Background:Recent international researches in trauma patients have shown that hyperglycemia usually goes along with increased mortality, ventilator time and post-operative complications. The role of blood glucose in trauma prognosis and treatment is a current concern. Objective: To evaluate blood glucose change and the relationship of hyperglycemia to severity of injury in the clinical in multiple trauma patients before operation. Subjects and method: A prospective, descriptive study was conducted at the Emergency Surgery Unit and Post-anesthesia Care Unit, Department of Anesthesia and Recovery, Viet Duc hospital, from March to September/2006. The participants were over 15 years old, multiple trauma patients who were operated within 48 hours after the accident, but they had not been used inotrope, sedatives and operated in other clinical. Results: Hypoglycemia (under 3.5 mmol/l) was seen in 4/926 multiple trauma patients. Three of four were in shock due to severe blood loss, of which 2 patients had breath and cardiac arrest. Both patients died from multi-organ dysfunction immediately and one week after operation. The average blood glucose level of patients with ISS 25-40 and over 40 was significantly higher than those with ISS 16-24. Hyperglycemia had a closely positive association with ISS (r=0.48, p< 0.01). Conclusion: Most of multiple trauma patients have hyperglycemia before operation. Hyperglycemia has a relationship with severity of injury, especially with severity of anatomical injury. 4.1% patients have hypoglycemia which is mainly associative with prolonged shock.
Multiple Trauma/ blood ; surgery ; Hyperglycemia/ pathology ; therapy

Gap junctions play a critical role in electrical synchronization and exchange of small molecules between neighboring cells; connexins are a family of structurally related transmembrane proteins that assemble to form vertebrate gap junctions. Hyperglycemia changes the structure gap junction proteins and their expression, resulting in obstruction of neural regeneration, vascular function and wound healing, and also promoting vascular atherosclerosis. These pathogenic factors would cause diabetic foot ulcers. This article reviews the involvement of connexins in pathogenesis of diabetic foot.
Atherosclerosis ; Connexins ; metabolism ; Diabetic Foot ; pathology ; Gap Junctions ; metabolism ; Humans ; Hyperglycemia ; physiopathology ; Regeneration ; Wound Healing

The prevalence of diabetes mellitus (DM) and associated diseases such as cancers are substantially increasing worldwide. About 80% of the patients with pancreatic cancer have glucose metabolism alterations. This suggests an association between type 2 DM and pancreatic cancer risk and progression. There are hypotheses that show metabolic links between the diseases, due to insulin resistance, hyperglycemia, hyperinsulinemia, low grade chronic inflammation, and alteration in the insulin-insulin-like growth factor axis. The use of diabetes medications can influence the extent of carcinogenesis of the pancreas. This study briefly reviews recent literature on investigation of metabolic link of type 2 DM, risk of carcinogenesis of the pancreas and their association, as well as the current understanding of metabolic pathways implicated in metabolism and cellular growth. The main finding of this review, although there are discrepancies, is that according to most research long-term DM does not raise the risk of pancreatic cancer. The longest duration of DM may reflect hypoinsulinemia due to treatment for hyperglycemia, but recent onset diabetes was associated with increased risk for pancreatic cancer due to hyperinsulinemia and hyperglycemia. In conclusion, the review demonstrates that type 2 DM and the duration of diabetes pose a risk for pancreatic carcinogenesis, and that there is biological link between the diseases.
Diabetes Mellitus, Type 2/complications/epidemiology/metabolism/*pathology ; Humans ; Hyperglycemia/pathology ; Insulin/metabolism ; Insulin Resistance ; Insulin-Like Growth Factor I/metabolism ; Pancreatic Neoplasms/epidemiology/*etiology ; Risk Factors

