Fatty Liver ; metabolism ; Glucose ; metabolism ; Humans ; Hyperglycemia ; metabolism ; Lipoproteins ; metabolism ; Metabolic Syndrome ; metabolism

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

Growth hormone (GH) is important for promotion of somatic growth and the regulation of substrate metabolism. Metabolic action of GH occurs in multiple tissues including the liver, muscle, fat and pancreas either directly or indirectly through insulin-like growth factor 1. The diabetogenic action of GH has been well-described in previous in vivo studies. In this paper, we review the metabolic effects of GH on peripheral tissues focusing on glucose metabolism and insulin resistance, and discuss results from human studies on the long-term effects of GH administration on insulin resistance and hyperglycemia.
Glucose* ; Growth Hormone* ; Humans* ; Hyperglycemia ; Insulin Resistance* ; Insulin* ; Liver ; Metabolism* ; Pancreas

BACKGROUND: Although impaired endothelial function is well known in patients with diabetes mellitus, the precise mechanism and the factors that contribute to this dysfunction remain to be clarified. We examined the effect of acute hyperglycemia on patients with impaired glucose metabolism in vivo by plethysmography. METHODS: Seven patients with diabetes mellitus or impaired glucose metabolism were studied. In each patient, endothelial function was examined in the fasting state and at two levels of hyperglycemia, which were achieved by the infusion of glucose, insulin, and somatostatin. Forearm blood flow was measured while acetylcholine was infused in increasing concentrations(7.5, 15, and 30 microgram/min) through the brachial artery. RESULTS: Glucose concentrations increased accordingly at each stage, from 135.3+/-18.4 mg/dl at stage 1(the fasting state), to 239.0+/-15.2 mg/dl at stage 2(the first level of hyperglycemia), and to 378.3+/-25.3 at stage 3 (the second level of hyperglycemia) [p<0.01]. Maximal acetylcholine-dependent vasodilation achieved by infusion of acetylcholine at 30 microgram/min was significantly aftenuated during stages 2 and 3 compared with stage 1(p<0.05 by AVOVA; forearm blood flow ratio was 2.87+/-0.18 and 2.56+/-0.14 versus 3.58+/-0.21, respectively). This was also evident during the infusion of 15 microgram/min and 7.5 microgram/min of acetylcholine. CONCLUSIONS: Endothelium-dependent vasodilation is significantly aftenuated by acute hyperglycemia in patients with diabetes mellitus or impaired glucose metabolism. Our findings suggest that elevated glucose may contribute to the endothelial dysfunction observed in patients with diabetes mellitus or impaired glucose metabolism.
Acetylcholine ; Brachial Artery ; Diabetes Mellitus* ; Endothelium ; Fasting ; Forearm ; Glucose* ; Humans ; Hyperglycemia* ; Insulin ; Metabolism* ; Plethysmography ; Somatostatin ; Vasodilation*

Cardiovascular diseases account for approximately 80% of deaths among individuals with diabetes mellitus, with diabetic cardiomyopathy as the major diabetic cardiovascular complication. Hyperglycemia is a symptom that abnormally activates multiple downstream pathways and contributes to cardiac hypertrophy, fibrosis, apoptosis, and other pathophysiological changes. Although glycemic control has long been at the center of diabetes therapy, multicenter randomized clinical studies have revealed that intensive glycemic control fails to reduce heart failure-associated hospitalization and mortality in patients with diabetes. This finding indicates that hyperglycemic stress persists in the cardiovascular system of patients with diabetes even if blood glucose level is tightly controlled to the normal level. This process is now referred to as hyperglycemic memory (HGM) phenomenon. We briefly reviewed herein the current advances that have been achieved in research on the underlying mechanisms of HGM in diabetic cardiomyopathy.
Cardiovascular Diseases ; Diabetes Complications ; Diabetes Mellitus ; Diabetic Cardiomyopathies/etiology* ; Humans ; Hyperglycemia/metabolism* ; Multicenter Studies as Topic

Stress induced hyperglycemia is the body's protect response against strong (patho-physiological and/or psychological) stress, sometimes the blood glucose level is too high due to out of the body's adjustment. Renal glucose threshold (about 9 mmol/L) is a window of glucose leak from capillary to interstitial tissue. It is important to keep blood glucose level < 9 mmol/L, for reducing vascular sclerosis as well as organs hypoperfusion, meanwhile pay attention to preventing more dangerous hypoglycemia. Glucose, as the main energy substrate, should be daily supply and its metabolism should be monitored. We used to talk "nutritional support". Support is conform the physiological ability of host, but therapy is to coordinate and change pathophysiology. So, nutritional support is not equal to nutritional therapy. For critical ill patients, we need to emphasize "nutritional therapy", i.e, do not give nutritional treatment without metabolic monitoring, make up for deficiencies and avoid metabolites overloading, rational adjustment to protect and coordinate organs function.
Humans ; Blood Glucose/metabolism* ; Critical Illness/therapy* ; Hyperglycemia/therapy* ; Nutritional Support ; Glucose

