Hepatic Glycogen Depletion Research Articles

Study of glucose tolerance and synthesis of hepatic glycogen from glucose and glycine-1-C 14 in tuberculous guinea pigs

A marked depletion of hepatic glycogen, an appreciable decrease in the hepatic glycogenesis, and a lowered glucose tolerance in tuberculous guinea pigs were demonstrated. Incorporation of glycine-1-C 14 into hepatic glycogen in vivo showed a tendency to increase as a result of experimental tuberculosis. Depletion of hepatic glycogen in experimental tuberculosis has been ascribed to the suppressed glycogenesis.

The depletion of liver glycogen in puromycin-treated animals

Mice and rats receiving puromycin dihydrochloride intraperitoneally (6.0 and 60 mg. per animal, respectively) in four equally divided doses over a 4-hr, period showed complete depletion of hepatic glycogen and inhibition of incorporation of glycine-C 14 into liver protein. Administration of a single dose of puromycin to mice was followed by rapid inhibition of synthesis of liver protein with concurrent loss of glycogen from the liver. Carbohydrate levels in liver, blood, and muscle were followed in mice up to 4 hr. after a single injection of puromycin. The decrease in liver glycogen was accompanied by an increase in blood sugar levels while muscle glycogen content was not appreciably affected during this period.

RENAL AMINO-ACIDURIA<subtitle>Report of Two Cases, with Studies of Amino Acid Excretion Patterns</subtitle>

AMONG the so-called inborn errors of metabolism as defined by Garrod 1 is a renal tubular defect originally described by Fanconi 2 in 1946 as nephrotic glycosuric dwarfism with hypophosphatemic rickets. Fanconi 3 later found this to be identical with what he termed cystine disease, or. because of the presence of increased amounts of acids other than cystine, amino acid diabetes. The syndrome is characterized by impaired renal tubular reabsorption of glucose, inorganic phosphate, and bicarbonate, as well as acids. Accompanying these defects in the kidney, and probably as a result of them, are acidosis and a negative calcium balance with the development of renal rickets. The increased losses of glucose may produce sufficient depletion of hepatic glycogen to produce a ketosis which enhances the acidosis. The amino-aciduria of this syndrome is the prominent feature which differentiates it from similar renal tubular defects, such as renal rickets or

Metabolism of fructose by the liver of diabetic and nondiabetic subjects.

Summary and ConclusionsThe metabolism of fructose in the liver was investigated by hepatic vein catheterization studies in 3 diabetic patients deprived of insulin and in 3 non-diabetic subjects. (1) There was a large hepatic uptake of fructose during the period of intravenous administration in both diabetic and non-diabetic subjects. (2) In all but one case there was a large hepatic output of pyruvic and lactic acid during the fructose infusion. The liver of one diabetic patient in ketosis continued to remove pyruvic and lactic acid from the blood; hepatic glycogen depletion may have accounted for this divergent result. (3) In half the cases (2 diabetic patients and 1 non-diabetic subject) the output of glucose by the liver was increased during fructose administration. (4) In the absence of ketosis, the liver of the diabetic subject without insulin, therefore, metabolized fructose in a manner similar to that of the liver of the non-diabetic individual. The presence of ketosis, however, was accompanied by ...

PHYSIOLOGIC BASIS OF INTRAVENOUS DEXTROSE THERAPY FOR DISEASES OF THE LIVER

Since Rosenbaum,1in 1882, called attention to the depletion of hepatic glycogen following chloroform narcosis, arsenic or phosphorus poisoning and excessive administration of morphine, there has been adequate confirmation of the fact that a damaged liver contains little glycogen.2Concomitant with the loss of glycogen, fatty changes appear in the liver after exposure to these hepatotoxic agents. Rosenfeld3observed that animals fed carbohydrate are, in general, less susceptible to any drug which produces accumulations of fat in the liver. Furthermore, after such poisonings the feeding of dextrose aids recovery of the animal. Since the early reports of Whipple and Sperry,4Opie and Alford5and Graham6on the resistance to chloroform or phosphorus poisoning of animals fed large amounts of carbohydrate or animals with livers containing large stores of glycogen, there have been many similar observations.7The protective action of high carbohydrate intake has also been noted in the prevention of