The mechanism of chorea underlying nonketotic hyperglycemia was controversial. Serial follow up of brain MRI, 99mTc-ECD SPECT, and 18F-FDG PET in conjunction with clinical observation was done to clarify the pathologic localization. From the functional neuroimages, according to the clinical improvement, the relevant pathology was localized on the lentiform nucleus, mainly on the putamen. In caudate, the mismatch between glucose metabolism and blood flow was observed during and after choreoballistic movement which suggested an important cue to understand the pathogenesis of chorea.
Basal Ganglia* ; Brain ; Chorea ; Corpus Striatum ; Cues ; Fluorodeoxyglucose F18 ; Follow-Up Studies* ; Glucose ; Humans ; Hyperglycemia* ; Magnetic Resonance Imaging ; Metabolism ; Pathology* ; Putamen ; Tomography, Emission-Computed, Single-Photon

BACKGROUNDHyperglycemia has been shown to be a powerful predictor of poor outcome after ST-segment elevation myocardial infarction (STEMI). This study aimed to evaluate the effect of admission glucose on microvascular flow after successful primary percutaneous coronary intervention (PCI) in patients with STEMI.

METHODSSuccessful primary PCI was performed in 267 patients with STEMI. The maximum ST elevation of single electrocardiogram (ECG) lead before and 60 minutes after PCI was measured, and patients were then divided into 3 groups according to the degree of ST-segment resolution (STR): absent (<30%), partial (30% to 70%) or complete (> or =70%).

RESULTSOf the 267 patients, 48 (18.0%) had absent STR, 137 (51.3%) experienced partial STR, and 82 (30.7%) had complete STR. The degree of STR decreased with increasing admission glucose levels (P=0.032), and patients with hyperglycemia (serum glucose level > or =11 mmol/L) were more likely to have absent STR (P=0.001). Moreover,hyperglycemia was an independent predictor of incomplete STR (odds ratio, 1.870; 95% confidence interval, 1.038 to 3.371, P=0.037).

CONCLUSIONSHyperglycemia on admission is associated with abnormal coronary microvascular reperfusion in patients with STEMI after successful primary PCI, which may contribute, at least in part, to the poor outcomes in these patients.

Adult ; Aged ; Angioplasty, Balloon, Coronary ; methods ; Electrocardiography ; Female ; Glucose ; metabolism ; Humans ; Hyperglycemia ; blood ; pathology ; physiopathology ; Male ; Middle Aged ; Myocardial Infarction ; blood ; physiopathology ; therapy ; Odds Ratio

This animal experiment was aimed at the questions whether high glucose concentration inhibits insulin secretion (glucose toxicity, GT) of beta-cell of islets from SHR and Wistar-Kyoto (WKY) rat and whether adrenomedullin (AM) enhances GT. Ten 6-week-old SHRs (test group) and ten 10-week-old Wistar-Kyoto rats (WKY) (control group) were selected. RAMI-1640 medium containing 5.6 mM glucose (normal glucose group) and 20 mM glucose (high glucose group) were applied. Various concentrations of AM (0, 10(-8), 10(-7), 10(-6) M) and RPMI-1640 medium containing high glucose were mixed, respectively. The isolated islets from rats were put into 12-well plates (90 islets/well). The islets were incubated in RAMI-1640 medium containing normal or high glucose for one hour. Then the supernatants from both incubations were determined by RIA for insulin. In SHR group, the insulin concentration in supernatants gained from high glucose group without AM was lower than that from normal glucose group (19.9+/-6.6 vs 60.9+/-33.6 mU/L, P<0.05). With the increment of the concentration of AM, insulin concentration in supernatants from islets incubated in high glucose and various concentrations of AM tended to be low further (19.9+/-6.6 vs 22.2+/-8.0 vs 21.5+/-5.6 vs 17.9+/-3.6 mU/L). The changing tendency in control group was the same as in SHR group. When the islets were incubated in normal glucose and high glucose medium, the insulin concentration in supernatant significantly decreased in SHR group compared with that in control group (P<0.01). The insulin secretion was inhibited by high glucose in beta-cell of islets from SHR and WKY. The results suggest GT to beta-cell of islets from SHR and WKY. AM tended to inhibit insulin secretion in a dose-dependent manner in beta-cell of islets from SHR and WKY. The inhibition of insulin secretion caused by high glucose in beta-cell of islets from SHR was more remarkable than from WKY. This may be related to secretion dysfunction in beta-cell of islets from SHR.
Adrenomedullin ; Animals ; Blood Glucose ; metabolism ; Cells, Cultured ; Female ; Glucose ; pharmacology ; Hyperglycemia ; blood ; Hypertension ; metabolism ; pathology ; Insulin ; secretion ; Insulin Resistance ; Islets of Langerhans ; drug effects ; pathology ; secretion ; Male ; Peptides ; pharmacology ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY

OBJECTIVETo investigate the relationship between insulin resistance and carotid atherosclerosis in patients with potential hyperglycemia.

