Homeostasis Model Assessment Adiponectin Research Articles

HOMA-IR as a Predictor of PAI-1 Levels in Women with Severe Obesity.

Obesity is a chronic inflammatory disorder that increases the risk of cardiovascular diseases (CVDs). Given the high CVD mortality rate among individuals with obesity, early screening should be considered. Plasminogen activator inhibitor (PAI-1), a cytokine that links obesity and CVDs, represents a promising biomarker. However, PAI-1 is not part of the clinical routine due to its high cost. Therefore, it is necessary to find good predictors that would allow an indirect assessment of PAI-1. This study enrolled 47 women with severe obesity (SO). The obtained anthropometric measurements included weight, height, neck (NC), waist (WC), and hip circumference (HC). Blood samples were collected to analyse glucose and lipid profiles, C-reactive protein, liver markers, adiponectin, and PAI-1 (determined by ELISA immunoassay). Homeostasis model assessment-adiponectin (HOMA-AD), homeostasis model assessment of insulin resistance (HOMA-IR), quantitative insulin sensitivity check index (QUICKI), triglyceride-glucose index (TyG), and atherogenic index of plasma (AIP) were calculated. The women were grouped according to PAI-1 levels. The data were analysed using IBM SPSS Statistics, version 21. The significance level for the analysis was set at 5%. Women with SO who have higher levels of PAI-1 have lower values of high-density lipoprotein cholesterol (HDL) (p = 0.037) and QUICKI (0.020) and higher values of HOMA-AD (0.046) and HOMA-IR (0.037). HOMA-IR was demonstrated to be a good predictor of PAI-1 in this sample (B = 0.2791; p = 0.017). HOMA-IR could be used as a predictor of PAI-1 levels, pointing out the relevance of assessing glycaemic parameters for the prevention of CVDs in women with SO.

Hepatic fibrosis: a manifestation of the liver disease evolution in patients with Ataxia-telangiectasia

BackgroundAtaxia-telangiectasia (A-T) is a DNA repair disorder characterized by changes in several organs and systems. Advances in clinical protocols have resulted in increased survival of A-T patients, however disease progression is evident, mainly through metabolic and liver changes.ObjectiveTo identify the frequency of significant hepatic fibrosis in A-T patients and to verify the association with metabolic alterations and degree of ataxia.MethodsThis is a cross-sectional study that included 25 A-T patients aged 5 to 31 years. Anthropometric data, liver, inflammatory, lipid metabolism and glucose biomarkers (oral glucose tolerance test with insulin curve—OGTT) were collected. The Cooperative Ataxia Rating Scale was applied to assess the degree of ataxia. The following were calculated: Homeostasis Model Assessment—Insulin Resistance, Homeostasis Model Assessment—Adiponectin (HOMA-AD), Matsuda index, aspartate aminotransferase (AST): platelet ratio index, nonalcoholic fatty liver disease fibrosis score and BARD score. Liver ultrasonography and transient liver elastography by FibroScan® were performed.ResultsSignificant hepatic fibrosis was observed in 5/25 (20%). Patients in the group with significant hepatic fibrosis were older (p < 0.001), had lower platelet count values (p = 0.027), serum albumin (p = 0.019), HDL-c (p = 0.013) and Matsuda index (p = 0.044); and high values of LDL-c (p = 0.049), AST (p = 0.001), alanine aminotransferase (p = 0.002), gamma-glutamyl transferase (p = 0.001), ferritin (p = 0.001), 120-min glycemia by OGTT (p = 0.049), HOMA-AD (p = 0.016) and degree of ataxia (p = 0.009).ConclusionsA non-invasive diagnosis of significant hepatic fibrosis was observed in 20% of A-T patients associated with changes in liver enzymes, ferritin, increased HOMA-AD, and the severity of ataxia in comparison with patients without hepatic fibrosis.

Effect of melatonin on stress-induced hyperglycemia and insulin resistance in critically-ill patients: A randomized double-blind, placebo-controlled clinical trial.

