glycogen and Potassium-Deficiency

Topics: Animals; Biological Transport, Active; Calcium Metabolism Disorders; Glycogen; Humans; Hydrogen-Ion Concentration; Hypernatremia; Hypokalemia; Hyponatremia; Magnesium; Membrane Potentials; Muscles; Myoglobinuria; Neuromuscular Diseases; Phosphorus Metabolism Disorders; Potassium Deficiency; Water-Electrolyte Imbalance

Topics: Animals; Carbohydrate Metabolism; Diazoxide; Glucocorticoids; Glycogen; Glycolysis; Humans; Hyperglycemia; Insulin; Insulin Secretion; Potassium; Potassium Deficiency; Rats; Sodium; Sulfonamides; Water-Electrolyte Balance

In order to evaluate the potential role of hyperkalemia and metabolic acidosis on the disturbances of carbohydrate metabolism normally seen in uremia, a specific model of acute uremia devoid of hyperkalemia and severe metabolic acidosis was chosen. Therefore, rats were deprived of potassium prior to induction of acute uremia. Potassium depletion caused a significant decrease of muscle and liver glycogen due to activation of phosphorylase kinase, whereas glycogen concentration in heart muscle was unchanged and elevated in the kidney of sham-operated and ureter-ligated animals. In contrast, glucose concentrations were enhanced in the liver and the kidney, unchanged in heart muscle and decreased in skeletal muscle. We conclude that carbohydrate abnormalities occur in acute uremia despite normokalemia and mild metabolic acidosis. Furthermore, acute uremia accompanied by prior potassium depletion results in no net effect on cardiac glycogen metabolism but stimulates glycogenolysis in both skeletal muscle and the liver.

Topics: Animals; Glucose; Glycogen; Kidney; Liver; Liver Glycogen; Male; Muscles; Potassium; Potassium Deficiency; Rats; Rats, Inbred Strains; Uremia

Carbohydrate metabolism was examined in different organs of rats with dietary potassium deprivation for 4 weeks. Thereafter, a 24- or 48-hour starvation period caused a significant decrease of skeletal muscle and liver glycogen content in K+-depleted (KD) rats, whereas kidney glycogen concentration increased and heart glycogen remained unchanged. In contrast, liver glucose concentration was significantly higher in starved KD animals without changes in muscle, heart, and kidney glucose concentrations. Potassium depletion caused a highly significant decrease of plasma and muscle potassium concentrations, metabolic alkalosis, reduced plasma insulin, and increased creatine phosphokinase levels. Blood lactate, pyruvate, and oxoglutarate levels were significantly enhanced in fasted KD rats, whereas blood citrate, beta-hydroxybutyrate, and glucose concentrations were unchanged. Blood acetoacetate level, however, was significantly reduced following potassium depletion. Therefore, beta-hydroxybutyrate/acetoacetate ratio increased significantly, whereas lactate/pyruvate ratio was not influenced. Our results clearly indicate impaired carbohydrate metabolism in potassium-depleted rats.

Topics: Acetoacetates; Animals; Blood Glucose; Carbohydrate Metabolism; Female; Glucose; Glycogen; Insulin; Ketoglutaric Acids; Kidney; Lactates; Lactic Acid; Liver; Muscles; Myocardium; Potassium; Potassium Deficiency; Pyruvates; Pyruvic Acid; Rats; Rats, Inbred Strains; Starvation

Topics: Adolescent; Biopsy; Glycogen; Humans; Male; Muscles; Paralyses, Familial Periodic; Pedigree; Potassium Deficiency

Diuretic therapy is the most common cause of potassium deficiency. Although the extent of potassium deficiency usually does not exceed 200 or 300 mEq, under appropriate circumstances such modest deficiency may have important consequences. Factors that tend to increase the incidence or severity of potassium deficiency in patients who take diuretics include high salt diets, large urine volumes, metabolic alkalosis, increased aldosterone production, and the simultaneous use of two diuretics that act on different sites in the renal tubule. There are many serious complications of potassium deficiency, including cardiac arrhythmias, muscle weakness, rhabdomyolysis, glucose intolerance, and several complications that result directly from increased ammonia production, such as protein and nitrogen wasting and hepatic coma. Emphasized herein are those conditions that impose potential danger in patients with mild hypokalemia. Important factors that identify specific causes of potassium deficiency and its treatment are discussed briefly.

