Sliding scale insulin was often applied for emergency patients. However there is no study on this therapy in Viet Nam. We used this therapy for 51 new onset hyperglycemic patients (glycemia > 200 mg/dl ) from 6/1998 to 2/2003. Regular insulin was injected when blood glucose>200 mg/dl, then blood glucose level was monitored by finger stick sugar Q4h. If glucose 200-300mg/dl, given 5IU of insulin, glucose>300 mg/dl, given 10 U.The goal blood glucose < 200mg/dl. Results: The average time to lower the blood glucose level to the target level was about 46h. The result after 7 days showed that glycemia was controlled < 200mg/dl and <150 mg/dl in 92% and 62% patientss, respectively.There was no severe hypoglycemia documented during the study.
Insulin ; Therapeutics ; Hyperglycemia ; Stress

Background: Hyperglycemia is commonly seen in cerebral vascular accidents in general and in acute phase in particular. It is difficult for doctors to treat. Objectives: To evaluate the effect of stress hyperglycemia on mortality risk and disability risk in patient with acute ischemic stroke. Subjects and method: 105 patients with acute ischemic stroke with admission blood glucose level >/= 8.0mmol/l without history of diabetes mellitus from 2004 to 2007. These patients were divided into two groups: group 1 with admission blood glucose level of 8.0-11.0mmol/l; group 2 with that level of >l1.0mmol/l. Results: There was a significant reverse correlation between blood glucose level and the Glasgow score scale on admission and after 24 hours. The mortality risk in hospital of group 2 was higher than that of group 1 and the disability level of group 2 was more severe than that of group 1. Conclusion: Stress hyperglycemia increased the risk of in-hospital mortality in acute ischemic stroke patients and risk of severe disability after leaving hospital. \r\n', u'\r\n', u'
Stress hyperglycemia ; acute ischemic stroke

Macrovascular and microvascular diseases are currently the principal causes of morbidity and mortality in subjects with diabetes. Disorders of the physiological signaling functions of reactive oxygen species (superoxide and hydrogen peroxide) and reactive nitrogen species (nitric oxide and peroxynitrite) are important features of diabetes. In the absence of an appropriate compensation by the endogenous antioxidant defense network, increased oxidative stress leads to the activation of stress-sensitive intracellular signaling pathways and the formation of gene products that cause cellular damage and contribute to the vascular complications of diabetes. It has recently been suggested that diabetic subjects with vascular complications may have a defective cellular antioxidant response against the oxidative stress generated by hyperglycemia. This raises the concept that antioxidant therapy may be of great benefit to these subjects. Although our understanding of how hyperglycemia-induced oxidative stress ultimately leads to tissue damage has advanced considerably in recent years, effective therapeutic strategies to prevent or delay the development of this damage remain limited. Thus, further investigation of therapeutic interventions to prevent or delay the progression of diabetic vascular complications is needed.
Compensation and Redress ; Diabetic Angiopathies ; Hydrogen ; Hyperglycemia ; Nitrogen ; Oxidative Stress ; Oxygen ; Reactive Nitrogen Species ; Reactive Oxygen Species

Low-carbohydrate diets have become increasingly popular in both media and clinical research settings. Although they may improve some metabolic markers, their effects on arterial function remain unclear. Endothelial dysfunction is the well-established response to cardiovascular risk factors and a pivotal feature that precedes atherosclerotic diseases. It has been demonstrated that a high carbohydrate-induced hyperglycemia and subsequent oxidative stress acutely worsen the efficacy of the endothelial vasodilatory system. Thus, in theory, a carbohydrate restricted diet may preserve the integrity of the arterial system. This review attempts to provide insight on whether low-carbohydrate diets have a favorable or detrimental impact on vascular function, or it is perhaps the quality of carbohydrate that should direct dietary recommendations. Research to date suggests that diets low in carbohydrate amount may negatively impact vascular endothelial function. Conversely, it appears that maintaining recommended carbohydrate intake with utilization of low glycemic index foods generates a more favorable vascular profile. Understanding these relationships will aid in deciphering the diverging role of modulating quantity and quality of carbohydrates on cardiovascular risk.
Carbohydrates* ; Cardiovascular Diseases ; Diet* ; Endothelium ; Glycemic Index ; Hyperglycemia ; Oxidative Stress ; Risk Factors

