Increased serum γ-glutamyltransferase in hypertriglyceridemia: Comparison with serum pseudocholinesterase

Cucuianu, M; Zdrenghea, Dumitru; M, Pop; Opincaru, A

doi:10.1016/0009-8981(76)90093-0

Cited by 23 publications

(5 citation statements)

References 21 publications

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“…There is evidence that, besides its proven cholinergic activity, this enzyme is involved in noncholinergic functions as well, such as the regulation of cell division, differentiation during early neuronal development (Mack and Robitzky, 2000) and the expression of AChE (Small et al, 1996). It has also been suggested that BChE may involved in the lipid metabolism (Cucuianu et al, 1976;Chu et al, 1978;Kutty et al, 1981;Kutty and Payne, 1994) since elevated serum pseudocholinesterase activity has been found in type IIa, IIb and IV hyperlipoproteinaemia (Cucuianu et al, 1975;Chu et al, 1978, Jain et al, 1983. Only the increased serum triglyceride levels were associated with changes in BChE activity, pure hypercholesterolaemia was affecting the enzyme activity (Cucuianu et al, 1975(Cucuianu et al, , 1976.…”

Section: Introductionmentioning

confidence: 95%

“…It has also been suggested that BChE may involved in the lipid metabolism (Cucuianu et al, 1976;Chu et al, 1978;Kutty et al, 1981;Kutty and Payne, 1994) since elevated serum pseudocholinesterase activity has been found in type IIa, IIb and IV hyperlipoproteinaemia (Cucuianu et al, 1975;Chu et al, 1978, Jain et al, 1983. Only the increased serum triglyceride levels were associated with changes in BChE activity, pure hypercholesterolaemia was affecting the enzyme activity (Cucuianu et al, 1975(Cucuianu et al, , 1976. On the other hand positive and negative correlations have been found with low density lipoprotein (LDL) and high density lipoprotein (HDL) cholesterol levels respectively (Kutty et al, 1981).…”

Section: Introductionmentioning

confidence: 97%

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Increased serum butyrylcholinesterase activity in type IIb hyperlipidaemic patients

Kálmán¹,

Juhász²,

Rakonczay³

et al. 2004

Life Sciences

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Section: Introductionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 97%

Increased serum butyrylcholinesterase activity in type IIb hyperlipidaemic patients

Kálmán¹,

Juhász²,

Rakonczay³

et al. 2004

Life Sciences

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“…In these studies, activity of serum yglutamyltransferase (EC 2.3.2.2) was employed as an index of hepatic microsomal enzyme induction (Rosalki, 1975;Goldberg, 1979). Support for this relationship has come from authors who have confirmed the association in humans between serum y-glutamyltransferase activity and triacylglycerol concentration (Cucuianu et al, 1976), whereas other workers reported parallel increases in serum triacylglycerol concentration, serum y-glutamyltransferase activity and urinary excretion of D-glucaric acid (another index of hepatic microsomal enzyme induction) in human subjects after starting phenobarbital therapy (Annoni et al, 1976). In order to elucidate the biochemical basis for these findings, we have determined, as presented in this paper, the activity of critical enzymes involved in triacylglycerol synthesis and have quantified the overall formation of glycerolipids in cell-free systems.…”