Topics: Animals; Arrhythmias, Cardiac; Cardiovascular System; Diuretics; Glycogen; Homeostasis; Humans; Hypokalemia; Muscle, Smooth; Muscles; Potassium Deficiency; Proteins

Potassium deficiency occurs in several conditions and is reported to cause muscle weakness and rhabdomyolysis. The mechanisms by which potassium deficiency cause muscle disease remain unknown, but the primary purpose of the present study was to determine whether abnormal muscle glycogen metabolism causes muscle weakness, as suggested by previous work. We monitored the natural history of potassium deficiency in two groups of dogs, one of which also received deoxycorticosterone acetate (DOCA), an agent commonly used in other studies to accelerate potassium loss. Group I dogs on potassium-free diet alone showed a 41% decrease in muscle potassium, no change in serum CO2, creatine kinase (CK), or muscle phosphorylase activity and only mild histopathologic abnormalities before death, after 198 +/- 42 days on the diet (mean +/- S.D.). In contrast, group II dogs on the same diet plus DOCA developed clinically similar severe weakness and died more rapidly than group I, 37 +/- 7 days (p less than 0.03). DOCA dogs showed a more rapid decrease in muscle potassium to the same level as group I, a 37% increase in serum CO2, an increase in serum CK to 1060 to 2775 IU/ml, a 23% decrease in muscle phosphorylase activity, and severe muscle histopathology, including rhabdomyolysis. Neither group showed any change in body weight, electromyogram (EMG), muscle glycogen concentration, glycogen synthetase activity, serum or muscle magnesium or phosphorus, or serum T3 or T4. In conclusion, dietary potassium deficiency in dogs causes severe weakness and death without causing rhabdomyolysis or abnormal muscle glycogen metabolism. Adding DOCA to the potassium-free diet creates a different model characterized by rapid clinical deterioration and rhabdomyolysis.

Topics: Animals; Carbon Dioxide; Creatine Kinase; Desoxycorticosterone; Dogs; Electromyography; Glycogen; Magnesium; Muscles; Phosphates; Potassium; Potassium Deficiency; Rhabdomyolysis

We have presented evidence that in an in vitro system, glycogenolysis and glycolysis function normally at potassium levels far below those observed in muscle cell water of severely deficient dogs. We suggest that a functional impairment of glycogenolysis or glycolysis is unlikely to be a mechanism by which potassium deficiency leads to rhabdomyolysis.

Topics: Animals; Dogs; Energy Metabolism; Glycogen; Glycolysis; Lactates; Muscles; Muscular Diseases; Physical Exertion; Potassium; Potassium Deficiency

Topics: Alkalosis; Animals; Blood Glucose; Diazoxide; Epinephrine; Glucagon; Glycogen; Heptoses; Hydrocortisone; Hypokalemia; Liver Glycogen; Male; Muscles; Potassium Deficiency; Rats

Topics: Animals; Bicarbonates; Diabetes Mellitus, Experimental; Glucose-6-Phosphatase; Glycogen; Insulin; Kidney; Liver; Muscles; Potassium Deficiency

Topics: Acidosis; Adolescent; Alkalosis; Child; Dehydration; Glycogen; Humans; Hyponatremia; Infant; Infant, Newborn; Metabolism; Parenteral Nutrition; Physiology; Potassium; Potassium Deficiency

Topics: Alanine; Animals; Carbohydrates; Glycogen; Glycogenolysis; Hypokalemia; Liver; Liver Glycogen; Potassium; Potassium Deficiency; Rats