BACKGROUND: We aimed to quantify stress-induced hyperglycemia and differentiate the glucose response between normal animals and those with diabetes. We also examined the pattern in glucose fluctuation induced by stress according to type of diabetes. METHODS: To load psychological stress on animal models, we used a predator stress model by exposing rats to a cat for 60 minutes and measured glucose level from the beginning to the end of the test to monitor glucose fluctuation. We induced type 1 diabetes model (T1D) for ten Sprague-Dawley rats using streptozotocin and used five Otsuka Long-Evans Tokushima Fatty rats as obese type 2 diabetes model (OT2D) and 10 Goto-Kakizaki rats as nonobese type 2 diabetes model (NOT2D). We performed the stress loading test in both the normal and diabetic states and compared patterns of glucose fluctuation among the three models. We classified the pattern of glucose fluctuation into A, B, and C types according to speed of change in glucose level. RESULTS: Increase in glucose, total amount of hyperglycemic exposure, time of stress-induced hyperglycemia, and speed of glucose increase were significantly increased in all models compared to the normal state. While the early increase in glucose after exposure to stress was higher in T1D and NOT2D, it was slower in OT2D. The rate of speed of the decrease in glucose level was highest in NOT2D and lowest in OT2D. CONCLUSION: The diabetic state was more vulnerable to stress compared to the normal state in all models, and the pattern of glucose fluctuation differed among the three types of diabetes. The study provides basic evidence for stress-induced hyperglycemia patterns and characteristics used for the management of diabetes patients.
Animals ; Cats ; Glucose ; Humans ; Hyperglycemia* ; Models, Animal ; Rats ; Rats, Sprague-Dawley ; Streptozocin ; Stress, Psychological

People whose diabetes is under good metabolic control should not experience more illness or infection than people without diabetes. However, when any illness occurs in someone with diabetes, the potential for hyperglycemia, hyperglycemia with ketosis, hyperglycemia with ketoacidosis, or hypoglycemia exists and requires education and treatment to prevent exacerbation or even possible death. In some parts of the world where access to medical care, insulin, or parenteral fluids is problematic, the added metabolic stress of an illness in someone with diabetes can be life threatening. Many illnesses are associated with higher levels of stress hormones which promote gluconeogenesis and insulin resistance. Education about the effects of concurrent illness ("sick days") is a critical component of diabetes management and must be adapted to the educational abilities and treatment possibilities of the particular situations in different parts of the world.
Diabetes Mellitus ; Gluconeogenesis ; Humans ; Hyperglycemia ; Hypoglycemia ; Insulin ; Insulin Resistance ; Ketosis ; Sick Leave ; Stress, Physiological

It is well established that diabetes mellitus is a major risk factor for cardiovascular disease (CVD), and tight glycemic control decreases CVD. Most physicians continue to depend on HbA1c and fasting plasma glucose levels as indicators for glycemic control. Increasing evidence suggests that increased postprandial glucose excursion is a strong contributing factor to the development of atherosclerosis and an independent risk factor for CVD in patients with or without diabetes. Glycemic excursions could exert their effects through oxidative stress, endothelial dysfunction, or formation of advanced glycation end-products. Several controlled interventional clinical trials have shown that treating postprandial hyperglycemia may have a beneficial effect on the endothelium and may reduce cardiovascular events. It is recommended that postprandial hyperglycemia be considered an important cardiovascular risk factor corresponding to other well known CV risk factors and should be monitored and managed properly.
Atherosclerosis ; Cardiovascular Diseases ; Diabetes Mellitus ; Endothelium ; Fasting ; Glucose ; Humans ; Hyperglycemia ; Oxidative Stress ; Plasma ; Risk Factors

