EZHI-14K MilliporeHuman Insulin ELISA

Effective management of diabetes mellitus, affecting tens of millions of patients, requires frequent assessment of plasma glucose. Patient compliance for sufficient testing is often reduced by the unpleasantness of current methodologies, which require blood samples and often cause pain and skin callusing. We propose that the analysis of volatile organic compounds (VOCs) in exhaled breath can be used as a novel, alternative non-invasive means to monitor glycemia in these patients. 17 healthy (9F/8M, 28.0±1.0 yrs) and 8 type 1 diabetic (T1DM) volunteers (5F/3M, 25.8±1.7 yrs) were enrolled in a 240 min triphasic intravenous dextrose infusion protocol (baseline, hyperglycemia, euglycemia-hyperinsulinemia). In T1DM patients, insulin was also administered (using differing protocols on 2 repeated visits to separate the effects of insulinemia on breath composition). Exhaled breath and room air samples were collected at 12 time points, and concentrations of ~100 VOCs were determined by gas chromatography and matched with direct plasma glucose measurements. Standard least squares regression was used on several subsets of exhaled gases to generate multi-linear models to predict plasma glucose for each subject. Plasma glucose estimates based on two groups of 4 gases each (Cluster A: acetone, methyl nitrate, ethanol, and ethyl benzene; Cluster B: 2-pentyl nitrate, propane, methanol, and acetone) displayed very strong correlations with glucose concentrations (0.883 and 0.869 for Clusters A and B, respectively) across nearly 300 measurements. Our study demonstrates the feasibility to accurately predict glycemia through exhaled breath analysis over a broad range of clinically relevant concentrations in both healthy and T1DM subjects.

Abstract Adipose tissue secretes the adipokine, adiponectin (ADPN), which increases insulin sensitivity. Because some of the metabolic effects of exercise and ADPN are similar, exercise has been proposed to increase ADPN. However, most short-term (≤3 mos) and constant-effort exercise protocols have not produced increases in ADPN. Furthermore, no direct comparisons of male and female subjects on the effect of exercise on ADPN levels have been reported. We hypothesized that long-term (6 mos), progressive training would increase ADPN levels in both males and females. We recruited middle-aged, untrained males and females to participate in an interventional study employing a marathon training regimen progressing from 9.7 to 88.5 km (6 to 55 miles) per week over 6 mos. At baseline, we matched the mean ages of the male and female groups. We collected and stored fasting plasma samples and recorded body measurements at 0 (baseline) and 6 mos. Stored samples were analysed for insulin, glucose, and ADPN. ADPN increased significantly among both males (from 5.89 ± 2.46 (mean ± SD) to 7.65 ± 3.18 μg/ml; p < 0.05) and females (from 8.48 ± 3.22 to 10.56 ± 4.05 μg/ml; p < 0.05). The extent of the increase in ADPN was similar in the male (40.7 ± 50%; median, 12.1%) and female (27.0 ± 31.1%; median, 22.3%) groups. However, there was no significant reduction in insulin resistance as measured by the HOMA-IR scores in either group. We conclude that long-term, progressive aerobic training increases circulating ADPN levels in middle-aged, untrained males and females.

The purpose of this study was to compare the effects of 3 different modalities of exercise on metabolic control, insulin resistance, inflammatory markers, adipocytokines, and tissue expression of insulin receptor substrate (IRS)-1 after 12 weeks of training among patients with type 2 diabetes mellitus. Forty-eight patients with type 2 diabetes mellitus were randomly assigned to 4 groups of training (3 times a week, 60 minutes per session): aerobic group (n = 12), resistance group (n = 12), combined (aerobic and resistance) group (n = 12), and control group (n = 12). Fasting and postprandial blood glucose, glycated hemoglobin, lipid profile, insulin resistance index (homeostasis model assessment of insulin resistance), adipocytokines (adiponectin, visfatin, and resistin), tumor necrosis factor, interleukin, and high-sensitivity C-reactive protein (hs-CRP) were measured at baseline and at the end of the study. Patients also underwent a muscle microbiopsy before and after training to quantify IRS-1 expression. All 4 groups displayed decreases in blood pressure, fasting plasma glucose, postprandial plasma glucose, lipid profile, and hs-CRP (P < .05); and there was no difference across the groups. After training, the IRS-1 expression increased by 65% in the resistance group (P < .05) and by 90% in the combined group (P < .01). Exercise training favorably affects glycemic parameters, lipid profile, blood pressure, and hs-CRP. In addition, resistance and combined training can increase IRS-1 expression.Copyright © 2011 Elsevier Inc. All rights reserved.