Background:Hyperglycemia is a common finding which is associated with increased mortality and morbidity among critically ill patients. There is currently no evidence that melatonin could improve stress induced hyperglycemia (SIH). In this study, we evaluated the effect of melatonin on blood sugar and insulin resistance (IR) in critically-ill patients.Methods:104 critically-ill patients with SIH divided into two groups, receiving melatonin (6 mg BD for 3 days) or placebo. Changes of blood sugar, IR indices including homeostasis model assessment for insulin resistance and homeostasis model assessment adiponectin (HOMA-AD) ratios, Glasgow coma scale (GCS) were evaluated on the 4th day of melatonin prescription. On the 7Th day of study, changes of ventilator dependency and delirium were considered. Mortality and intensive care unit (ICU) stay were also compared between groups.Results:On day 4, patients in the melatonin group had significantly lower blood glucose and HMOA-IR level compared with the placebo group (P=0.04 and P=0.03, respectively) whereas HOMA-AD level did not differ significantly from placebo group (p>0.2). Also, we did not observe any significant difference in GCS level at this time between groups (p>0.2). On day 7, melatonin could not improve ventilator dependency and delirium significantly (p>0.2) and also could not reduce mortality and ICU stay in comparison with placebo (p>0.2, P=0.2, respectively).Conclusion:Melatonin supplementation showed positive effect on blood sugar and somehow insulin resistance whereas it could not improve ICU complications.

Impact of Adiponectin Resistance on Coronary Artery Disease Severity.

The serum adiponectin level (AD), adiponectin resistance (AD-R) may reflect the degree of metabolic syndrome (MetS). The role parameter AD-R, The Homeostasis Model Assessment-Adiponectin (HOMA-AD) index on the coronary artery disease (CAD) severity is not still understood. To determine adiponectin concentration and HOMA-AD index in patients with CAD with/without MetS and to evaluate their prognostic importance on severity of CAD. This cross-sectional study involved selected 130 examinees which were divided into three groups: CAD+MetS, CAD-MetS, control group (no CAD/MetS). In all examinees values of biochemical and anthropometric parameters were determined. We analyzed the severity of coronary artery lesions from coronary angiography. Total serum adiponectin concentration was measured by ELISA. We calculated atherogenic Gensini scoring system, Duke prognostic index, and HOMA-AD-index. Serum adiponectin level was significantly lower in the group with CAD+MetS (p < 0.001) and in CAD-MetS group (p < 0.01), compared to the control group. The HOMA-AD index showed statistically significant positive correlation with the key parameters of MetS, as well as with the parameters of CAD, number of CAD and modified Gensini score. After applying logistic regression analysis the best predictors for CAD were: adiponectin, blood pressure, HOMA-IR index, and HOMA-AD index. The cut-off values of adiponectin ≤1506.38 pg/mL, HOMA-IR index ≥3.91 and HOMA-AD index ≥0.67 were associated with a higher risk of CAD. Patients with CAD with or without MetS had low adiponectin levels and this hypoadiponectinemia indicates that AD and HOMA-AD index may be a useful marker for identifying patients at risk for CAD.

Insulin Resistance and Renal Sodium Handling Influence Arterial Stiffness in Hypertensive Patients with Prevailing Sodium Intake.

Insulin resistance and renal tubular sodium handling influence arterial structure and function and play an essential role in salt-sensitive forms of hypertension. In a population with prevailing sodium consumption, we assessed the relationship between cardiovascular phenotypes (peripheral and central blood pressures, elastic properties of large arteries, the left ventricular structure) and sodium handling parameters (daily urinary sodium excretion, fractional urinary lithium excretion in proximal-FELi and distal tubules), as a function of insulin sensitivity-measured by homeostasis model assessment-insulin resistance (HOMA-IR), leptin-to-adiponectin (L/A) ratio, and homeostasis model assessment-adiponectin (HOMA-AD). In patients with FELi below the median value (corresponding to the group with increased proximal sodium reabsorption) and higher insulin resistance as measured by HOMA-IR, pulse wave augmentation indexes were significantly higher-AIxP (99.4% vs. 86.2%; P = 0.007), AIxC1 (159.4% vs. 144.2%; P = 0.04), and AIxC2 (36.1% vs. 28.3%; P = 0.02), than in patients with lower insulin resistance. The same trend was observed in relation to L/A ratio-AIxP (98.7% vs. 87.1%; P = 0.005), AIxC1 (158.6% vs. 144.5%; P = 0.02), and AIxC2 (35.6% vs. 28.5%; P = 0.01) and HOMA-AD-AIxP (99.7% vs. 83.8%; P = 0.001), AIxC1 (160.5% vs. 140.3%; P = 0.007), and AIxC2 (36.6% vs. 26.3%; P = 0.003). Such relationships were not observed in patients with FELi above the median value. In the hypertensive population with prevailing sodium intake, insulin resistance and increased sodium reabsorption in proximal tubules may affect arterial wall function.

