Studies on Gluconeogenesis in Galactosamine Induced Hepatitis

Monier, D; Wagle, S.R.

doi:10.3181/00379727-136-35268

Cited by 22 publications

(6 citation statements)

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“…The undifferentiated enzyme pattern in the injured liver was caused not only by the loss or diminished activities of adult type liver enzymes or 'luxury' molecules (GK, G6Pase, FDPase, ALD-B and PK-L) but also by the increase in activities of prototype or fetal type liver enzymes or 'essential' molecules (HK, G6PD, PFK, ALD-A and PK-M2). These enzyme alterations are not likely to be specific to CCI4, since similar results have been obtained with other agents known as hepatotoxins, such as thioacetamide, allyl formate or galacto samine [2,8,39,40] and with hepatitis virus [41]. Furthermore, among tissues of CCl4-treated rats the changes in enzyme activities appeared to be limited to the liver [42].…”

Section: Discussionmentioning

confidence: 71%

Undifferentiated Patterns of Key Carbohydrate-Metabolizing Enzymes in Injured Livers. I. Acute Carbon-Tetrachloride Intoxication of Rat

Taketa

Tanaka

Watanabe

et al. 1976

Enzyme

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In acute CCI(4), intoxication of rats significantly increased activities of hepatic low-K(m) hexokinases, glucose-6-phosphate dehydrogenase, phosphofructokinase, aldolase A and pyruvate kinase M(2) with concurrently decreased activities of glucokinase, glucose- 6-phosphatase, fructose-1,6-diphosphatase, aldolase B and pyruvate kinase L were observed. The resulting enzyme pattern was apparently different from that in dietary induction. Principal component analysis revealed that the degree of enzyme deviation in the injured liver was much greater than that in the regenerating liver after partial hepatectomy and was closer to that in fetal liver or hepatoma tissue.

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Section: Discussionmentioning

confidence: 71%

Undifferentiated Patterns of Key Carbohydrate-Metabolizing Enzymes in Injured Livers. I. Acute Carbon-Tetrachloride Intoxication of Rat

Taketa

Tanaka

Watanabe

et al. 1976

Enzyme

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“…It has been suggested that reduction in activity is related to disorders in protein metabolism during D-galactosamine hepatitis (1,21,28).…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, following ¿»-galac tosamine injection, accumulation of uridine diphosphate-hexosamines (UDP-hexosamines) has been described in association to a marked decrease of uridine diphosphate-hexoses (UDPglucose, UDP-galactose) and uridine phosphates (UTP, UDP, UMP) (13,14). Inhibition of hepatic intracellular metabolism (including ribonucleic acid and protein synthesis) has also been reported (15,21,28,29).…”

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confidence: 99%

Changes in Glycoproteins of Liver Plasma Membranes from Rats Treated with <i>D</i>-Galactosamine

Bertrand¹,

Veissière²,

Picard³

1979

Digestion

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D-Galactosamine administration to rats (400mg/kg) by intraperitoneal injection induced biochemical alterations in liver plasma membranes. Alterations were studied 4, 16 and 24 h after D-galactosamine injection. Plasma membrane 5’-mononucleotidase activity decreased to 40% of control values. Carbohydrate composition was significantly changed. After 24 h D-galactosamine administration, the diminution in plasma membrane sialic acids and hexoses reached 30% of control values. As detected by SDS-acrylamide gel electrophoresis, high molecular weight glycoproteins of D-galactosamine-treated plasma membranes were modified. Moreover, the incorporation of [³⁵S]-sulfate into membrane glycoproteins decreased after D-galactosamine administration (40–60% of control). The present results show that biochemical alterations in rat liver plasma membranes appear soon after D-galactosamine injection. Marked changes are observed in cell surface glycoproteins, especially in sialoglycoproteins and sulfated glycoproteins.