Hyperglycemia can result in severe adverse effects on the body. The mortality and morbidity of surgery are increased significantly in diabetic patients. The surgical stress-related hyperglycemia and insulin resistance can also produce the same adverse consequences. The metabolic state of the surgical patients, anesthesia method, glucose infusion, stress-induced neuroendocrine responses and insulin resistance can affect the perioperative blood glucose levels, resulting in poor clinical outcomes. The relationship between tight glycemic control and reducing post-operative mortality and morbidity is not clear. It's necessary to control blood sugar level during the perioperative period but the ideal state of glycemic control still needs a mult-center clinical trial evidence. It is generally believed that perioperative blood glucose level should be controlled below 10 mmol/L. The efficacy and safety of tight glycemic control needs further study.
Blood Glucose ; metabolism ; Humans ; Hyperglycemia ; etiology ; therapy ; Hypoglycemia ; prevention & control ; Perioperative Care

To explore the effects of serum insulin on the expression of ChREBP, ACC and FAS in vivo, KKAy mice which were characterized with high levels of both serum insulin and glucose and DIO mice which were characterized with high serum insulin level alone were utilized, separately. The age-matched C57BL/6J mice fed with standard chow were used as normal control (Con). Expressions of hepatic ChREBP, ACC and FAS were detected by Western blotting. As the results, in KKAy mice, a positive correlation between the levels of serum insulin and glucose (r = 0.902, P < 0.000), as well as between the levels of serum insulin and TG (r = 0.732, P < 0.000), was observed. Meanwhile, the expressions of hepatic ChREBP, ACC and FAS increased significantly and accompanied with its hyperinsulinemia and hyperglycemia, separately. In DIO mice, correlation between the levels of serum insulin and TG (r = 0.722, P < 0.001) also showed positive, and the expressions of hepatic ChREBP, ACC and FAS increased significantly and also accompanied with its hyperinsulinemia. However, their blood glucose values were almost normal. These demonstrated that hyperinsulinemia may cause glycolipid metabolic disorders by up-regulating the expression of ChREBP in vivo.
Animals ; Blood Glucose ; metabolism ; Hyperglycemia ; metabolism ; Hyperinsulinism ; metabolism ; Insulin ; blood ; Liver ; metabolism ; Mice ; Mice, Inbred C57BL ; Nuclear Proteins ; metabolism ; Transcription Factors ; metabolism

To investigate the influence of hyperglycemia on ischemic brain damage, we measured brain ATP, lactate and malondialdehyde (MDA) levels in global cerebral ischemic models of Wistar rats. We induced global cerebral ischemia by the 4-vessel occlusion method. After 30 or 60 min of occlusion, and after 30 min of reperfusion, we measured brain ATP, lactate and MDA levels. During the ischemic period, brain ATP levels decreased to 30-70% of sham groups both in normoglycemic and hyperglycemic groups. But during the reperfusion period, the recovery rate of ATP levels was significantly lower in the hyperglycemic than in the normoglycemic groups (p less than 0.05). After 60 min of global ischemia, brain lactate increased much more in the hyperglycemic than in the normoglycemic group, and, during reperfusion, was washed out slowly in the hyperglycemic group. The MDA level, a parameter of lipid peroxidation, increased more in the hyperglycemic group than in the normoglycemic group during reperfusion periods (p less than 0.05). We conclude that hyperglycemia increases lactate accumulation, delays the recovery of energy metabolism, and enhances the lipid peroxidation in the transient global ischemia of rat brain. These findings may suggest the harmfulness of hyperglycemia in clinical cerebral ischemia.
3,4-Methylenedioxyamphetamine/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Hyperglycemia/complications/*metabolism ; Ischemic Attack, Transient/complications/*metabolism ; Lactates/metabolism ; *Lipid Peroxidation ; Male ; Rats ; Rats, Wistar

Metabolic syndrome is a cluster of diseases that include central obesity, hyperglycemia, dyslipidemia, and hypertension. Metabolic syndrome is a risk factor for type 2 diabetes and cardiovascular disease and the key pathophysiology is insulin resistance. Thyroid hormone has been known to play an important role in lipid and glucose metabolism and hypothyroidism causes atherosclerosis and insulin resistance. A number of clinical studies reported overt or subclinical hypothyroidism is associated with metabolic syndrome, and there has been the efforts elucidating a link between these two diseases. Recently, thyroid hormone analogue or thyromimetics has been developed to improve metabolic syndrome including dyslipidemia. I reviewed recently reported mechanisms explaining the association between hypothyroidism and metabolic syndrome, and current status of the development of thyromimetics was also reviewed.
Atherosclerosis ; Cardiovascular Diseases ; Dyslipidemias ; Glucose ; Hyperglycemia ; Hypertension ; Hypothyroidism* ; Insulin Resistance ; Metabolism ; Obesity, Abdominal ; Risk Factors ; Thyroid Gland