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At least 1,405 records · Page 78Linked to original sources
PubMed1993

Hormonal control of glycogenolysis in isolated chick embryo hepatocytes.

Hepatocytes were isolated from 15-, 16-, 17-, and 18-day-old chick embryos. Glucagon, adrenaline, and dibutyryl cAMP (Bt2cAMP), individually or in combination, activated glycogenolysis in the isolated hepatocytes. The alpha-adrenergic agonist phenylephrine did not increase glycogen breakdown. The action of adrenaline was abolished upon treatment of hepatocytes with a combination of the hormone and propranolol, a beta-adrenergic blocker. The effects of glucagon, adrenaline, and dibutyryl cAMP on glycogenolysis were not additive. Either hormone induced an increase in the concentration of cAMP. The activities of dephosphophosphorylase kinase and phosphorylase a were stimulated by each hormone or Bt2cAMP. It appears likely that glucagon and adrenaline serve as physiological regulators of hepatic glycogen breakdown during embryogenesis in chickens.

Adenosine Triphosphate↗
PubMed1979

Progressive extrinsic ophthalmoplegia with peripheral neuropathy and storage of muscle glycogen.

A case of progressive extrinsic ophthalmoplegia associated with peripheral neuropathy and hypertriglyceridemia type IV is described. Motor and sensory conduction velocities of the spinal nerves were severely decreased, while the EMG of the facial muscles was more suggested of a myopathic disorder. Electron microscopic study of biopsies of biceps and peroneus brevis muscles disclosed many ragged red fibers, mainly type I, which contained typical abnormal mitochondria. Other fibers, all type II, contained increased amounts of glycogen between myofibrils or beneath the sarcolemmal membrane, but the mitochondria were normal. These fibers were more abundant in the peroneus brevis than in the biceps muscle. Nerve biopsy revealed marked loss of myelinated fibers, but neither mitochondrial changes nor glycogen storages were evident in Schwann's cells. Biochemical investigations confirmed the increased amount of glycogen in both muscle biopsies and revealed a decrease of guanilcyclase. Phosphorylase, phosphorylase b kinase, adenilcyclase, and carnitine concentrations were all normal. The pathogenesis of this syndrome is discussed and the relationship between mitochondrial abnormalities and glycogen accumulation in muscle tissue are considered.

Adult↗
PubMed1988

Glycogen storage disease: recommendations for treatment.

A workshop was held on "Aspects of treatment of patients with glycogen storage disease" within the framework of the Concerted Action "Inborn errors of metabolism" of the European Communities. Consensus was reached on the main issues of treatment of patients with deficiency of glucose-6-phosphatase, glucose-6-phosphate translocase, debranching enzyme, liver phosphorylase and phosphorylase-b-kinase. The resulting recommendations are reported.

Adolescent↗
PubMed1975

Multiple regulation of nucleoside catabolizing enzymes: regulation of the deo operon by the cytR and deoR gene products.

The protein and repressor nature of two regulatory gene products in E. coli has been demonstrated, employing mutants with either amber or thermosensitive mutations. The regulatory genes are the cytR and the deoR genes, both of which contribute to the regulation of the synthesis of nucleoside catabolizing enzymes. Enzyme levels in strains with concurrent mutations in both regulatory genes are considerably higher than the sum of the levels in strains with a cytR or a deoR mutation alone, indicating a certain co-operativity between the two repressor proteins. The glucose repression of enzyme levels observed in the double regulatory mutant is similar to that found in a cytR mutant, and much more pronounced than the glucose effect in a deoR mutant. A model of the promoter-operator region in the deo operon is proposed.

Cytidine Deaminase↗
PubMed1980

Inherited metabolic disease in laboratory animals: a review.

Research on the screening for and study of animal models of inherited metabolic disease is reviewed. It is emphasized that an animal model, to be of value, must be an inherited deficiency of the same enzyme as the one deficient in the human syndrome. If this criterion is adhered to there is a remarkable identity in aetiology between animal and man. Specific examples of inherited metabolic disease in laboratory animals are described for: amino acid metabolism; lysosomal storage diseases, carbohydrate metabolism, transport disorders and trace element metabolism; the mutants found in mice being the easiest to manipulate biochemically and genetically. There is still a lack of adequate screening programmes for animal homologues of the more serious human inborn errors (such as lysosomal storage diseases) where laboratory studies could provide significant advances in therapy.

Amino Acid Metabolism, Inborn Errors↗