BACKGROUND: Diabetes is characterized by chronic hyperglycemia, which can increase reactive oxygen species (ROS) production by the mitochondrial electron transport chain. The formation of ROS induces oxidative stress and activates oxidative damage-inducing genes in cells. No research has been published on oxidative damage-related extracellular superoxide dismutase (EC-SOD) protein levels in human diabetic skin. We investigated the expression of EC-SOD in diabetic skin compared with normal skin tissue in vivo. METHODS: The expression of EC-SOD protein was evaluated by western blotting in 6 diabetic skin tissue samples and 6 normal skin samples. Immunohistochemical staining was also carried out to confirm the EC-SOD expression level in the 6 diabetic skin tissue samples. RESULTS: The western blotting showed significantly lower EC-SOD protein expression in the diabetic skin tissue than in the normal tissue. Immunohistochemical examination of EC-SOD protein expression supported the western blotting analysis. CONCLUSIONS: Diabetic skin tissues express a relatively small amount of EC-SOD protein and may not be protected against oxidative stress. We believe that EC-SOD is related to the altered metabolic state in diabetic skin, which elevates ROS production.
Blotting, Western ; Diabetes Mellitus ; Electron Transport ; Humans ; Hyperglycemia ; Oxidative Stress ; Reactive Oxygen Species ; Skin ; Superoxide Dismutase ; Superoxides

Pancreatic beta-cells are major cells responsible for glucose metabolism in the body. Hyperglycemia is known to be a primary factor in the induction of diabetes mellitus. Glutamate is also an excitatory neurotransmitter in diverse organs. Oxidative stress also plays a pivotal role in the development of diabetes mellitus. However, the effect of hyperglycemia in glutamate uptake in the pancreas is not clear. Furthermore, the relationship between high glucose-induced glutamate uptake and oxidative stress has not been investigated. Therefore, this study was conducted to investigate the effect of high glucose on glutamate uptake in pancreatic beta-cells. In the present study, 25 mM glucose stimulated the glutamate uptake in HIT-15 cells of hamster pancreatic beta-cells. The treatment of 25 mM glucose and 1 mM glutamate also decreased the cell viability in HIT-15 cells. In addition, the treatment of 25 mM glucose induced an increase of lipid peroxide formation. High glucose-induced increase of LPO formation was prevented by the treatment of antioxidants such as N-acetyl-L-cysteine and quercetin. Furthermore, high glucose-induced stimulation of glutamate uptake and decrease of cell viability were also blocked by the treatment of N-acetyl-L-cysteine and quercetin. In conclusion, high glucose stimulated glutamate uptake via oxidative stress in pancreatic beta-cells.
Acetylcysteine ; Animals ; Antioxidants ; Cell Survival ; Cricetinae ; Diabetes Mellitus ; Glucose ; Glutamic Acid ; Hyperglycemia ; Neurotransmitter Agents ; Oxidative Stress ; Pancreas ; Quercetin

Blood sugar levels were measured in patients anesthetized with halothane and compared to those with Thalamonal. The effect of preoperative starvation, surgical and anesthetic tension and postoperative pain on the level of blood sugar were also studied. The results were as follows: 1) None of the patient has showed hypoglycemia of under 60mg% by 10~14 hours of fasting before anesthesia. 2) Preoperative apprehension or anxiety without premedication had not seemed to raise the blood sugar level. 3) At 15 minutes after induction, increase in blood sugar level was remarkable in Thalsmonal group, while it was insignificant in halothane group(p<0.01). 4) At 5 minutes after skin incision, there was again a remarkable increase in blood sugar level in Thalsmonal group and insignificant change in halothane group. 5) At 1 hour after induction, blood sugar level has increased significantly in both group(p<0.01). 6) At 30 minutes after termination of anesthesia, blood sugar levels were significantly high compared to preoperative levels. 7) There was no significant difference in change in blood sugar level between two groups. 8) Conclusively, surgery and/or anesthesia regardless of agents could be stressful enough to cause elevation of blood sugar level but it did not seem to cause clinically significant hyperglycemia because all the blood sugar values obtained from this study were within 60 to 200mg%.
Anesthesia* ; Anesthetics* ; Anxiety ; Blood Glucose* ; Fasting ; Halothane ; Humans ; Hyperglycemia ; Hypoglycemia ; Pain, Postoperative* ; Premedication ; Skin ; Starvation* ; Stress, Psychological*