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confidence: 95%

Effects of phenobarbital upon triacylglycerol metabolism in the rabbit

Goldberg¹,

Roomi²,

Yu³

et al. 1980

Biochemical Journal

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1. The association between hepatic microsomal enzyme induction and triacylglycerol metabolism was examined in fasting male rabbits (2kg body wt.) injected intra-peritoneally with 50 mg of phenobarbital per kg for 10 days. 2. Occurrence of enzyme induction was established by a significant increase in hepatic aminopyrine N-demethylase activity and cytochrome P-450 content, as well as a doubling of microsomal protein per g of liver and a 54% increase in liver weight. Parallel increments in hepatic gamma-glutamyltransferase (EC 2.3.2.2) activity occurred; these were more pronounced in the whole homogenate than in the microsomes, which only accounted for 12.5% of the total enzyme activity in the controls and 17.0% in the animals given phenobarbital. Increased activity of gamma-glutamyltransferase activity was also observed in the blood serum of the test animals. 3. The rabbits given phenobarbital manifested increased hepatic triacylglycerol content and the triacylglycerol concentration of blood serum was also elevated. These changes were accompanied by a significantly enhanced ability of cell-free fractions of liver from the test animals (postmitochondrial supernatant and microsomal fractions) to synthesize glycerolipids in vitro from sn-[14C] glycerol 3-phosphate and fatty acids, when expressed per whole liver. Relative to the protein content of the fraction, glycerolipid synthesis in vitro was significantly decreased in the microsomes, presumably consequent upon the dramatic increase in their total protein content, whereas no change occurred in the postmitochondrial supernatant, possibly due to the protective effect of cytosolic factors present in this fraction and known to enhance glycerolipid synthesis. 4. Microsomal phosphatidate phosphohydrolase accounted for 85% of the total liver activity of this enzyme and its specific activity was 20-fold higher than that of the cytosolic phosphatidate phosphohydrolase (EC 3.1.3.4), when each was measured under optimal conditions. A significant increase in the activity of both enzymes per whole liver occurred in the rabbits given phenobarbital. A closer correlation between hepatic triacylglycerol content and and microsomal phosphatidate phosphohydrolase, as well as the above observation, suggest that this, rather than the cytosolic enzyme, may be rate-limiting for triacylglycerol synthesis in rabbit liver. 5. Significant correlations were observed between the various factors of hepatic microsomal-enzyme induction (aminopyrine N-demethylase and gamma-glutamyltransferase activity as well as cytochrome P-450 content) and hepatic triacylglycerol content, suggesting that that microsomal enzyme induction may promote hepatic triacylglycerol synthesis and consequently hypertriglyceridaemia in the rabbit.

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“…Slight hepatic abnormalities, especially steatosis, are often found in situations where PAI-l is increased (obesity, hypertriglyceridemia and insulin resistance). Furthermore, steatosis is associated with increased synthesis of a variety of proteins, including hepatic enzymes, apolipoprotein and coagulation factors X and XIII (10)(11)(12). We recently observed that the slight hepatic impairment often found in patients who are hypertriglyceridemic is linked to raised levels of factor VII and protein C (13).…”

Section: Introductionmentioning

confidence: 99%

Relation between Plasminogen Activator Inhibitor-1 and Hepatic Enzyme Concentrations in Hyperlipidemic Patients

et al. 1994

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SummaryPlasminogen activator inhibitor type-1 (PAI-1) is a key determinant of the fibrinolytic capacity. Its activity correlates with most of the characteristic features of insulin resistance syndrome, i. e. obesity, high blood pressure and hyperlipidemia.We measured plasma PAI-1 antigen levels in 131 asymptomatic men (aged 44.2 ± 11 years) who had been referred for hyperlipidemia. Those taking medication and those with a secondary hyperlipidemia were excluded.We confirmed the correlation between PAI-1 levels and the following variables: body mass index, blood pressure, triglyceride concentration, and blood glucose and insulin levels before and after an oral glucose tolerance test. We also found a significant and independent correlation between PAI-1 and the concentration of the hepatic enzymes glutamyl transferase, alanine aminotransferase and aspartate aminotransferase.Mild liver abnormalities (presumably steatosis) may thus be one of the factors accounting for high plasma PAI-1 levels in hyperlipidemic patients.

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Increased serum γ-glutamyltransferase in hypertriglyceridemia: Comparison with serum pseudocholinesterase

Cited by 23 publications

References 21 publications

Increased serum butyrylcholinesterase activity in type IIb hyperlipidaemic patients

Increased serum butyrylcholinesterase activity in type IIb hyperlipidaemic patients

Effects of phenobarbital upon triacylglycerol metabolism in the rabbit

Relation between Plasminogen Activator Inhibitor-1 and Hepatic Enzyme Concentrations in Hyperlipidemic Patients

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