Homoeostasis Model Assessment Index Research Articles

Oxidative stress and nitric oxide are increased in obese children and correlate with cardiometabolic risk and renal function.

Oxidative stress and nitric oxide (NO) appear to represent important links between obesity and cardiovascular, metabolic and/or renal disease. We investigated whether oxidative stress and NO production/metabolism are increased in overweight and obese prepubertal children and correlate with cardiometabolic risk and renal function. We performed a cross-sectional evaluation of 313 children aged 8-9 years. Anthropometrics, 24-h ambulatory blood pressure, pulse wave velocity (PWV), insulin resistance (homoeostasis model assessment index (HOMA-IR)), inflammatory/metabolic biomarkers, estimated glomerular filtration rate (eGFR), plasma total antioxidant status (TAS), plasma and urinary isoprostanes (P-Isop, U-Isop), urinary hydrogen peroxide (U-H2O2), and plasma and urinary nitrates and nitrites (P-NOx, U-NOx) were compared among normal weight, overweight and obese groups, according to WHO BMI z-score reference. U-Isop were increased in the obese group, whereas U-NOx were increased in both overweight and obese children. U-Isop were positively correlated with U-H2O2, myeloperoxidase (MPO), high-sensitivity C-reactive protein, HOMA-IR and TAG. TAS correlated negatively with U-Isop and MPO and positively with PWV. HOMA-IR and U-H2O2 were associated with higher U-Isop, independently of BMI and eGFR, and total cholesterol and U-H2O2 were associated with U-NOx, independently of BMI, eGFR values and P-NOx concentration. In overweight and obese children, eGFR decreased across P-NOx tertiles (median: 139·3 (25th, 75th percentile 128·0, 146·5), 128·0 (25th, 75th percentile 121·5, 140·4), 129·5 (25th, 75th percentile 119·4, 138·3), P for linear trend=0·003). We conclude that oxidant status and NO are increased in relation to fat accumulation and, even in young children, they translate into higher values of cardiometabolic risk markers and affect renal function.

Effect of vitamins C and E on insulin resistance indiabetes: a meta-analysis study.

Data regarding the effect of vitamin C (VC) and vitamin E (VE) supplementation on insulin resistance in type 2 diabetes mellitus (T2DM) are controversial. We aimed to systematically review the current data on this topic. All randomized controlled trials (RCTs) conducted to assess the effect of VC and/or VE on insulin resistance in diabetes published in Google Scholar and PubMed web databases until January 2014 were included. Exclusion criteria were studies conducted in animal, type 1 DM, children or pregnant women. Main outcome measure was insulin resistance by homoeostasis model assessment (HOMA) index. According to degree of heterogeneity, fixed- or random-effect model was employed by stata software (11.0). We selected 14 RCTs involving 735 patients with T2DM. VE or mixture-mode supplementation did not have any significant effect on HOMA with a standardized mean difference (SMD): 0·017, 95% CI: -0·376 to 0·411 (P=0·932); and SMD: -0·035, 95% CI: -0·634 to 0·025 (P=0·070), respectively, by random-effect model. VC supplement alone did not improve insulin resistance with a SMD: -0·150, 95% CI: -0·494 to 0·194 (P=0·391), by fixed-effect model. Meta-regression test demonstrated that HOMA index may have not been influenced by the year of publication, dosage or duration of treatment. The sole intake of VC, VE or their combination with other antioxidants could not improve insulin resistance in diabetes.

Independent association of elevated serum hepatocyte growth factor levels with development of insulin resistance in a 10‐year prospective study

Hepatocyte growth factor (HGF) receptors form a hybrid complex with insulin receptors in the liver of mice, which lead to robust signalling to regulate glucose metabolism. Serum HGF levels are high in subjects with metabolic syndrome and/or obesity. Accordingly, we prospectively investigated the relationship between HGF and the development of insulin resistance (IR) in a general population without IR at baseline. A total of 1492 subjects received health examinations. After excluding subjects with diabetes and/or IR (n=402) at baseline, the remaining subjects (n=1090) were followed-up 10 years later. Complete data sets were available from 716 subjects for prospective analysis. Logistic regression was performed to determine factors associated with the development of IR after 10years. In subjects without diabetes at baseline, serum HGF levels were higher (0·26±0·10ng/ml, n=259) in subjects with IR than without it (0·22±0·09ng/ml, n=1090). After deleting subjects who developed liver disease during follow-up, 188 were found to have developed IR at 10years after the original screening. HGF (P<0·05), age (P<0·001), homoeostasis model assessment index (P<0·001), HDL-c (P<0·05; inversely) and hypertensive medication (P<0·05) were significantly associated with the development of IR by multivariate stepwise logistic regression analysis. A significant (P<0·05) relative risk [1·75 (95%CI: 1·01-3·12)] for the development of IR was observed in the highest (≥0·30ng/ml) vs the lowest categories (<0·15ng/ml) of HGF after adjustments for confounders. Our 10-year prospective study suggests that elevated serum HGF levels were significantly associated with the development of IR.

