الفهرس 
Normal glucose metabolismOnly 14 pages are availabe for public view
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Abstract
Glucose metabolism is a remarkable process that provides glucose to the body for energy and a constant source of glucose to the brain while preventing hyperglycemia. the body maintains strict blood glucose levels through a remarkable network between the pancreas, liver, adipose tissue, muscle, and brain. Glucose production is governed by the liver, which can generate free glucose from hepatic glycogen stores and de novo through gluconeogenesis. Specific glucose transporters found on every cell of the body administer glucose utilization. Each transporter works with a different serum glucose level.
Diabetic ketoacidosis (DKA) and the hyperosmolar hyperglycemic state (HHS) are the two most serious acute metabolic complications of diabetes. The triad of uncontrolled hyperglycemia, metabolic acidosis, and increased total body ketone concentration characterizes DKA. Hyperglycemic hyperosmolar state is characterized by severe hyperglycemia, hyperosmolality, and dehydration in the absence of significant ketoacidosis. These metabolic derangements result from the combination of absolute or relative insulin deficiency and an increase in counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). Most patients with DKA have autoimmune type 1 diabetes; however, patients with type2 diabetes are also at risk during the catabolic stress of acute illness such as trauma, surgery, or infections.
Stress hyperglycemia occurs in response to the chemical, hormonal and metabolic changes in the body that occur during stress. Thus, it can be considered as a physiological adaptation during the fight and flight response.
During acute illness growth hormone starts to increase causing lipolysis and inhibiting lipid uptake by cells. T3and T4 decrease during acute illness while TSH remains normal or low normal. Cortisol increases during acute illness causing energy production and shift of energy to vital organs and delays anabolism.
Alteration of glucose metabolism occurs under stress as in trauma, burn, major surgery, myocardial infarction, cerebrovascular accidents, sepsis and acute pancreatitis. Stress hyperglycemia increases sympathetic activity, counter-regulatory hormones and pro-inflammatory cytokines.
In myocardial infarction, stress hyperglycemia is reported to cause thrombosis and increase platelet aggregation. Moreover, hyperglycemia produces rise in inflammatory immune reactions. Oxidative stress process is supported by hyperglycemia with the production of free radicals and activation of coagulation that lead to impaired endothelial function and inflammation.
In cerebro-vascular stroke, insulin resistance is a risk factor for onset of stroke acting through thrombophilia, endothelial dysfunction, and inflammation, and increased free fatty acids. In evaluation of acute infarction, the ischemic time seems to be faster in patients with diabetes or grave hyperglycemia.
In burns, hyperglycemia arises from glycogen breakdown and gluconeogenesis and starts to appear after 6 hours from injury and reaches its peak by the fourth day of injury. Burns cause hormonal changes as increased epinephrine, norepinephrine, glucagon, cortisol and GH which lead to increased hepatic outcome of glucose by 50% of healthy person. Burns inhibit normal effect of insulin on glucose metabolism by catabolic breakdown and glucose release seen during the injury. Patients remain in the hypermetabolic and catabolic state until wound closure. Hyperglycemia remains for 6 months after injury while the effect on insulin remains for 3 years after injury.
In trauma, injury causes immediate release of catecholamines in the blood. Stress response to trauma causes a hypermetabolic state characterized by protein and fat catabolism, negative nitrogen balance, hyperglycemia and insulin resistance.
Surgical patients who undergo elective and urgent surgery may have unrecognized diabetes or develop stress hyperglycemia that contributes to increased postoperative complications. Patients with hospital-induced stress hyperglycemia have a greater risk than those with pre-existing diabetes.