259 research outputs found
Association between one-hour post-load plasma glucose levels and vascular stiffness in essential hypertension
Objectives: Pulse wave velocity (PWV) is a surrogate end-point for cardiovascular morbidity and mortality. A plasma glucose
value 155 mg/dl (NGT155 had a worse insulin sensitivity and higher hs-CRP than NGT,155, similar to IGT subjects. In addition, NGT 155 subjects, compared with NGT,155, have higher PWV and its hemodynamic correlates
that increase their cardiovascular risk profile
Serum IgG2 levels are specifically associated with whole-body insulin-mediated glucose disposal in non-diabetic offspring of type 2 diabetic individuals. a cross-sectional study
.Preclinical studies suggested that IgG2c isotype may specifically impair skeletal muscle insulin
sensitivity in mice. In this study we investigated the association between serum levels of the four IgG
subclasses and insulin sensitivity in non-diabetic individuals. Total IgG, IgG1, IgG2, IgG3 and IgG4
levels were measured in 262 subjects. Whole-body insulin sensitivity was assessed by euglycemic
hyperinsulinemic clamp. IgG2 levels were positively correlated with BMI, waist circumference, 2-h postload
glucose levels and complement C3. Serum IgG2, but not IgG1, IgG3 and IgG4 levels were negatively
correlated with whole-body insulin sensitivity (r = −0.17; P = 0.003) and muscle insulin sensitivity index
(r = −0.16; P = 0.03) after adjustment for age and gender. No significant correlation was found between
IgG2 levels and hepatic insulin resistance assessed by HOMA-IR and liver IR index. In a multivariable
regression analysis including variables known to affect insulin sensitivity such as age, gender, BMI,
smoking, lipids, inflammatory markers, fasting and 2-h post-load glucose levels, IgG2 levels were
independently associated with insulin-stimulated glucose disposal (β = −0.115, 95% CI: −0.541 to
−0.024; P = 0.03). These data demonstrate the independent association between higher levels of IgG2
and decreased whole-body insulin sensitivity, thus confirming in humans the animal-based evidence
indicating the pathogenic role of IgG2 in insulin resistance
Obese patients with a binge eating disorder have an unfavorable metabolic and inflammatory profile
To evaluate whether obese patients with a binge eating disorder (BED) have an altered metabolic and inflammatory profile related to their eating behaviors compared with non-BED obese.A total of 115 White obese patients consecutively recruited underwent biochemical, anthropometrical evaluation, and a 75-g oral glucose tolerance test. Patients answered the Binge Eating Scale and were interviewed by a psychiatrist. The patients were subsequently divided into 2 groups according to diagnosis: non-BED obese (n = 85) and BED obese (n = 30). Structural equation modeling analysis was performed to elucidate the relation between eating behaviors and metabolic and inflammatory profile.BED obese exhibited significantly higher percentages of altered eating behaviors, body mass index (P < 0.001), waist circumference (P < 0.01), fat mass (P < 0.001), and a lower lean mass (P < 0.001) when compared with non-BED obese. Binge eating disorder obese also had a worse metabolic and inflammatory profile, exhibiting significantly lower high-density lipoprotein cholesterol levels (P < 0.05), and higher levels of glycated hemoglobin (P < 0.01), uric acid (P < 0.05), erythrocyte sedimentation rate (P < 0.001), high-sensitive C-reactive protein (P < 0.01), and white blood cell counts (P < 0.01). Higher fasting insulin (P < 0.01) and higher insulin resistance (P < 0.01), assessed by homeostasis model assessment index and visceral adiposity index (P < 0.001), were observed among BED obese. All differences remained significant after adjusting for body mass index. No significant differences in fasting plasma glucose or 2-hour postchallenge plasma glucose were found. Structural equation modeling analysis confirmed the relation between the altered eating behaviors of BED and the metabolic and inflammatory profile.Binge eating disorder obese exhibited an unfavorable metabolic and inflammatory profile, which is related to their characteristic eating habits
Insulin sensitivity, β-cell function, and incretin effect in individuals with elevated 1-hour postload plasma glucose levels
OBJECTIVE: Individuals with normal glucose tolerance (NGT), whose 1-h postload plasma glucose is ≥155 mg/dL (NGT 1h-high), have an increased risk of type 2 diabetes. The purpose of this study was to characterize their metabolic phenotype.
