:adiponectin ratio were higher in asthma compared to controls and were higher again in subjects with a severe vs. mild-to-moderate asthma pattern. Amongst asthmatic subjects, resistin was not modified by gender or obesity, while adiponectin was lower in males and obese subjects. As a result, resistin:adiponectin ratio was higher in obese males, non-obese males and obese females, compared to non-obese females. In a logistic regression model, plasma resistin concentration was a predictor of asthma risk. In a multiple linear regression model, plasma resistin:adiponectin ratio was a negative predictor of FEV1 in asthma. Following weight loss, neither resistin, adiponectin nor resistin:adiponectin ratio was changed. However, the change (∆) in %body fat was associated with ∆ resistin:adiponectin ratio. Post-intervention ∆ resistin was negatively correlated with both ∆FRC and ∆RV. This study demonstrates that resistin and resistin:adiponectin ratio are higher in asthma and are higher again in subjects who have more severe disease. Resistin:adiponectin ratio is highest in obese male asthmatics. As resistin is a predictor of asthma risk and resistin:adiponectin is a predictor of FEV1 in asthma, these adipokines may be contributing to the obese asthma phenotype, thus providing a potential therapeutic target for obese asthma.

Effects of antihypertensive treatment on plasma apelin, resistin, and visfatin concentrations

INTRODUCTION Adipose tissue has been recently recognized as an endocrine organ secreting a number of adipokines contributing to the development of atherosclerosis, hypertension, chronic kidney disease, endothelial dysfunction, insulin resistance, and vascular remodeling. OBJECTIVES The aim of this study was to determine whether treatment with a β-blocker, calcium antagonist, thiazide-like diuretic, or angiotensin II receptor type 1 influences plasma concentrations of apelin, resistin, and visfatin in obese hypertensive patients. PATIENTS AND METHODS The study included 84 obese patients with essential hypertension. One control group included obese subjects without hypertension, and the other, lean subjects without hypertension. Patients with hypertension were randomized into 4 groups treated for 6 weeks with bisoprolol, amlodipine, indapamide, or candesartan, respectively. RESULTS Mean daily plasma apelin concentrations in patients treated with amlodipine was significantly higher than the baseline values, whereas the difference in plasma apelin concentrations in other treatment groups was not significant. Mean daily plasma resistin concentrations were significantly lower after 6-week treatment with amlodipine, bisoprolol, or indapamide compared with the baseline values. In patients treated with candesartan, no significant differences in resistin concentrations were shown. After 6-week treatment with bisoprolol, mean daily plasma concentrations of visfatin were significantly lower compared with the baseline values. Treatment with amlodipine, candesartan, or indapamide did not significantly affect plasma visfatin levels. CONCLUSIONS Antihypertensive treatment exerts significant and varied effects on adipokine secretion in obese hypertensive patients. Changes in apelin secretion, caused by the use of different antihypertensive drugs, may protect the cardiovascular system and kidneys. The involvement of adipokins in the mechanism of diverse protective effects of antihypertensive drugs, independently of the effect on blood pressure, requires further research.

D-Allulose supplementation normalized the body weight and fat-pad mass in diet-induced obese mice via the regulation of lipid metabolism under isocaloric fed condition.

A number of findings suggest that zero-calorie d-allulose, also known as d-psicose, has beneficial effects on obesity-related metabolic disturbances. However, it is unclear whether d-allulose can normalize the metabolic status of diet-induced obesity without having an impact on the energy density. We investigated whether 5% d-allulose supplementation in a high fat diet(HFD) could normalize body fat in a diet-induced obesity animal model under isocaloric pair-fed conditions. Mice were fed an HFD with or without various sugar substitutes (d-glucose, d-fructose, erytritol, or d-allulose, n = 10 per group) for 16 wk. Body weight and fat-pad mass in the d-allulose group were dramatically lowered to that of the normal group with a simultaneous decrease in plasma leptin and resistin concentrations. d-allulose lowered plasma and hepatic lipids while elevating fecal lipids with a decrease in mRNA expression of CD36, ApoB48, FATP4, in the small intestine in mice. In the liver, activities of both fatty acid synthase and β-oxidation were downregulated by d-allulose to that of the normal group; however, in WAT, fatty acid synthase was decreased while β-oxidation activity was enhanced. Taken together, our findings suggest that 5% dietary d-allulose led to the normalization of the metabolic status of diet-induced obesity by altering lipid-regulating enzyme activities and their gene-expression level along with fecal lipids.

Circulating resistin concentrations are independently associated with aortic pulse wave velocity in a community sample.

The role of the adipokine, resistin in mediating increases in aortic stiffness is uncertain. We aimed to determine independent relations between circulating resistin concentrations and aortic pulse wave velocity (PWV) and wave reflection in a community-based sample with a high prevalence of untreated hypertension and obesity. Plasma resistin, adiponectin, and C-reactive protein concentrations (ELISA); carotid-femoral (aortic) PWV and the aortic reflected wave index (applanation tonometry and SphygmoCor software) were determined in 683 randomly selected participants of African ancestry from SOWETO, South Africa who had never received antihypertensive therapy. Resistin concentrations were not independently associated with office or 24-h (n = 492) blood pressure (BP). In a stepwise regression model with BMI included in the model, age (P < 0.0001), mean arterial pressure (P < 0.0001), plasma resistin concentrations (P < 0.005), female sex (P = 0.01), and creatinine concentrations (P < 0.01) contributed independently to variations in PWV. Independent relations between resistin concentrations and PWV persisted with further adjustments for C-reactive protein concentrations (P < 0.005), and the homeostasis model of insulin resistance (P < 0.02). Similar relations were noted with waist circumference rather than BMI in the model. Resistin concentrations were not independently associated with aortic reflected wave index or aortic BP. Resistin is independently and directly associated with aortic stiffness and these effects occur beyond BP, insulin resistance, and general inflammation.

Epigenome-wide association study suggests that SNPs in the promoter region of RETN influence plasma resistin level via effects on DNA methylation at neighbouring sites.

To investigate epigenetic regulation of the plasma concentration of resistin, we performed an epigenome-wide association study for this variable and DNA methylation (DNAm) in an elderly Japanese cohort and then assessed the relation of single nucleotide polymorphisms (SNPs) associated with the plasma resistin concentration to DNAm level at identified sites. The association of plasma resistin level with DNAm status was examined in 191 nondiabetic elderly men with the Illumina Infinium HumanMethylation450 BeadChip array. The association between DNAm status at specific sites in the flanking region of the resistin gene (RETN) and RETN mRNA abundance was then evaluated with a public data set for 1202 monocyte samples from a multi-ethnic cohort. Finally, the association of DNAm status and SNPs in the promoter region of RETN was assessed in two cohorts comprising a total of 478 Japanese individuals. DNAm status at cg02346997 located in the RETN promoter region showed a negative genome-wide significant association with the plasma resistin level (p = 6.02 × 10(-10)). Four DNAm sites in the RETN promoter region including cg02346997 (p = 4.23 × 10(-70)) showed a negative genome-wide significant association with RETN mRNA abundance in monocytes. Furthermore, the number of minor alleles of the RETN promoter SNPs rs34861192 and rs3219175 was negatively associated with DNAm level at cg02346997 (p = 4.43 × 10(-17)). Our results suggest that RETN promoter SNPs might influence the circulating resistin level through an effect on DNAm at cg02346997 and on RETN mRNA abundance in monocytes.