The oxidation/reduction state of the extramitochondrial DPNDPNH system in rat liver and the hormonal control of substrate levels invivo

Hohorst, H. J.; Kreutz, F.; Reim, Martin; Hübener, H. J.

doi:10.1016/0006-291x(61)90263-7

Cited by 86 publications

(18 citation statements)

References 2 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…There was an increase in hepatic fructose-1,6-diphosphate, dihydroxyacetone phosphate, and a-glycerophosphate. The normal ratio of a-glycerophosphate to dihydroxyacetone phosphate is approximately 8-10 in the rat (14). In our patient a ratio of 260 was found.…”

Section: Resultssupporting

confidence: 47%

“…Marked differences in the lactate-pyruvate ratios between the two species were also apparent. The rat livers demonstrated a normal ratio of 17.5 (14) (Table II) making it unlikely that anoxic changes in the patient's liver before analysis could account for the differences observed (15). The liver biopsy in our patient was performed under ideal conditions consisting of intravenous glucose infusion to maintain plasma glucose normal (80-95 mg/100 ml) and prevent lactic acidosis (blood lactates 2-2.5 mM).…”

Section: Resultsmentioning

confidence: 99%

“…Reinstitution of the high carbohydrate diet corrected the metabolic defects (days 8-12). On the high fat diet severe lactic acidosis, hypoglycemia, and ketonemia rapidly developed (days [12][13][14]. When switched to the therapeutic diet these changes rapidly reversed (days 15-17) (Fig.…”

Section: Resultsmentioning

confidence: 99%

See 2 more Smart Citations

Hepatic fructose-1,6-diphosphatase deficiency

Pagliara¹,

Karl²,

Keating³

et al. 1972

J. Clin. Invest.

View full text Add to dashboard Cite

A B S T R A C T An 8-month-old female, maintained on breast feeding for 6 months, experienced numerous attacks of hyperventilation when weaned to baby food and was admitted with severe lactic acidosis (20 mM) and hypoglycemia. Physical examination was negative except for hepatomegaly. Fasting (18 hr) after stabilization on a high carbohydrate diet resulted in hypoglycemia (plasma glucose 40 mg/100 ml), lactic acidosis (6-10 mM), and a rise in plasma alanine. Glucagon produced a glycemic response after 6 hr, but not after 18 hr fasting. Intravenous galactose increased plasma glucose (A 45 mg/100 ml) but intravenous fructose, glycerol, and alanine caused a 40-50% fall in plasma glucose and a significant rise in lactate (A 3-4 mM).Liver biopsy showed fatty infiltration. Liver slices incubated with galactose, lactate, fructose, alanine, or glycerol converted only galactose to glucose. Hepatic glycolytic intermediates were increased below the level of fructose-1,6-diphosphate and decreased above. Hepatic phosphorylase, glucose-6-phosphatase, amylo-1,6-glucosidase, phosphofructokinase, fructose-i-phosphate aldolase, and fructose-1,6-diphosphate aldolase levels were normal, but no fructose-1,6-diphosphatase (FDPase) activity was detected. Further studies on the liver homogenate of this patient revealed the presence of an acid-precipitable activator of FDPase.Normal plasma glucose and lactate levels were maintained on an 800 cal diet of 66% carbohydrate (sucrose and fructose excluded), 5% protein, and 20% fat. When carbohydrate was reduced to 35% and protein or fat This work was presented in part at the meeting of the

show abstract

Section: Resultssupporting

confidence: 47%

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Hepatic fructose-1,6-diphosphatase deficiency

Pagliara¹,

Karl²,

Keating³

et al. 1972

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…The concentration of aspartic acid in the liver falls dramatically in diabetic rats, whereas that of glutamic acid remains relatively unchanged (Kirsten, Kirsten, Hohorst & Biucher, 1961). This, together with the increase in the amount of NADH relative to NAD+ (Glock & McLean, 1955;Hohorst, Kreutz & Reim, 1961) (a point, incidentally, on which there is no general agreement; see also Helmreich, Holzer, Lamprecht & Goldschmidt, 1954;Greenbaum & Graymore, 1956), suggests that these substrate and coenzyme changes are in part a result of rather than a causative effect of the increased urea output in diabetic rats.…”

Section: Resultsmentioning

confidence: 99%

Influence of pancreatic hormones on enzymes concerned with urea synthesis in rat liver