Increased insulin sensitivity in individuals with neurofibromatosis type 1.

Objects To compare insulin resistance (IR) and metabolic aspects of patients with neurofibromatosis type 1 (NF1) and individuals without the disease. Subjects and methods Forty patients with NF1 were matched by sex, age, and body mass index (BMI) to 40 controls from the community. Blood samples were collected for biochemical assessment. Homeostasis model assessment adiponectin (HOMA-AD), Homeostasis model assessment insulin resistance (HOMA-IR), and adiponectin/leptin ratio (ALR) were used to identify IR. Results The median HOMA-IR values were similar between the groups. However, the HOMA-AD value was significantly lower and the ALR significantly higher in the NF1 group. Fasting blood glucose (FBG), leptin, and visfatin levels of patients with NF1 were significantly lower, although adiponectin levels were significantly higher than those in the controls. Fasting insulin and blood glucose levels 2 hours after administration of 75 g of dextrose, glycated hemoglobin, and resistin showed no significant differences between groups. The HOMA-AD correlated with BMI, FBG, blood glucose levels 2 hours after administration of 75 g of dextrose, fasting insulin, glycated hemoglobin, adiponectin, leptin, visfatin, ALR, and HOMA-IR. The ALR correlated with BMI leptin, visfatin, and adiponectin. Conclusions Lower levels of FBG, leptin, visfatin, and HOMA-AD, and higher adiponectin levels and ALR may be related to increased insulin sensitivity and lower occurrence of type 2 diabetes mellitus in patients with NF1.

Inhibition of Interleukin-1 Receptor-Associated Kinases 1/4, Increases Gene Expression and Serum Level of Adiponectin in Mouse Model of Insulin Resistance.

Insulin resistance is a feature of most patients with type 2 diabetes mellitus. Epidemiological evidence suggest a correlation between inflammation and insulin resistant states such as obesity, but the underlying mechanisms are largely unknown. Interleukin-1 receptor-associated kinases (IRAK) play a central role in inflammatory responses by regulating the expression of various inflammatory genes in immune cells. This study was aimed to investigate the effect of IRAK inhibitor on gene transcription and serum concentration of adiponectin in insulin-resistant mice. Experimental mice were randomly divided into 6 groups: the healthy control group was fed a regular chow diet while other groups were fed with a high-fat diet for 12 weeks. After this period, the animals were treated with IRAK inhibitor, pioglitazone, both IRAK and pioglitazone, and DMSO, for two weeks. Adiponectin gene expression level was analyzed by real-time PCR. Additionally, serum adiponectin levels were measured by ELISA. Homeostasis model assessment-adiponectin (HOMA-AD) as an insulin sensitivity index was calculated. IRAK inhibitor and pioglitazone increased significantly the expression of adiponectin gene. Also, adiponectin concentration in the control group (9.67±1.1 μg/ml) increased to 25.34±2.04 μg/ml in pioglitazone treatment group. IRAK inhibitor also increased adiponectin concentration (18.24±1.53 μg/ml) but did not show a synergistic effect with pioglitazone when administered simultaneously (26.66±2.5 μg/ml). HOMA-AD was 0.33±0.04 in pioglitazone treated group, 0.6±0.13 in IRAK inhibitor group, and 0.31±0.03 in animals that received IRAKi and pioglitazone. Our findings suggest that increased adiponectin secretion from adipose tissue mediated by IRAK inhibitor may increase the insulin sensitivity in an animal model of insulin resistance.

Surrogates of Insulin Sensitivity and Indices of Cardiometabolic Profile in Obesity.

