ABSTRACT
Many patients with hypertension suffer from impaired glucose tolerance or type 2 diabetes mellitus. Although these diagnoses are generally simple and reliable, it is more difficult to diagnose impaired glucose tolerance. As the gold standard (oral glucose tolerance test (OGTT)) is complicated to perform, a simpler alternative would be useful. The aims of the Pre-Diabetes Score study are to correlate demographic and/or laboratory parameters that are clinically simple to determine with the results of the OGTT and to determine the diagnostic significance of the combinations of parameters with regard to impaired glucose tolerance. A total of 260 patients were included in the evaluation; 39% had impaired glucose tolerance and 12% had diabetes mellitus. A combination of HbA1c of > or =6%, a venous fasting glucose of > or =110 mg/dl, an age of > or =55 years, a systolic blood pressure of > or =140 mmHg and an enlarged waist size is highly predictive of impaired glucose tolerance.
Subject(s)
Diabetes Mellitus, Type 2/diagnosis , Glucose Intolerance/diagnosis , Glucose Tolerance Test/methods , Hypertension/complications , Analysis of Variance , Blood Glucose/metabolism , Female , Humans , Male , Middle Aged , Predictive Value of TestsABSTRACT
Glutamate has been shown to play an important role in delayed neuronal cell death occurring due to ischemia. Attenuation of synaptically released glutamate can be accomplished by modulators such as adenosine and baclofen. This study focused on the ability of adenosine to attenuate the excitotoxicity secondary to glutamate receptor activation in vitro after exposure to potassium cyanide (KCN) in hippocampal neuronal cell cultures. For this study, hippocampal cell cultures were obtained from 1-day-old rats and trypan blue staining was used for assessment of cell viability. It was found that the N-methyl-D-aspartate-specific antagonist MK801 (10 microM) attenuated neuronal cell death resulting from exposure to 1 mM KCN for 60 minutes. Adenosine (10 to 1000 microM) decreased neuronal cell death secondary to the same concentration of KCN in a dose-dependent manner. This same neuroprotective effect is mimicked by the adenosine A1-specific receptor agonist N6-cyclopentyladenosine (10 microM). The A1-specific receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine (10 to 1000 nM) blocked the neuroprotective effect of adenosine in a dose-dependent manner. Therefore, neuronal cell death produced by KCN in the experimental model described was mediated at least in part by glutamate. This neuronal cell death was attenuated by adenosine via the A1-specific mechanism.
