Ana Maria Garcia Bellon has completed her PhD from Granada University and Post-doctoral studies from Malaga University School of Medicine. She currently works at the University Regional Hospital of Malaga, Spain.
Objective: To analyze the value of glycosylated hemoglobin (HbA1c), determined at admission, as predictor of developing type 2 diabetes mellitus in non-diabetic patients, hospitalized for coronary disease. Material & Methods: We collected 578 consecutive patients, admitted for (ACS) in our department, from May 2014 to September 2015. Their levels of Hb1Ac were requested at admission systematically. Finally, 199 patients (34%) were included with diagnosed coronary disease and without known diabetes. We collected clinical data, cardiovascular risk factors (CVRF), anthropometric and laboratory values (fasting glucose and HbA1c). Two months after hospital discharge, all patients were re-evaluated clinically and analytically undergoing an oral glucose tolerance test (OGTT). Patients were grouped into four categories according to the criteria of the American Diabetes Association (ADA): a) normal fasting glucose <110 mg/dL and OGTT <140 mg/dL, b) altered basal glucose (ABG): fasting glucose 110-126 mg/dL, c) glucose intolerance (GI): a 2-h OGTT 140-200 mg/dL, d) ABG + IG, e) DM: fasting glucose> 126 mg/dL and 2 hours OGTT> 200 mg/dL We conducted a descriptive analysis of the data. We determine the odds ratio (OR) of having DM or any disorder of carbohydrate metabolism in relation to the values of HbA1c at admission. Results: Mean age was 68.3 years. 69.2% were male and 30.8%, female. Mean body mass index (BMI): 28.4 kg/m². The prevalence of cardiovascular risk factors is: 74.6% hypertensive, 34.7% dyslipidemic, 32.9% active smokers. Prior history of heart disease: 26.5% acute myocardial infarction (AMI), 19.3% prior stable angina, 41.6% with no history of heart disease. Mean fasting blood glucose 104 mg / dL ± 24, and 6% on HbA1c. The evaluation at 2 months by fasting glucose and OGTT: Normal result 24.1%, 3.5% GBA, IG 33.7%, 11.1% GBA + IG, 27.6% DM. The OR of having any disorder of carbohydrate metabolism in terms of HbA1c levels was 6.65 (95% CI, 1.25-35) (p <0.029). The cutoff point that best discriminated Hb1Ac was Hb1Ac risk = 6.5%. Conclusions: HbA1c level at admission is a good predictor of the risk of developing DM or other alterations in carbohydrate metabolism. This small measure would be useful for an early detection of DM, allowing to start a suitable dietary and pharmacological prevention.
Andrea Pereira Rosa received her MSc in Biochemistry from Federal University of Rio Grande do Sul. She is currently a PhD student in Biochemistry. She has published 15 papers in prestigious scientific journals.
Diabetes is an endocrine disorder of carbohydrate metabolism characterized by hyperglycemia due to deficiency of insulin secretion or action. Recently, the impact of diabetes on the central nervous system (CNS) has been received great attention, but the mechanisms by which hyperglycemia can cause brain damage remain poorly understood. In addition, recent studies have shown that hyperglycemia induces brain damage in adult rat. In this regard, there is a paucity of studies addressing the deleterious effects of hyperglycemia on the rat brain during CNS development. Therefore, in the present study, we investigated if neonatal hyperglycemia was able to alter the expression of proteins associated with survival/death signaling. Seven-day-old Wistar rats were subjected to a single administration of streptozotocin (100 mg/Kg body weight) while controls received saline. Glycemia was verified every day (>200 mg/dL are considered hyperglycemic). Five days after injection of streptozotocin, animals were killed and the brain homogenates were utilized for analyses. The expression of proteins JNK, GSK3β, Bax, Bcl2, p38, Total AKT and phosphosforylated AKT (p-AKT) was quantified by “western blot”. No significant changes were detected in JNK, GSK3β, Bax and Total AKT protein expression. On the other hand, brain of neonatal hyperglycemic group presented increased p38 and Bcl2 protein expression. Furthermore, brain of neonatal hyperglycemic rats showed decreased p-AKT protein expression as compared to control group. Finally, these results suggest that neonatal hyperglycemia induces death signaling activation, indicating the potential harmful effect of hyperglycemia on the central nervous system.