Obesity is often associated with insulin resistance (IR). We considered different IR indexes: the Homeostasis Model Assessment-Insulin Resistance (HOMA-IR) index, the two specimen (0 and 120 min) oral glucose tolerance test Matsuda Index (MI) and the Homeostasis Model Assessment-Adiponectin (HOMA-AD) index. These IR indexes were compared with indicators of the cardiometabolic profile. This cross-sectional study enrolled 60 obese individuals without previous history of diabetes. Anthropometrical, ultrasound and laboratory examinations were conducted. All 3 indexes significantly correlated with indicators of central obesity, systolic and diastolic blood pressure, inflammation parameters, liver enzymes, HbA1c and some lipid parameters. The majority of correlation coefficients were the highest for HOMA-AD, but only the difference in correlation with waist circumference comparing with MI was statistically significant. HOMA-IR directly, and MI indirectly, significantly correlated with age, while HOMA-AD significantly directly correlated with the mean carotid artery intima media thickness (CAIMT). MI showed the best performances in predicting non-alcoholic fatty liver disease and pathologically increased CAIMT; HOMA-AD was the best in predicting metabolic syndrome, while HOMA-IR demonstrated the poorest performances in the prediction of all 3 conditions. There were no statistically significant differences in predicting performances of the analysed indexes. The HOMA-AD and MI are not superior compared with the HOMA-IR, in the identification of obese individuals with a proatherogenic cardiometabolic profile.

The HOMA-Adiponectin (HOMA-AD) Closely Mirrors the HOMA-IR Index in the Screening of Insulin Resistance in the Brazilian Metabolic Syndrome Study (BRAMS).

BackgroundThe major adverse consequences of obesity are associated with the development of insulin resistance (IR) and adiposopathy. The Homeostasis Model Assessment-Adiponectin (HOMA-AD) was proposed as a modified version of the HOMA1-IR, which incorporates adiponectin in the denominator of the index.ObjectivesTo evaluate the performance of the HOMA-AD index compared with the HOMA1-IR index as a surrogate marker of IR in women, and to establish the cutoff value of the HOMA-AD.Subjects/MethodsThe Brazilian Metabolic Syndrome Study (BRAMS) is a cross-sectional multicenter survey. The data from 1,061 subjects met the desired criteria: 18–65 years old, BMI: 18.5–49.9 Kg/m² and without diabetes. The IR was assessed by the indexes HOMA1-IR and HOMA-AD (total sample) and by the hyperglycemic clamp (n = 49). Metabolic syndrome was defined using the IDF criteria.ResultsFor the IR assessed by the clamp, the HOMA-AD demonstrated a stronger coefficient of correlation (r = -0.64) compared with the HOMA1-IR (r = -0.56); p < 0.0001. In the ROC analysis, compared with the HOMA1-IR, the HOMA-AD showed higher values of the AUC for the identification of IR based on the clamp test (AUC: 0.844 vs. AUC: 0.804) and on the metabolic syndrome (AUC: 0.703 vs. AUC: 0.689), respectively; p < 0.001 for all. However, the pairwise comparison did not show evidence of superiority for the HOMA-AD in comparison with the HOMA1-IR in the diagnosis of IR and metabolic syndrome (p > 0.05). The optimal cutoff identified for the HOMA-AD for the diagnosis of IR was 0.95.ConclusionsThe HOMA-AD index was demonstrated to be a useful surrogate marker for detecting IR among adult women and presented a similar performance compared with the HOMA1-IR index. These results may assist physicians and researchers in determining which method to use to evaluate IR in light of the available facilities.

The role of multicomponent therapy in the metabolic syndrome, inflammation and cardiovascular risk in obese adolescents.