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“…43 Adenosine monophosphate is an important allosteric inhibitor of fructose 1,6-bisphosphatase and stimulator of 6-phospho-1-fructokinase. Furthermore, decreased activity of gluconeogenic enzymes 22,66 and increased pyruvate kinase activity 56 have been reported in response to D-galactosamine treatment in rats. With the induction of glycolysis in FHF rat livers, there was no concomitant activation of pyruvate dehydrogenase to convert pyruvate to acetyl-CoA, which led to a significant increase in lactate release.…”

Section: Discussionmentioning

confidence: 99%

Intrahepatic Amino Acid and Glucose Metabolism in A D–Galactosamine-Induced Rat Liver Failure Model

et al. 2001

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A better understanding of the hepatic metabolic pathways affected by fulminant hepatic failure (FHF) would help develop nutritional support and other nonsurgical medical therapies for FHF. We used an isolated perfused liver system in combination with a mass-balance model of hepatic intermediary metabolism to generate a comprehensive map of metabolic alterations in the liver in FHF. To induce FHF, rats were fasted for 36 hours, during which they received 2 D-galactosamine injections. The livers were then perfused for 60 minutes via the portal vein with amino acid-supplemented Eagle minimal essential medium containing 3% wt/ vol bovine serum albumin and oxygenated with 95% O 2 /5% CO 2 . Control rats were fasted for 36 hours with no other treatment before perfusion. FHF rat livers exhibited reduced amino acid uptake, a switch from gluconeogenesis to glycolysis, and a decrease in urea synthesis, but no change in ammonia consumption compared with normal fasted rat livers. Mass-balance analysis showed that hepatic glucose synthesis was inhibited as a result of a reduction in amino acid entry into the tricarboxylic acid cycle by anaplerosis. Furthermore, FHF inhibited intrahepatic aspartate synthesis, which resulted in a 50% reduction in urea cycle flux. Urea synthesis by conversion of exogenous arginine to ornithine was unchanged. Ammonia removal was quantitatively maintained by glutamine synthesis from glutamate and a decrease in the conversion of glutamate to ␣-ketoglutarate. Mass-balance analysis of hepatic metabolism will be useful in characterizing changes during FHF, and in elucidating the effects of nutritional supplements and other treatments on hepatic function. (HEPATOLOGY 2001;34:360-371.)Since the late 1980s, orthotopic liver transplantation has become the only widely accepted treatment for fulminant hepatic failure (FHF). [1][2][3][4] Because of the severe shortage in donor organs, various alternatives aimed at providing a "substitute" liver, such as xenogeneic whole liver perfusion 5 and extracorporeal bioartificial liver devices, 6,7 are being developed. Such systems, which can be used as a bridge to transplantation or provide temporary relief during the most acute phase of hepatic failure, are promising, although technically complex and expensive. It has been hypothesized that hepatic encephalopathy may result from the elevation of circulating levels of putative toxins such as ammonia, mercaptans, short-chain fatty acids, [8][9][10] and an abnormal amino acid profile. [11][12][13] In FHF patients, alterations in amino acid concentrations in systemic plasma have been characterized by several investigators, 14,15 which led to the use of solutions rich in branchedchain amino acids (BCAA) for the treatment of hepatic encephalopathy. 16,17 These approaches, which were largely unsuccessful, aimed at counteracting the observed shifts in metabolite levels in the systemic circulation; however, systemic changes in metabolite levels do not solely reflect alterations in liver function, but also changes in whole-b...

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Studies on Gluconeogenesis in Galactosamine Induced Hepatitis

Cited by 22 publications

References 0 publications

Undifferentiated Patterns of Key Carbohydrate-Metabolizing Enzymes in Injured Livers. I. Acute Carbon-Tetrachloride Intoxication of Rat

Undifferentiated Patterns of Key Carbohydrate-Metabolizing Enzymes in Injured Livers. I. Acute Carbon-Tetrachloride Intoxication of Rat

Changes in Glycoproteins of Liver Plasma Membranes from Rats Treated with <i>D</i>-Galactosamine

Intrahepatic Amino Acid and Glucose Metabolism in A D–Galactosamine-Induced Rat Liver Failure Model

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