McLean¹,

Novello²

1965

Biochemical Journal

View full text Add to dashboard Cite

1. The activities of enzymes of the urea cycle [carbamoyl phosphate synthetase, ornithine transcarbamoylase, argininosuccinate synthetase, argininosuccinase (these last two comprising the arginine-synthetase system) and arginase] have been measured in control, alloxan-diabetic and glucagon-treated rats. In addition, measurements were made on alloxan-diabetic rats treated with protamine-zincinsulin. 2. Treatment of rats with glucagon for 3 days results in a marked increase in the activities ofthree enzymes ofthe urea cycle (carbamoyl phosphate synthetase, argininosuccinate synthetase and argininosuccinase). The pattern of change in the alloxan-diabetic group is very similar to that of the glucagon-treated group, although the magnitude of the change was much greater. 3. Comparison was made of the actual and potential rate of urea synthesis in normal and diabetic rats. In both groups the potential rate of urea production, as measured by the activity of the rate-limiting enzyme, argininosuccinate synthetase, slightly exceeds the actual rate of synthesis by liver slices in the presence of substrates. The relative activities of the actual and potential rates were similar in the two groups of animals, this ratio being 1: 0-70. 4. In the alloxan-diabetic rats treated with protamine-zinc-insulin for 2-5 or 4 days there was a marked increase in liver weight. This was associated with a rise in the total hepatic activity of the urea-cycle enzymes located in the soluble fraction of the cell (the arginine-synthetase system and arginase) after 2-5 days of treatment. After 4 days of treatment the concentration of these enzymes/g. of liver decreased, and the total hepatic content then reverted to the untreated alloxan-diabetic value. 5. No effects of glucagon or of insulin in vitro could be found on the rate of urea production by liver slices. 6. The present results are discussed in relation to how far this pattern of change is typical of conditions resulting in a high urea output, and comparison has been made with other values in the literature.It has been known for many years that the diabetic state is associated with a greatly increased nitrogen excretion, and this and the effect of insulin in causing nitrogen retention have been widely studied (Minkowski, 1893;Atchley, Loeb, Richards, Benedict & Driscoll, 1933;Soskin & Levine, 1946;Chaikoff & Forker, 1950). More recently glucagon has been shown to be a hormone closely associated with protein catabolism, increased amino acid breakdown and increased urea synthesis (Tyberghein, 1953;Salter, Davidson & Best, 1957;Best, 1959;Miller, 1960). Thus these two hormones, secreted by the pancreas, have powerful and antagonistic effects on both carbohydrate and nitrogen metabolism (see de Duve, 1953;Lukens, 1959;Randle, 1963 Though certain of the urea-cycle enzymes have been studied in alloxan-diabetic-rat liver, namely arginase (Folley & Greenbaum, 1949) and the overall arginine-synthetase system (Freedland & Sodikoff, 1962), there has as yet been no systematic study of the overall pat...

show abstract

“…Hohorst et al (6) have concluded that the steady state of this system is very close to mass action equilibrium and therefore, it should be possible to estimate the NAD+/NADH ratio in the cellular compartment of the liver cell.…”

mentioning

confidence: 99%

Cellular Oxidation-Reduction State of Some NAD-linked Reactions in Diabetic Rat Liver, and the Effect of Coenzyme Q Administration

et al. 1968

View full text Add to dashboard Cite

The cytoplasmic reduction-oxidation state of some NAD-linked reactions has been investigated in the liver in vivo under normal and diabetic conditions with or without CoQ7 administration.1. In the liver, the close relationships among lactate/pyru vate, malate/oxaloacetate and glycerol-1-phosphate/dihydrox yacetone phosphate ratios were found in all the metabolic con ditions studied. In diabetic rats, these systems were found to be more reduced.2. CoQ7 administration to diabetic rats for four days in tramuscularly tended to restore these ratios to normal. This effect was followed by a significant drop in malate concentration.Present findings would indicate that the effect of CoQ7 on the reduced state in diabetic rats seems to be mediated via malate removal.

show abstract

The oxidation/reduction state of the extramitochondrial DPNDPNH system in rat liver and the hormonal control of substrate levels invivo

Cited by 86 publications

References 2 publications

Hepatic fructose-1,6-diphosphatase deficiency

Hepatic fructose-1,6-diphosphatase deficiency

Influence of pancreatic hormones on enzymes concerned with urea synthesis in rat liver

Cellular Oxidation-Reduction State of Some NAD-linked Reactions in Diabetic Rat Liver, and the Effect of Coenzyme Q Administration

Contact Info

Product

Resources

About