Obesity is characterised by low-grade inflammation, which increases the metabolic syndrome (MetS) and cardiovascular risks. The aim of the present study was to verify the role of multicomponent therapy in controlling the MetS, inflammation and carotid intima-media thickness (cIMT) in obese adolescents. The second aim was to investigate the relationships between adipokines, the MetS parameters and cIMT. A total of sixty-nine obese adolescents participated in the present study and completed 1 year of multicomponent therapy (a combination of strategies involving nutrition, psychology, physical exercise and clinical therapy), and were divided according to their MetS diagnosis as follows: MetS (n 19); non-MetS (n 50). Blood analyses of glucose, lipid and adipokine concentrations (adiponectin, leptin, plasminogen activator inhibitor 1 (PAI-1) and C-reactive protein) were collected. Insulin resistance was assessed using the homeostasis model assessment for insulin resistance, quantitative insulin sensitivity check index and homeostasis model assessment-adiponectin. cIMT and visceral and subcutaneous fat were estimated using ultrasonography. At baseline, the MetS group presented higher waist circumference, glucose and insulin levels, and systolic and median blood pressures compared with the non-MetS group. After therapy, both groups showed improvements in the anthropometric profile, body composition, insulin level, insulin resistance, insulin sensibility, TAG and VLDL-cholesterol, adiponectin, leptin and PAI-1 levels, blood pressure and cIMT. The prevalence of the MetS was reduced from 27·5 to 13·0%. Metabolic syndrome patients showed resistance in the attenuation of total cholesterol and LDL-cholesterol (LDL-C) levels and leptin:adiponectin and adiponectin:leptin ratios. In the MetS group, the variation in the adiponectin:leptin ratio was correlated with variations in glucose, insulin sensibility, total cholesterol, LDL-c and systolic blood pressure. Additionally, the number of MetS parameters was correlated with the carotid measurement. Moreover, the variation in cIMT was correlated with the variations in insulin sensibility, total cholesterol and LDL-c. For the entire group, the number of MetS alterations was correlated with the leptin level and leptin:adiponectin ratio and adiponectin:leptin ratio after therapy. In conclusion, multicomponent therapy was effective in controlling the MetS, inflammation and cIMT in the obese adolescents. However, the MetS patients showed resistance in the attenuation of the atherogenic lipid profile and leptin:adiponectin ratio and adiponectin:leptin ratio. These results suggest that the MetS patients have increased cardiovascular risks, and that it is important to attempt to control the inflammatory process that occurs due to obesity in clinical practice in order to improve the health of adolescents.

The Homeostasis Model Assessment-adiponectin (HOMA-AD) is the most sensitive predictor of insulin resistance in obese children

ObjectivesThe aim of this study was to examine the efficacy of three indices i.e. adiponectin/leptin ratio, HOMA-IR and HOMA-AD in assessing insulin resistance among obese children. Patients and methodsOne hundred and twenty-two obese children (57 girls, 65 boys): mean age 13.7±1.3 years, BMI 30.1±4.5kg/m2, eight tanner stage I, 48 tanner stage II-III, 66 tanner stage IV-V, participated in this study. They were classified into four groups according to sex and the presence of metabolic syndrome characteristics: with metabolic syndrome (MS; 21 girls and 36 boys) and controls without metabolic syndrome (CON, 36 girls and 29 boys). The correlations between these three indices of insulin resistance and the MS criteria were analyzed using linear and multiple regressions and receiver operating characteristics (ROC) curves analysis. ResultsThe majority of anthropometric and biological parameters as well as adiponectin/leptin ratio, HOMA-IR and HOMA-AD were significantly different between MS and CON in both sexes. Both HOMA-AD and HOMA-IR were significantly correlated with the majority of metabolic syndrome components than was the adiponectin/leptin ratio in MS of both sexes. In boys and girls with and without MS, multiple regression analyses highlighted that both HOMA-AD and adiponectin/leptin ratio (r=−0.99 and r=−0.54 for MS girls and boys respectively, 0.05<P<0.001), and HOMA-AD and HOMA-IR (r=0.66 and r=0.31 for MS girls and boys respectively, 0.05<P<0.01) affected each other but did not adiponectin/leptin ratio and HOMA-IR. Additionally, the area under the ROC curves for predicting insulin resistance were 0.69 (CI 95%, 0.60–0.77), 0.68 (CI 95%, 0.59–0.76) and 0.71 (CI 95%, 0.62–0.79) for adiponectin/leptin ratio, HOMA-IR and HOMA-AD, respectively. ConclusionThe current study strengthens the validity of the HOMA-AD as an adequate tool for determining insulin resistance among obese children with MS.