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Recently we observed increased adipose tissue (AT) expression of CD40-related signaling proteins but no activation of tumor necrosis factor-α or CD68 in patients with chronic sustained hypoxia resulting from chronic obstructive pulmonary disease (COPD). Transcription factor nuclear factor-κB (NFκB) is involved in cellular responses to hypoxia and activates the proinflammatory gene expression with concomitant upregulation of its own repressors-inhibitors of κB (IκB) in an auto feedback loop. Inhibitor of kappaB kinase (IKK)-γ and inhibitor of kappaB kinase complex-associated protein (IKAP) are further regulatory proteins involved in NFκB signaling. In this study, we hypothesized that chronic sustained hypoxia significantly relates to IκBα, IKKγ and IKAP within the AT in COPD patients. In 20 patients with stable disease, samples of subcutaneous AT were analyzed using real-time PCR. Although no significant differences were observed between two groups categorized by median PaO in NFκB ( p = 0.065), gene expressions of IκBα, IKKγ and IKAP were all higher in hypoxemic patients ( p = 0.033; p = 0.050; p = 0.010, respectively). In multivariate analyses, PaO independently predicted AT IκBα, IKKγ and IKAP ( R = 0.490, p = 0.012; R = 0.586, p = 0.002; R = 0.504, p = 0.009, respectively). In conclusion, our data suggest significant AT upregulation of IκBα, IKKγ and IKAP by chronic sustained hypoxia in COPD patients. [ABSTRACT FROM AUTHOR]

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The continuous delivery of glucose to the brain is critically important to the maintenance of normal metabolic function. However, elucidation of the hormonal regulation of in vivo cerebral glucose metabolism in humans has been limited by the lack of direct, noninvasive methods with which to measure brain glucose. In this study, we sought to directly examine the effect of insulin on glucose concentrations and rates of glucose transport/metabolism in human brain using (1)H-magnetic resonance spectroscopy at 4 Tesla. Seven subjects participated in paired hyperglycemic (16.3 +/- 0.3 mmol/l) clamp studies performed with and without insulin. Brain glucose remained constant throughout (5.3 +/- 0.3 micromol/g wet wt when serum insulin = 16 +/- 7 pmol/l vs. 5.5 +/- 0.3 micromol/g wet wt when serum insulin = 668 +/- 81 pmol/l, P = NS). Glucose concentrations in gray matter-rich occipital cortex and white matter-rich periventricular tissue were then simultaneously measured in clamps, where plasma glucose ranged from 4.4 to 24.5 mmol/l and insulin was infused at 0.5 mU. kg(-1). min(-1). The relationship between plasma and brain glucose was linear in both regions. Reversible Michaelis-Menten kinetics fit these data best, and no differences were found in the kinetic constants calculated for each region. These data support the hypothesis that the majority of cerebral glucose uptake/metabolism is an insulin-independent process in humans. [ABSTRACT FROM AUTHOR]

The aim of the present study was to analyse effects of sulphonylurea treatment on parameters of glycaemic control in relation to transcription factor 7-like 2 ( TCF7L2) genotypes. In 87 patients with type 2 diabetes who failed to achieve glycaemic control on metformin monotherapy, effects of 6-month sulphonylurea in addition to metformin on reductions in haemoglobin A1c (HbA1c) and fasting plasma glucose (FPG) levels were evaluated. Reduction in HbA1c and FPG in response to 6-month sulphonylurea treatment was significantly higher in patients with CC genotype compared to those with the CT+TT genotype (1.16 ± 0.07 vs. 0.86 ± 0.07%, p = 0.003; 1.57 ± 0.12 vs. 1.14 ± 0.14 mmol/l, p = 0.031, respectively). In the multivariate analysis, baseline HbA1c and the TCF7L2 genotype were the only significant predictors of HbA1c reduction. In conclusion, the magnitude of HbA1c and FPG reductions after 6-month sulphonylurea treatment in addition to metformin is related to the TCF7L2 gene polymorphism. [ABSTRACT FROM AUTHOR]

The article presents an abstract of the research paper "In Vivo 1H NMR Spectroscopy of the Developing Rat Hippocampus." The study aimed at determining the biochemical changes in neonatal rat hippocampus. Researchers also determined concentrations of 15 metabolites by LCModel including alanine, aspartate, cholinc groups, creatine, and phosphocreatine.

The article presents an abstract of a medical research related to the direct measurements of glycogen concentrations and metabolism in rat brain in vivo. It has been concluded by researchers that brain glycogen metabolism is transiently perturbed towards net synthesis from steady-state during hyperglycemia, possibly mediated by a transient activation of the glucose-6-phosphate dependent glycogen synthase.

The article presents an abstract of the paper "Non-Invasive Assessment of the Diffusion Characteristics of Glucose in the Rat Brain in Vivo," which will be presented at the 30th Annual Meeting of the American Society for Neurochemistry to be held from March 14-17, 1999 in New Orleans, Louisiana. The paper concludes that the analysis of glucose in vivo during hyperglycemia is consistent with a considerable portion of glucose signal being intracellular.

The article presents an abstract of the paper "In Vivo Measurements of Neurochemical Changes in Quinolinic Acid-Lesioned Rat Stratum by 1H NMR Spectroscopy," which will be presented at the 30th Annual Meeting of the American Society for Neurochemistry to be held from March 14-17, 1999 in New Orleans, Louisiana. Examining graft survival in experimental models of Huntington disease is made possible by the paper.