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  • Plasma levels of MCP-1 and adiponectin in obstructive sleep apnea syndrome. 20855682

    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.
    Document Type:
    Reference
    Product Catalog Number:
    EZHI-14K
    Product Catalog Name:
    Human Insulin ELISA

  • Effect of trans-fat, fructose and monosodium glutamate feeding on feline weight gain, adiposity, insulin sensitivity, adipokine and lipid profile. 21429276

    The incidence of obesity and type 2 diabetes mellitus (T2DM) is increasing, and new experimental models are required to investigate the diverse aspects of these polygenic diseases, which are intimately linked in terms of aetiology. Feline T2DM has been shown to closely resemble human T2DM in terms of its clinical, pathological and physiological features. Our aim was to develop a feline model of diet-induced weight gain, adiposity and metabolic deregulation, and to examine correlates of weight and body fat change, insulin homeostasis, lipid profile, adipokines and clinical chemistry, in order to study associations which may shed light on the mechanism of diet-induced metabolic dysregulation. We used a combination of partially hydrogenated vegetable shortening and high-fructose corn syrup to generate a high-fat-high-fructose diet. The effects of this diet were compared with an isoenergetic standard chow, either in the presence or absence of 1·125 % dietary monosodium glutamate (MSG). Dual-energy X-ray absorptiometry body imaging and a glucose tolerance test were performed. The present results indicate that dietary MSG increased weight gain and adiposity, and reduced insulin sensitivity (P < 0·05), whereas high-fat-high-fructose feeding resulted in elevated cortisol and markers of liver dysfunction (P < 0·01). The combination of all three dietary constituents resulted in lower insulin levels and elevated serum β-hydroxybutyrate and cortisol (P < 0·05). This combination also resulted in a lower first-phase insulin release during glucose tolerance testing (P < 0·001). In conclusion, markers of insulin deregulation and metabolic dysfunction associated with adiposity and T2DM can be induced by dietary factors in a feline model.
    Document Type:
    Reference
    Product Catalog Number:
    EZCL-31K
    Product Catalog Name:
    Canine Leptin ELISA

  • PPARβ/δ Activation Induces Enteroendocrine L Cell GLP-1 Production. 21300064

    BACKGROUND & AIMS: Glucagon-like peptide (GLP)-1, an intestinal incretin produced by L cells through proglucagon processing, is secreted after nutrient ingestion and acts on endocrine pancreas beta cells to enhance insulin secretion. Peroxisome proliferator-activated receptor (PPAR) β/δ is a nuclear receptor that improves glucose homeostasis and pancreas islet function in diabetic animal models. Here, we investigated whether PPARβ/δ activation regulates L cell GLP-1 production.METHODS: Proglucagon regulation and GLP-1 release were evaluated in murine GLUTag and human NCI-H716 L cells and in vivo using wild-type, PPARβ/δ-null, and ob/ob C57Bl/6 mice treated with the PPARβ/δ synthetic agonists GW501516 or GW0742.RESULTS: PPARβ/δ activation increased proglucagon expression and enhanced glucose- and bile acid-induced GLP-1 release by intestinal L cells in vitro and ex vivo in human jejunum. In vivo treatment with GW0742 increased proglucagon messenger RNA levels in the small intestine in wild-type but not in PPARβ/δ-deficient mice. Treatment of wild-type and ob/ob mice with GW501516 enhanced the increase in plasma GLP-1 level after an oral glucose load and improved glucose tolerance. Concomitantly, proglucagon and GLP-1 receptor messenger RNA levels increased in the small intestine and pancreas, respectively. Finally, PPARβ/δ agonists activate the proglucagon gene transcription by interfering with the β-catenin/TCF-4 pathway.CONCLUSIONS: Our data show that PPARβ/δ activation potentiates GLP-1 production by the small intestine. Pharmacologic targeting of PPARβ/δ is a promising approach in the treatment of patients with type 2 diabetes mellitus, especially in combination with dipeptidyl peptidase IV inhibitors.Copyright © 2011 AGA Institute. Published by Elsevier Inc. All rights reserved.
    Document Type:
    Reference
    Product Catalog Number:
    EGLP-35K
    Product Catalog Name:
    Glucagon Like Peptide-1 (Active) ELISA

  • Atherogenecity of LDL and unfavorable adipokine profile in metabolically obese, normal-weight woman. 18239579

    OBJECTIVE: The relationship of visceral adiposity with adipocytokines and low-density lipoprotein (LDL) particle distribution and oxidation in Asian metabolically obese, normal-weight (MONW) individuals has not been evaluated. We aimed to investigate the association between visceral adiposity and adipocytokines and cardiovascular disease (CVD) risk factors in MONW Korean women with normal glucose tolerance. METHODS AND PROCEDURES: We examined the metabolic characteristics of 135 non-obese (BMI 25 kg/m(2)) women aged 25-64 years. Twenty-five women (BMI 25 kg/m(2) and visceral fat adiposity (VFA) > or =100 cm(2)) were classified as MONW and 25 women (BMI 25 kg/m(2) and VFA 100 cm(2)), pair-matched for age, weight, height, and menopausal status, as control group. Plasma lipid profiles and adipocytokines were evaluated in these two groups. RESULTS: MONW subjects had higher systolic (P 0.05) and diastolic blood pressure (P 0.005) and higher concentrations of triacylglycerol (TG) (P 0.005), insulin (P 0.01), and free fatty acid (FFA) (P 0.05) than control subjects. There was no significant difference between two groups in LDL-cholesterol (LDL-C) concentrations; however, MONW subjects had smaller LDL particles (P 0.01) and higher concentrations of oxidized LDL (ox-LDL) (P 0.05) compared with controls. Moreover, MONW subjects had higher concentrations of tumor necrosis factor-alpha (TNF-alpha) (P 0.05), interleukin-6 (IL-6) (P 0.05) and leptin (P 0.05), and lower plasma adiponectin concentrations (P 0.05). Higher intake of saturated fat with lower ratio of polyunsaturated fatty acids (PUFAs) to saturated fatty acids (SFA) and lower fiber intake than normal subjects were found in MONW women. DISCUSSION: We found an unfavorable inflammatory profile and a more atherogenic LDL profile in MONW female subjects even in the absence of a known CVD risk factors. Moreover, MONW consumed more saturated fat and less fiber than the control group.
    Document Type:
    Reference
    Product Catalog Number:
    5005

  • Acute d-psicose administration decreases the glycemic responses to an oral maltodextrin tolerance test in normal adults. 19155592

    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.
    Document Type:
    Reference
    Product Catalog Number:
    EZHI-14K
    Product Catalog Name:
    Human Insulin ELISA

  • Non-invasive Measurement of Plasma Glucose from Exhaled Breath in Healthy and Type 1 Diabetic Mellitus Subjects. 21467303

    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.
    Document Type:
    Reference
    Product Catalog Number:
    EZHI-14K
    Product Catalog Name:
    Human Insulin ELISA

  • Dose-dependent relationship between severity of pediatric obesity and blunting of the growth hormone response to exercise. 19875716

    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.
    Document Type:
    Reference
    Product Catalog Number:
    EZHI-14K
    Product Catalog Name:
    Human Insulin ELISA
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