METHODSA total of 221 patients were recruited among those with potential hyperglycemia. All participants underwent physical examination, medical history interview, and 75 g oral glucose tolerance test. Venous blood was sampled for measurement of insulin and cholesterol levels. The intima-media thickness (IMT) in bilateral common carotid arteries was observed by B-mode ultrasound. Insulin resistance index was calculated by homeostasis model assessment (HOMA-IR). Subjects were stratified in quintiles according to HOMA-IR values. Risk factors and atherosclerotic parameters were analyzed.

RESULTSWith HOMA-IR value increase, incidence of impaired glucose tolerance, diabetes mellitus, hypertension, and coronary artery disease increased, the levels of triglyceride (TG), low density lipoprotein cholesterol (LDL-C), fasting plasma glucose, 2 hour plasma glucose, and fasting insulin increased as well, while the level of high density lipoprotein cholesterol (HDL-C) decreased. Meanwhile, all atherosclerotic parameters increased. Multivariate regression analysis showed that TG, total cholesterol, HDL-C, LDL-C levels, and ln(HOMA-IR) were related to IMT, hence were risk factors for IMT increase.

CONCLUSIONInsulin resistance is implicated in atherogenesis.

Aged ; Blood Glucose ; metabolism ; Carotid Artery Diseases ; blood ; etiology ; Carotid Artery, Common ; pathology ; ultrastructure ; Female ; Glucose Tolerance Test ; Humans ; Hyperglycemia ; blood ; Insulin ; blood ; Insulin Resistance ; Lipids ; blood ; Male ; Middle Aged ; Risk Factors ; Tunica Media ; pathology

BACKGROUNDEarly intensive insulin therapies in newly diagnosed type 2 diabetic patients may improve beta-cell function and yield prolonged glycemic remissions. This study was performed to evaluate the relationship between the glycemic remission and beta-cell function and assess the variables predictive of long-term near-normoglycemic remission.

METHODSEighty-four newly diagnosed type 2 diabetic patients were treated with 2-week continuous subcutaneous insulin infusion (CSII) and followed up longitudinally. Intravenous glucose tolerance tests (IVGTTs) were performed, and blood glucose, hemoglobin A1c (HbA1c) and insulin were measured at baseline, after CSII and at 2-year visit. The patients who maintained glycemic control for two years were defined as the remission group and those who relapsed before the 2-year visit were the non-remission group.

RESULTSThe duration to be diagnosed of the patients (from the time that patients began to have diabetic symptoms until diagnosis) in the remission group was shorter than that in the non-remission group (1.00 month vs 4.38 months, P = 0.040). The increase of the acute insulin response (AIR) was maintained after 2 years in the remission group compared with AIR measured immediately after intervention (413.05 pmol*L(-1)*min(-1) vs 408.99 pmol*L(-1)*min(-1), P = 0.820). While AIR in the non-remission group significantly declined (74.71 pmol*L(-1)*min(-1) vs 335.64 pmol*L(-1)*min(-1), P = 0.030). Cox model showed that a shorter duration to be diagnosed positively affected the duration of near-nomoglycemic remission with an odds ratio (OR) 1.019, P = 0.038, while fasting plasma glucose (FPG) and post-breakfast plasma glucose (PPG) after CSII were the risk factors (OR 1.397, P = 0.024 and OR 1.187, P = 0.035, respectively).

CONCLUSIONThe near-normoglycemic remission is closely associated with long-term maintenance of beta-cell function and occurs more commonly in patients with shorter duration to be diagnosed and better glycemic control during CSII.