Increased Toll-Like Receptor 2 Expression in Peptidoglycan-Treated Blood Monocytes Is Associated with Insulin Resistance in Patients with Nondiabetic Rheumatoid Arthritis

The close relationship between increased TLR-2 expression in blood monocytes and insulin resistance in RA patients is shown in this study. Traditional risk factors for metabolic disorders, including the waist circumstance, body mass index (BMI), triglyceride (TG), and ratio of TG to high density lipoprotein (HDL) cholesterol, were closely correlated with HOMA (homoeostasis model assessment) index in patients with nondiabetic RA. Expressions of TLR2 in peripheral blood monocytes, following stimulation with peptidoglycan which is known as a TLR2 agonist, were closely correlated with the HOMA index, TNF-α, and IL-6 concentrations. Accordingly, TLR-2 receptor and its related inflammatory cytokines could be potential therapeutic targets in managing insulin resistance in RA patients.

Homocysteine levels are associated with hippocampus volume in type 2 diabetic patients

Elevated total plasma homocysteine (tHcy) levels are associated with cognitive dysfunction, in which changes in the hippocampus plausibly play a pivotal role. We tested the hypothesis that elevated tHcy levels are correlated with hippocampus volume and insulin resistance in nondementia patients with type 2 diabetes. The study included 43 nondementia patients with type 2 diabetes, who were divided into two groups: a high tHcy group (age: 65 ± 8 years, mean ± standard deviation, n = 16) and a normal tHcy group (64 ± 9 years, n = 27). Hippocampus volume was quantified with a computer-assisted analysis using a magnetic resonance imaging (MRI) voxel-based specific regional analysis system developed for the study of Alzheimer's disease (VSRAD), which yields a Z-score as the end point for the assessment of hippocampal volume. Results The Z-score was higher in the high tHcy group compared to the normal tHcy group (P < 0·0001). The fasting plasma glucose (P < 0·01) and insulin (P < 0·0001) concentrations and the homoeostasis model assessment (HOMA) index (P < 0·0001) were higher in the high tHcy group than in the normal tHcy group. Multiple regression analysis showed that the main factors that influenced tHcy levels may be the Z-score and the HOMA index. Our results indicate that the elevated levels of tHcy in Japanese nondementia patients with type 2 diabetes are characterised by hippocampal atrophy and insulin resistance and that the Z-score and HOMA index may be the primary factors that influence tHcy levels.

An increase in plasma adiponectin multimeric complexes follows hypocaloric diet-induced weight loss in obese and overweight pre-menopausal women

Adiponectin is involved in the regulation of glucose and fatty acid metabolism, influences whole-body insulin sensitivity and protects arterial walls against the development of atherosclerosis. Plasma adiponectin is decreased in obese, insulin-resistant and Type 2 diabetic patients. Adiponectin circulates in plasma as high-, medium- and low-molecular-weight ('mass') forms (HMW, MMW and LMW respectively). The HMW form is believed to be closely associated with insulin sensitivity. The aim of the present study was to investigate whether diet-induced changes in body weight and insulin sensitivity were associated with changes in the quantity of adiponectin multimeric complexes. A total of 20 overweight or obese women (age, 39.4+/-9.5 years; body mass index, 32.2+/-6.4 kg/m(2)) underwent 12 weeks of low caloric diet (600 kcal/day less than energy requirements; where 1 kcal is approximately 4.184 kJ). Plasma samples were drawn before and after the study for biochemical analysis and Western blot detection of adiponectin multimeric complexes. The hypocaloric diet resulted in a weight reduction (89.8+/-16.4 kg compared with 83.1+/-15.6 kg; P<0.001) and an improvement in whole-body insulin sensitivity, as measured by HOMA (homoeostasis model assessment index; 1.9+/-0.8 compared with 1.5+/-0.7; P=0.013). Increases in the quantities of the HMW, MMW and LMW forms by 5.5, 8.5 and 18.1% respectively, were observed (P<0.05 for all of the forms). Total plasma adiponectin was increased by 36% with borderline significance (P=0.08). No correlations between changes in adiponectin complexes and changes in indices of insulin sensitivity were observed. In conclusion, diet-induced weight loss improved insulin sensitivity as well as increased the amount of HMW, MMW and LMW adiponectin complexes in plasma.

Residual C-peptide secretion and endothelial function in patients with Type II diabetes

Recent studies have demonstrated that C-peptide exerts beneficial effects on endothelial function. To investigate the relationship between residual pancreatic C-peptide secretion and endothelial function in patients with well controlled or poorly controlled Type II diabetes, we studied 100 patients with Type II diabetes that were free from diabetic neuropathy. In all patients, insulin resistance, residual pancreatic C-peptide secretion, endothelial function and oxidative stress were investigated using the homoeostasis model assessment (HOMA) index, glucagon bolus test, brachial reactivity, Trolox equivalent antioxidant capacity (TEAC) and thiobarbituric acid-reacting substances (TBARS). The patients were categorized into quartiles on the basis of plasma HbA(1c) (glycated haemoglobin) concentration. Analysis of the data showed significant increases in plasma glucose concentration, HOMA index, microalbuminuria and TBARS, and significant decreases in plasma C-peptide, AUC (area under the curve) plasma C-peptide and TEAC, through the different quartiles (from the lowest to the highest HbA(1c) concentration). With regard to parameters of endothelial function, changes in diameter showed a significant declining trend through the different quartiles. Endothelial-dependent changes in diameter were independently and significantly associated with AUC C-peptide levels, TEAC and TBARS. In conclusion, our study demonstrated that patients with Type II diabetes with good residual C-peptide secretion are better protected from endothelial dysfunction that those with poor C-peptide secretion.