glycogen and Diabetic-Coma

Topics: Adipose Tissue; Blood Glucose; Cell Membrane Permeability; Cytoplasm; Diabetes Mellitus; Diabetic Coma; Gluconeogenesis; Glucose; Glycogen; Glycolysis; Glycosuria, Renal; Humans; Hyperglycemia; Insulin; Lipid Metabolism; Liver; Mitochondria; Muscles; Pancreas; Pancreatectomy; Proteins; Time Factors

Vacuolization of the renal tubular epithelial cells (the Armanni-Ebstein lesion) associated with diabetic hyperglycemia is usually regarded as an accumulation of glycogen. In a case of death of diabetic coma, the vacuoles were stained strongly for lipids. This observation may have both clinical and therapeutic consequences, and may increase our knowledge of the metabolism in diabetes.

Topics: Diabetic Coma; Fatal Outcome; Female; Glycogen; Humans; Hyperglycemia; Kidney Tubules, Proximal; Lipids; Middle Aged

Topics: Blood Glucose; Diabetic Coma; Diabetic Nephropathies; Glycogen; Humans; Kidney Tubules, Proximal

The significance of ketosis in this syndrome has been evaluated from several viewpoints. With respect to acid-base considerations (pH, anion gap), ketosis was not very significant. However, with respect to sustained hyperglycemia, the combustion of less glucose than normal by the brain is critical and it is likely that ketone body metabolism plays an important role in this regard. This point can be underscored by a quantitative example. First, assume that the maximum rate of new glucose production in a fasted subject is less than 100 g of glucose per day. Second, since the brain will burn 100 g of glucose per day in a non-ketotic subject, it follows that, even in the absence of glucosuria, there will be a net daily consumption of glucose. Since the hyperglycemic individual has only an extra 100 or so g of glucose, it follows that the blood glucose concentration would approach the renal threshold in several days in the absence of ketosis. Recall that this is a minimum estimate because glucose oxidation in other organs and glucosuria will remove an additional quantity of glucose. Hyperglycemia can only be maintained in the absence of glucose intake if there is a reduced rate of glucose metabolism in the brain. The brain can diminish its rate of glucose catabolism by several mechanisms, including a diminished metabolic rate in the brain and/or the consumption of non-glucose fuels (free fatty acids or beta-hydroxybutyrate) by this organ.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acetone; Acidosis; Brain; Diabetic Coma; Glucose; Glycerides; Glycerol; Glycogen; Humans; Hyperglycemia; Hyperglycemic Hyperosmolar Nonketotic Coma; Ketosis; Proteins; Syndrome

Two concepts are advanced to explain some fo the puzzling biochemical features found in nonketotic hyperosmolar diabetic coma. It is firstly suggested that an insulinised liver (reflecting residual beta-cell secretory activity) coexists with a diabetic periphery, thereby inactivating intrahepatic oxidation of incoming free fatty acids, which are directed largly along nonketogenic metabolic pathways such as triglyceride synthesis. This could account for the lack of hyperketonaemia. Secondly, it is hypothesised that within the liver enhanced neoglucogenesis occurs, due to the prevailing portal-vein into ratio of glucagon to insulin, and is mainly responsible for the development of massive hyperglycaemia.

Topics: Animals; Diabetes Mellitus; Diabetic Coma; Fatty Acids, Nonesterified; Glucagon; Glycogen; Humans; Hyperglycemia; Insulin; Islets of Langerhans; Liver; Metabolic Clearance Rate; Osmolar Concentration; Oxidation-Reduction; Rats; Triglycerides

Topics: Animals; Antigens; Blood Glucose; Carbon Dioxide; Chlorides; Diabetes Mellitus, Experimental; Diabetic Coma; Diabetic Ketoacidosis; Disease Models, Animal; Fatty Acids, Nonesterified; Glycogen; Hydrocortisone; Insulin; Ketone Bodies; Liver; Male; Osmolar Concentration; Potassium; Rats; Sodium; Urea

Topics: Adenosine Triphosphate; Anesthetics; Brain; Brain Edema; Cerebral Cortex; Cerebrovascular Circulation; Cerebrovascular Disorders; Coma; Consciousness; Diabetic Coma; Glucose; Glycogen; Hepatic Encephalopathy; Humans; Hypoglycemia; Lactates; Oxygen Consumption; Seizures; Sleep

Topics: Dehydration; Diabetic Coma; Diabetic Ketoacidosis; Fructose; Glucagon; Glucose; Glycogen; Humans; Hypoglycemia; Hypotonic Solutions; Injections, Intravenous; Insulin; Insulin Secretion; Ketone Bodies; Lipid Metabolism; Male; Oxygen Consumption; Potassium; Water; Water-Electrolyte Balance

Topics: Adolescent; Body Weight; Child; Dehydration; Diabetic Coma; Diabetic Ketoacidosis; Drug Therapy; Fluid Therapy; Glycogen; Glycosuria; Humans; Hyperglycemia; Infant; Infant, Newborn; Insulin; Metabolism; Parenteral Nutrition; Water-Electrolyte Balance