OBJECTIVES: To evaluate the correlation between concentrations of the proinflammatory cytokines monocyte chemotactic protein 1 (MCP-1), adiponectin, interleukin 6 (IL-6), interleukin 8 (IL-8), and tumor necrosis factor (TNF) and patients with obstructive sleep apnea syndrome (OSAS). Repeated apnea attacks in patients with OSAS constitute a hypoxic condition, which induces tissue inflammation by mediation of these proinflammatory cytokines.

In children, exercise modulates systemic anabolism, muscle growth, and overall physiological development through the growth hormone (GH)-insulin-like growth factor I (IGF-I) axis. GH secretion, at rest and during exercise, changes with age and maturational status and can be blunted by hyperlipidemia and obesity, with possible negative effects on physiological growth. However, little is known about the effect of progressively more severe pediatric obesity on the GH response to exercise and its relationship to pubertal status. We therefore studied 48 early- or late-pubertal obese children [body mass index (BMI) >95th percentile, separated in tertiles with progressively greater BMI] and 42 matched controls (BMI <85th percentile), who performed ten 2-min cycling bouts at approximately 80% of maximal O2 consumption, separated by 1-min rest intervals. Plasma GH and IGF-I were measured at baseline and end exercise. GH responses were systematically blunted in obese children, with more pronounced blunting paralleling increasing BMI. Although overall the GH response to exercise was greater in late-pubertal than in younger children, this blunting pattern was observed in early- and late-pubertal children. Our results reveal insight into the interaction between pediatric obesity and key modulators of physiological growth and development and underscore the necessity of optimizing physical activity strategies for specific pediatric dysmetabolic conditions.

The reason for weight loss at high altitudes is largely unknown. To date, studies have been unable to differentiate between weight loss due to hypobaric hypoxia and that related to increased physical exercise. The aim of our study was to examine the effect of hypobaric hypoxia on body weight at high altitude in obese subjects. We investigated 20 male obese subjects (age 55.7 +/- 4.1 years, BMI 33.7 +/- 1.0 kg/m(2)). Body weight, waist circumference, basal metabolic rate (BMR), nutrition protocols, and objective activity parameters as well as metabolic and cardiovascular parameters, blood gas analysis, leptin, and ghrelin were determined at low altitude (LA) (Munich 530 m, D1), at the beginning and at the end of a 1-week stay at high altitude (2,650 m, D7 and D14) and 4 weeks after returning to LA (D42). Although daily pace counting remained stable at high altitude, at D14 and D42, participants weighed significantly less and had higher BMRs than at D1. Food intake was decreased at D7. Basal leptin levels increased significantly at high altitude despite the reduction in body weight. Diastolic blood pressure was significantly lower at D7, D14, and D42 compared to D1. This study shows that obese subjects lose weight at high altitudes. This may be due to a higher metabolic rate and reduced food intake. Interestingly, leptin levels rise in high altitude despite reduced body weight. Hypobaric hypoxia seems to play a major role, although the physiological mechanisms remain unclear. Weight loss at high altitudes was associated with clinically relevant improvements in diastolic blood pressure.