Adult ; Aged ; Diabetes Mellitus, Type 2 ; blood ; drug therapy ; pathology ; Female ; Follow-Up Studies ; Humans ; Hyperglycemia ; pathology ; Hypoglycemic Agents ; therapeutic use ; Insulin ; therapeutic use ; Kaplan-Meier Estimate ; Male ; Middle Aged ; Young Adult

This article reviews the clinical and experimental researches on cognitive impairment related to diabetes in the recent decade. Most clinical studies indicate that the cognitive impairment in patients with type 1 diabetes mellitus is related to recurrent hypoglycemia closely. There is little research about whether or not hyperglycemia is related to cognitive impairment in patients with type 1 diabetes mellitus. Most studies indicate that the cognitive impairment in type 2 diabetes involves multiple factors through multiple mechanisms, including blood glucose, blood lipid, blood pressure, level of insulin, medication, chronic complication, etc. But, there has been no large-scale, multi-center, randomized controlled clinical trial in China recently. And what is more, some problems exist in this field of research, such as the lack of golden criterion of cognitive function measurement, different population of studied objects, and incomprehensive handling of confounding factors. Experimental studies found that hippocampal long-term potentiation (LTP) was impaired, which were manifested by impairment of spatial memory and decreased expression of LTP, but it's relation to hyperglycemia, the duration of diabetes, learning and memory has always been differently reported by different researches. Thus, there are a lot of unknown things to be explored and studied in order to clarify its mechanism. TCM has abundant clinical experience in treating cerebral disease with medicine that enforces the kidney and promotes wit. However, there has been no research on treating diabetic cognitive impairment, which requires work to be done actively and TCM to be put into full play, in order to improve the treatment of diabetes and enhance living quality of patients.
Animals ; Cognition Disorders ; etiology ; pathology ; physiopathology ; Diabetes Mellitus, Experimental ; pathology ; physiopathology ; psychology ; Diabetes Mellitus, Type 1 ; pathology ; physiopathology ; psychology ; Diabetes Mellitus, Type 2 ; pathology ; physiopathology ; psychology ; Drugs, Chinese Herbal ; therapeutic use ; Hippocampus ; pathology ; physiopathology ; Humans ; Hyperglycemia ; complications ; Hypoglycemia ; complications ; Long-Term Potentiation ; Neuronal Plasticity

Prolonged administration of anterior hypophyseal, adrenocortical, or thyroid hormones is known to cause degeneration, degranulation and necrosis of the beta-cells in the Langerhans islets of the pancreas. However, the effects of extirpation of these endocrine glands upon the Langerhans islets has not been reported, a1though it is known that removal of any of these glands bring about hypoglycemia, decreased tissue uptake of glucose, and increased tissue sensitivity to insulin. The present investigation is studies of the morphologic alterations of the beta-cells in the Langerhans islets following hypophysectomy, adrenalectomy, or thyroidectomy in rats. Hypophysectomy, adrenalectomy, and thyroidectomy, all induce similar morphologic alterations in the beta-cells of the islets. These consist of increased beta-cell population, the accumlnation of beta-granules, and atrophy of the individual betacell. Therefore, these changes are considered to be not specific following the withdrawal of specific hormones but a common effect of the hypoglycemia due to removal of the hypophysis, adrenals, or thyroid glands. A similar common degeneration of the beta-cells due to hyperglycemia occurs when hormones of these endocrine glands are given excessively.
Adrenal Cortex Hormones/physiology ; Adrenalectomy* ; Animal ; Atrophy/etiology ; Blood Glucose ; Diabetes Mellitus/etiology ; Glycogen/metabolism ; Hyperglycemia/etiology ; Hypoglycemia/etiology ; Hypophysectomy* ; Insulin/secretion ; Islets of Langerhans/pathology* ; Liver Glycogen/metabolism ; Muscles/metabolism ; Myocardium/metabolism ; Necrosis/etiology ; Rats ; Staining and Labeling ; Thyroidectomy* ; Thyroxine/physiology