Effects of Glucose Feeding, Cortisol, and Insulin on Liver Glycogen Synthesis in the Rat

Friedmann, Bernice; Goodman, Edward H.; Weinhouse, Sidney

doi:10.1210/endo-81-3-486

Cited by 67 publications

(47 citation statements)

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“…The results of the chemical analyses of liver for glycogen, protein, fat and water are summarized in table 11. When compared to controls, a significant increase in the hepatic glycogen concentration was noted in all groups receiving prednisone.…”

Section: Resultsmentioning

confidence: 99%

Prednisone-Induced Morphologic and Chemical Changes in the Liver of Dogs

Fittschen¹,

Bellamy²

1984

Vet Pathol

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Abstract. Glucocorticoid treatment in dogs is known to cause hepatocellular swelling due to accumulation of cytoplasmic compounds which variably have been identified histochemically as fat, glycogen, or water. In the present study changes in dog liver, after treatment for 15 days with two different doses of oral or intramuscular prednisone, were examined using histological, histochemical, and ultrastructural techniques as well as quantitative chemical analysis.Thirty mongrel dogs were divided into two control groups and three treatment groups of six dogs each. Dogs which received prednisone orally at I .2 mg/kg body weight/day, or 4 mg/kg body weight/day, respectively, or received intramuscular prednisone injections of 4 mg/kg body weight/day had hepatomegaly due primarily to hepatocellular accumulation of glycogen. Compared to controls, no changes in the hepatic water concentration were observed, whereas the relative amounts of liver fat were decreased slightly and those of protein were decreased markedly. Hepatocellular glycogen could be demonstrated histochemically in tissues fixed in absolute alcohol, but not in tissues treated with aqueous fixative, such as 10% buffered formalin or Bouin's solution. Glycogen deposition occurred predominantly in the midzone of hepatic acini. Affected hepatocytes varied in size and shape. The most severely affected cells were enlarged five to ten fold with glycogen occupying most of the cytoplasmic space restricting the mitochondria, endoplasmic reticulum, and other organelles to a narrow zone around the cell periphery and the nucleus. It was concluded that treatment with prednisone causes hepatomegaly due to glycogenosis in the dog.

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Section: Resultsmentioning

confidence: 99%

Prednisone-Induced Morphologic and Chemical Changes in the Liver of Dogs

Fittschen¹,

Bellamy²

1984

Vet Pathol

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“…1) which would be in accord with the view that this enzyme catalyzes a rate-limiting step. That interpretation was advanced in earlier investigations showing that in both organs during starvation and diabetes [32,33] and in kidney during metabolic acidosis [34,35] and experimental impairment of liver function by galactosamine or CC14 [3 -51 gluconeogenesis from lactate or pyruvate [26,36,37] and the level of phosphoenolpyruvate carboxykinase [16,38 -401 were altered in parallel. Also the metabolite crossover pattern observed during glucagon treatment in liver [41] and during metabolic acidosis in kidney [42] is consistent with a regulation of gluconeogenesis at the phosphoenolpyruvate carboxykinase reaction.…”

Section: Increased Gluconeogenesis After Partial Hepatectomymentioning

confidence: 90%

Correlation between Rates and Enzyme Levels of Increased Gluconeogenesis in Rat Liver and Kidney after Partial Hepatectomy

Katz

1979

European Journal of Biochemistry

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The metabolic rates and key enzymes of gluconeogenesis and glycolysis were determined and correlated in perfused livers, isolated hepatocyte suspensions and kidney cortex slices of rats after two-thirds hepatectomy. Fed unoperated, sham operated and fasted animals served as controls.In liver the following results were obtained. In kidney cortex the following results were obtained. Firstly, after partial hepatectomy gluconeogenesis from lactate was enhanced in tissue slices to 217 % after 24 h. Gluconeogenesis from fructose was unchanged. These rates coincided with an increase of the level of phosphoenolpyruvate carboxykinase to 193 % and of glucose-6-phosphatase to 151 %. Secondly, after a 24-h fast similar changes for the gluconeogenic rate to 200 % and of phosphoenolpyruvate carboxykinase to 240 % as well as of glucose-6-phosphatase to 136 % were observed. Thirdly, neither the rates of glycolysis nor the levels of hexokinase, phosphofructokinase and pyruvate kinase were altered after partial hepatectomy or a 24-h fast. No significant changes neither in liver nor in kidney cortex occurred after sham operation. Thus the drastic reduction of liver tissue after partial hepatectomy was compensated by an increase of gluconeogenesis in the liver remnant and in kidney cortex, both accompanied by an enhancement of the phosphoenolpyruvate carboxykinase level, in order to maintain the glucose homeostasis.

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“…We shall use only the a and b nomenclature, which conforms to that initially introduced by Cori and Green [17] for the 2 forms of muscle phosphorylase. 19] and in diabetic rats [20,21 ] as well as in normal animals.…”

Section: The Rate Limiting Enzymes; Their Phosphorylation and Dephospmentioning

confidence: 99%

“…It is poorly active in preparations obtained from fasted animals, but recovers its full activity if 0.5% glycogen is: added [6,55]. The enzyme is also inactive in liver extracts [56] and in perfused livers [25] obtained from fasted adrenalectomized rats, despite the fact that glycogen synthesis rapidly occurs in vivo upon refeeding of these animals [18,19].…”

Section: The Control Of Synthetase Phosphatase By Phosphorylasementioning

confidence: 99%