BACKGROUND: Serum adiponectin inversely correlates with the extent of coronary artery disease (CAD). OBJECTIVES: To investigate the clinical significance of measuring high molecular weight (HMW) adiponectin in addition to total adiponectin from different samples (peripheral veins and ostia of coronary arteries) in patients with CAD. METHODS: We studied 134 patients; 57 with acute coronary syndrome (ACS), 44 with stable angina and 33 healthy patients. Total and HMW adiponectin were measured in the coronary ostia and peripheral veins simultaneously. Venous levels of lipid profile, C-reactive protein, tumour necrosis factor-alpha, interleukin-6 and insulin were measured. RESULTS: Mean levels of HMW adiponectin in the coronary ostia were significantly correlated with the venous levels of total (r = 0.33, P = 0.002) and HMW (r = 0.37, P = 0.002) adiponectin. Mean levels of total and HMW adiponectin were lower in CAD patients versus controls (6.9 +/- 0.5 versus 7.9 +/- 0.7 mug/ml, P = 0.3 and 1.9 +/- 0.2 versus 3.1 +/- 0.3 mug/ml, P = 0.003). In the coronary ostia, levels of HMW adiponectin were higher in ACS than those with stable angina (1.1 +/- 0.1 versus 0.8 +/- 0.1 mug/ml, P = 0.2). In patients with CAD, levels of ostial adiponectin (total and HMW) were significantly lower in diabetic than non-diabetic patients (6.5 +/- 0.8 versus 9.4 +/- 1.1 mug/ml, P = 0.04 and 0.8 +/- 0.12 versus 1.2 +/- 0.1 mug/ml, P = 0.03). Mean levels of venous adiponectin (total and HMW) were non-significantly lower in diabetic patients (5.9 +/- 0.7 versus 7.7 +/- 0.7, P = 0.12 and 1.8 +/- 0.4 versus 1.9 +/- 0.1, P = 0.8). CONCLUSION: Measurement of HMW adiponectin and its ratio to total adiponectin may be a better marker for CAD than total adiponectin levels. Ostial levels of adiponectin in ACS may indicate re-distribution of adiponectin molecules towards the acute lesions. The low HMW adiponectin levels in diabetes mellitus may in part explain the worse outcome of CAD in diabetics.

An examination was conducted to verify D-psicose suppressed the elevation of blood glucose and insulin concentration in a dose-dependent manner under the concurrent administration of maltodextrin and D-psicose to healthy humans. Twenty subjects aged 20-39 y, 11 males and 9 females were recruited. A load test of oral maltodextrin was conducted as a randomized single blind study. The subjects took one of five test beverages (7.5 g D-psicose alone, 75 g maltodextrin alone, 75 g maltodextrin +2.5, 5 or 7.5 g D-psicose). Blood was collected before an intake and at 30, 60, 90 and 120 min after an intake. Intervals of administration were at least 1 wk. The load test with 75 g maltodextrin showed significant suppressions of the elevation of blood glucose and insulin concentration under the doses of 5 g or more D-psicose with dose dependency. An independent administration of 7.5 g D-psicose had no influence on blood glucose or insulin concentration. D-Psicose is considered efficacious in the suppression of the elevation of blood glucose concentration after eating in humans.

OBJECTIVE: Islet amyloid, formed by aggregation of the beta-cell peptide islet amyloid polypeptide (IAPP; amylin), is a pathological characteristic of pancreatic islets in type 2 diabetes. Toxic IAPP aggregates likely contribute to the progressive loss of beta-cells in this disease. We used cultured human islets as an ex vivo model of amyloid formation to investigate whether suppression of proIAPP expression would inhibit islet amyloid formation and enhance beta-cell survival and function. RESEARCH DESIGN AND METHODS: Islets from cadaveric organ donors were transduced with a recombinant adenovirus expressing a short interfering RNA (siRNA) designed to suppress human proIAPP (Ad-hProIAPP-siRNA), cultured for 10 days, and then assessed for the presence of islet amyloid, beta-cell apoptosis, and beta-cell function. RESULTS: Thioflavine S-positive amyloid deposits were clearly present after 10 days of culture. Transduction with Ad-hProIAPP-siRNA reduced proIAPP expression by 75% compared with nontransduced islets as assessed by Western blot analysis of islet lysates 4 days after transduction. siRNA-mediated inhibition of IAPP expression decreased islet amyloid area by 63% compared with nontransduced cultured islets. Cell death assessed by transferase-mediated dUTP nick-end labeling staining was decreased by 50% in transduced cultured human islets, associated with a significant increase in islet insulin content (control, 100 +/- 4 vs. +Ad-siRNA, 153 +/- 22%, P 0.01) and glucose-stimulated insulin secretion (control, 222 +/- 33 vs. +Ad-siRNA, 285 +/- 21 percent basal, P 0.05). CONCLUSIONS: These findings demonstrate that inhibition of IAPP synthesis prevents amyloid formation and beta-cell death in cultured human islets. Inhibitors of IAPP synthesis may have therapeutic value in type 2 diabetes.