Metabolism: clinical and experimental
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Tumor necrosis factor-alpha (TNF-alpha) seems to be increased in obese subjects, suggesting its role as a proinflammatory cytokine to insulin resistance and metabolic abnormalities in obesity. The aim of this study was to evaluate the relationship between serum TNF-alpha, soluble TNF-alpha receptor 1 (sTNF-R1), TNF-alpha receptor 2 (sTNF-R2), and metabolic syndrome (MS) components and anthropometric indices in obese and non-obese adolescents. A cross-sectional study was performed on obese and non-obese adolescents. ⋯ The serum TNF-alpha was positively correlated with triglyceride (TG) and DBP, and negatively with high-density lipoprotein-cholesterol (HDLC). The sTNF-R1 and sTNF-R2 were correlated with TG and DBP, and TG, respectively. Obese compared with non-obese adolescents exhibited higher concentrations of TNF-alpha and its soluble receptors, and the higher TNF-alpha concentrations were associated with several components of MS in obese adolescents.
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Subjects with impaired glucose tolerance (IGT) are usually overweight and exhibit insulin resistance with a defective compensation of insulin secretion. In this study, we sought to establish the interrelation between insulin secretion and insulin sensitivity after oral glucose in non-obese subjects with IGT and we also examined this interrelation in relation to the 2 main incretins, glucagon-like peptide (GLP-1) and gastric inhibitory polypeptide (GIP). To that end, 13 women with IGT and 17 women with normal glucose tolerance (NGT) underwent an oral glucose tolerance test (OGTT) with measurements of glucose, insulin, C-peptide, GLP-1, and GIP. ⋯ However, the 30-minute increase in GLP-1 concentrations was lower in IGT than in NGT (P =.036). We conclude that also in non-obese subjects with IGT, when adiposity is controlled for in relation to NGT, defective early insulin secretion after oral glucose is a key factor. This defective beta-cell function is associated with, and may be caused by, a reduced early GLP-1 response.
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In this crossover study, we compared the peak responses of cortisol to low-dose (1 microg/1.73 m(2)) and standard-dose (250 microg/1.73 m(2)) adrenocorticotropic hormone (ACTH) stimulation tests in 90 full-term newborns (37 to 42 weeks gestational age, birthweight > 2,500 g, aged 4 to 7 days): 30 with sepsis syndrome, 30 with respiratory distress (RD) and 30 normal infants. Basal cortisol and ACTH were measured in a fasting venous sample. Serum cortisol concentrations were measured 30 minutes after low-dose ACTH and 60 minutes after standard-dose ACTH by radioimmunoassay (RIA). ⋯ These data suggest that the low-dose ACTH test may be more disciminatory than the standard-dose test among babies under stress. Increasing the cut-point level of basal cortisol in stressed infants to the lowest level of cortisol response to low-dose ACTH in normal newborns, followed by the use of a low-dose ACTH test, appears to select some newborns who need and may improve on corticosteroid therapy. Further studies are required to investigate whether supplementation with stress doses of hydrocortisone may improve the outcome in these patients.
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Recent reports have suggested a link between acylation-stimulating protein (ASP) and complement C3 with obesity, insulin resistance, coronary artery disease, and hyperlipidemia. Our aim was to examine the mRNA expression of C3 and other factors related to ASP production (such as factor B and adipsin) in adipose tissue. The influence of gender and obesity was examined in subcutaneous (SC) and omental (OM) tissues from 16 males and 16 females with body mass index (BMI) from 20 to 54 kg/m(2). ⋯ These results suggest that in female SC adipose tissue, there is downregulation of factors related to ASP production in obesity, perhaps to limit further expansion of adipose tissue. In males, there is increased expression in OM tissue. In addition, relative OM/SC expression increases with obesity and these changes may contribute to the development of visceral adipose tissue.
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Clinical Trial
Is there a threshold of visceral fat loss that improves the metabolic profile in obese postmenopausal women?
It is presently unclear how much visceral adipose tissue (VAT) loss is needed to induce favorable metabolic changes. Cross-sectional studies have proposed that a threshold level of VAT exceeding 110 cm(2) in women induces deleterious changes in the metabolic profile. It is presently unclear, however, if significant decreases in VAT below this given threshold significantly improve the metabolic profile more as compared to decreases that remain below 110 cm(2). ⋯ These results do not favor the idea that attaining levels of VAT below a threshold of 110 cm(2) is necessary to favorably improve the metabolic profile in obese postmenopausal women. Achieving or not the proposed threshold of VAT, independently of baseline values, appears to yield similar metabolic improvements in obese postmenopausal women. More moderate losses of VAT appear to yield similar metabolic improvements as large losses.