RESEARCH DESIGN AND METHODS: A total of 305 nondiabetic offspring of type 2 diabetic patients was consecutively recruited. Insulin secretion was assessed using both indexes derived from oral glucose tolerance test (OGTT) and intravenous glucose tolerance test (IVGTT). Insulin sensitivity was measured by hyperinsulinemic-euglycemic clamp.
RESULTS: Compared with individuals with a 1-h postload plasma glucose <155 mg/dL (NGT 1h-low), NGT 1h-high individuals exhibited lower insulin sensitivity after adjustment for age, sex, and BMI. Insulin secretion estimated from the OGTT did not differ between the two groups of individuals. By contrast, compared with NGT 1h-low individuals, the acute insulin response during an IVGTT and the disposition index were significantly reduced in NGT 1h-high individuals after adjustment for age, sex, and BMI. Incretin effect, estimated as the ratio between total insulin responses during OGTT and IVGTT, was higher in NGT 1h-high individuals compared with NGT 1h-low individuals.
CONCLUSIONS: NGT 1h-high individuals may represent an intermediate state of glucose intolerance between NGT and type 2 diabetes characterized by insulin resistance and reduced β-cell function, the two main pathophysiological defects responsible for the development of type 2 diabetes. Postload hyperglycemia is the result of an intrinsic β-cell defect rather than impaired incretin effec
Fertilización de Eucalyptus grandis en el NE de Entre Ríos: resultados al turno y algunas implicancias para el manejo de las plantaciones
Fil: Graciano, Corina. Universidad Nacional de La Plata. Facultad de Ciencias Agrarias y Forestales; ArgentinaFil: Goya, Juan F.. Universidad Nacional de La Plata. Facultad de Ciencias Naturales y Museo. Laboratorio de Investigaciones de Sistemas Ecológicos y Ambientales; ArgentinaFil: Arturi, Marcelo. Universidad Nacional de La Plata. Facultad de Ciencias Naturales y Museo. Laboratorio de Investigaciones de Sistemas Ecológicos y Ambientales; ArgentinaFil: Burns, Sarah L.. Universidad Nacional de La Plata. Facultad de Ciencias Naturales y Museo. Laboratorio de Investigaciones de Sistemas Ecológicos y Ambientales; ArgentinaFil: Pérez, Carolina. Universidad Nacional de La Plata. Facultad de Ciencias Naturales y Museo. Laboratorio de Investigaciones de Sistemas Ecológicos y Ambientales; Argentin
Recovery of NIS expression in thyroid cancer cells by overexpression of Pax8 gene
BACKGROUND: Recovery of iodide uptake in thyroid cancer cells by means of obtaining the functional expression of the sodium/iodide symporter (NIS) represents an innovative strategy for the treatment of poorly differentiated thyroid cancer. However, the NIS gene expression alone is not always sufficient to restore radioiodine concentration ability in these tumour cells. METHODS: In this study, the anaplastic thyroid carcinoma ARO cells were stably transfected with a Pax8 gene expression vector. A quantitative RT-PCR was performed to assess the thyroid specific gene expression in selected clones. The presence of NIS protein was detected by Western blot and localized by immunofluorescence. A iodide uptake assay was also performed to verify the functional effect of NIS induction and differentiation switch. RESULTS: The clones overexpressing Pax8 showed the re-activation of several thyroid specific genes including NIS, Pendrin, Thyroglobulin, TPO and TTF1. In ARO-Pax8 clones NIS protein was also localized both in cell cytoplasm and membrane. Thus, the ability to uptake the radioiodine was partially restored, associated to a high rate of efflux. In addition, ARO cells expressing Pax8 presented a lower rate of cell growth. CONCLUSION: These finding demonstrate that induction of Pax8 expression may determine a re-differentiation of thyroid cancer cells, including a partial recovery of iodide uptake, fundamental requisite for a radioiodine-based therapeutic approach for thyroid tumours
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