glycogen and Asthma

High dose glucocorticoid may induce a significant myopathy with loss of thick myofilament from muscle, particularly if administered in conjunction with depolarizing drugs. Remarkably, the effect of chronic low dose glucocorticoid in muscle is vastly different, although it may induce changes in muscle glycogen metabolism as evidenced in animal experimental trials. However, there is no clear confirmation that these changes could develop similarly in patients. We evaluate clinical, functional, histological and metabolic muscle changes during chronic low-dose glucocorticoid treatment in 11 asthmatic patients. Remarkably, these patients did not develop clinical symptoms of myopathy nor significant muscle weakness or morphological changes in muscle histology. However, glycogen concentration and the activity of the main regulatory enzymes of glycogen metabolism, aldolase and creatine kinase were modified in comparison with controls. An increase in the synthesis and muscle cell deposition of glycogen and a decrease in the muscle glycogen degradation process have been suggested. These changes were not related with malnutrition. There was not correlation between histological and biochemical changes. We conclude that chronic treatment with glucocorticoid causes clear changes in glycogen metabolism in the skeletal muscle, resulting in glycogen muscle storage. The significance of these biochemical changes is unknown, but it can be well an associated phenomenon with glucocorticoid treatment.

Topics: Adult; Aged; Alanine Transaminase; Aspartate Aminotransferases; Asthma; Creatine Kinase; Energy Metabolism; Female; Fructose-Bisphosphate Aldolase; Glycogen; Glycogen Synthase; Humans; Isoenzymes; L-Lactate Dehydrogenase; Male; Middle Aged; Muscle Contraction; Muscle Proteins; Muscles; Phosphorylases; Prednisone

Forty-six patients with bronchial asthma and preasthma and 6 normal persons were examined before and after graded exercise. Measurements were made of changes in glycogenolysis in peripheral lymphocytes, in blood plasma osmolarity, external respiration function ad diffusion capacity of the lungs, and of blood and sputum eosinophilia. Some of the patients were also examined for blood content of catecholamines. The group of patients with asthma of effort showed, in contrast to those without that illness, the signs of allergic inflammation of the distal parts of the bronchi and a direct correlation between changes in plasma osmolarity and glycogen content in lymphocytes, a decrease in the grade of the glycogenolytic response to adrenaline after exercise. It seems likely that in the pathogenesis of asthma of effort, of certain importance is inadequate reaction of the adrenoreceptor apparatus of the cells to the changes in the microenvironment provoked by exercise, which is manifested by the lack of the rise of beta-adrenoreactivity.

Topics: Asthma; Asthma, Exercise-Induced; Glycogen; Humans; Osmolar Concentration; Respiratory Function Tests

Leukosuspensions from 217 patients with bronchial asthma and 73 normal subjects were examined for alterations in the levels of cAMP and cGMP under the effect of incubation with adrenaline, propranolol, acetylcholine. A study was also made of the activity of cAMP PDE and glycogen metabolism. Simultaneous measurement of the basal and stimulated levels of cyclic nucleotides and their ratios revealed a decrease in cell adrenoreactivity and a rise in cholinoreactivity. Variation of the beta-adrenoblocking action of propranolol typical for the atopic mechanism of bronchial asthma was demonstrated. Comparison of the adrenodependent glycogenolysis and alterations in the cAMP level, analysis of the action of analgin on these characteristics allowed the conclusion about the secondary nature of alterations in cAMP metabolism dependent on the features of prostaglandin metabolism. A significant decrease in the adrenodependent glycogenolysis was revealed in lymphocytes, with that decrease induced by drug, dust and pollen allergens. It was demonstrated that in verified viral infection, cAMP PDE was significantly reduced.

Topics: 3',5'-Cyclic-AMP Phosphodiesterases; Asthma; Cyclic AMP; Cyclic GMP; Glycogen; Humans; In Vitro Techniques; Leukocytes

Topics: Asthma; Epinephrine; Glycogen; Humans; Leukocytes

Topics: Adrenergic beta-Agonists; Adrenergic beta-Antagonists; Asthma; Epinephrine; Glycogen; Humans; Lymphocytes; Propranolol

Topics: Asthma; Cyclic AMP; Cyclic GMP; Glycogen; Humans; Leukocytes

Topics: Adolescent; Adult; Asthma; Female; Glycogen; Histocytochemistry; Humans; Male; Middle Aged; Neutrophils; Peroxidase

Decreased beta adrenergic regulation of cyclic adenosine monophosphate (cAMP) in lymphocytes has been described in asthma. We investigated adrenergic stimulation of glycogenolysis and responses to prostaglandin E1 (PGE1). Lymphocytes from 24 normal and 24 mild asthmatic subjects who had no drugs for at least 2 weeks were separated on Ficoll-hypaque and incubated in medium 199 with Hepes buffer. Beta adrenergic stimulation of cAMP and glycogenolysis was reduced in the asthmatics (p less than 0.05). PGE produced less of a rise in cAMP in asthmatics than in normals, but the difference was not significant (p greater than 0.05) and glycogenolysis was normal. Cortisol added in vitro potentiates the effect of isoproterenol and PGE1--but in the presence of cortisol the response of the asthmatic cells to isoproterenol is still lower than that of normal cells. This observation would support that "beta adrenergic blockade" is the major defect of asthmatic cells. The conclusion is further supported by the observation that the degree of the blockade is associated with a pathologic condition.

Topics: Adrenergic beta-Agonists; Asthma; Cells, Cultured; Cyclic AMP; Drug Therapy, Combination; Epinephrine; Glycogen; Humans; Hydrocortisone; Isoproterenol; Lymphocytes; Phentolamine; Phenylephrine; Propranolol; Prostaglandins E

Topics: Adolescent; Asthma; Child; Child, Preschool; Glycogen; Humans; Lipids; Neutrophils; Peroxidases; Phagocytosis

Topics: Adolescent; Adult; Aged; Asthma; Autolysis; Female; Glycogen; Granulocytes; Humans; Leukocytes; Male; Middle Aged

Topics: Adenine Nucleotides; Adrenal Cortex Hormones; Adrenalectomy; Alloxan; Aminophylline; Animals; Antigens; Asthma; Blood Glucose; Carbohydrate Metabolism; Diazoxide; Drug Hypersensitivity; Epinephrine; Glycogen; Gold; Histamine; Humans; Hydrocortisone; Hyperglycemia; Liver; Mice; Muscles; Obesity; Sympatholytics

Topics: Adolescent; Adrenal Insufficiency; Adult; Aged; Asthma; Cell Membrane Permeability; Cholesterol; Female; Glycogen; Homeostasis; Humans; Lipoproteins; Liver; Male; Middle Aged; Protein Binding; Sympathetic Nervous System

Topics: Adolescent; Asthma; Blood Glucose; Child; Epinephrine; Female; Glycogen; Humans; Male; Prognosis

Topics: Asthma; Cell Nucleus; Colitis, Ulcerative; Eosinophils; Eye Injuries; Glycogen; Hepatitis; Humans; Leukemia; Leukocytes; Lung Diseases; Schistosomiasis; Skin Window Technique

Topics: Adult; Asthma; Blood Glucose; Cortisone; Diabetes Complications; Diabetes Mellitus; Glucose Tolerance Test; Glycogen; Humans; Insulin; Lipase; Middle Aged