Elevated Glutamic Pyruvic Transaminase Research Articles

Elevation of glutamic pyruvic transaminase and .GAMMA.-glutamyl transpeptidase in obesity.

Study was made of glutamic pyruvic transaminase (GPT), glutamic oxalacetic transaminase (GOT), and gamma-glutamyl transpeptidase (gamma-GTP) in 729 obese subjects in various groups, namely, primary school children, high school children, university students, and outpatients. The incidences of abnormal GPT, GOT, and gamma-GTP in the obese subjects were frequently significantly higher than in the controls. It was most clearly shown in GPT. The incidences of abnormal GPT in the obese females were significantly lower than those in the obese males, but were significantly higher than the controls. Higher incidences of abnormality in the school children were ascribed to the higher degree of obesity in the children. The extent of increase in GPT was considerable. GPT was sometimes higher than 6 times the normal upper limit.

Biological effects of alkali-treated soya protein and lactalbumin in the rat and mouse

Diets containing 20% alkali-treated soya protein and providing 1370–2630 ppm dietary lysinoalanine produced nephrocytomegaly in the pars recta of the proximal tubule in male Sprague-Dawley and Wistar rats. The frequency of abnormally large pars recta nuclei exceeded 33% in rats fed alkali-treated soya protein providing dietary lysinoalanine levels of 2080 or 2630 ppm. There were no quantitative or qualitative differences between the renal responses of Sprague-Dawley and Wistar rats fed the same diets. Swiss-Webster mice fed alkali-treated soya protein had slightly more than twice as many enlarged pars recta nuclei as did the control group, but the shift in size distribution was not significant at the 5% level. Sprague-Dawley rats developed only minimal karyomegaly on a diet of 20% alkali-treated lactalbumin, despite a dietary lysinoalanine level of 4970 ppm. Diets containing 8 or 10% untreated lactalbumin in addition to 12% alkali-treated soya protein or 10% alkali-treated lactalbumin did not induce nephrocytomegaly or karyomegaly, despite providing dietary lysinoalanine levels of 1753 and 2490 ppm, respectively. Sprague-Dawley and Wistar rats fed 20% alkali-treated soya protein showed elevated plasma levels of glutamic-pyruvic transaminase (GPT) and blood urea nitrogen (BUN), and had a significantly lower plasma protein content than control animals after 8 or 12 wk on the diet. Sprague-Dawley rats fed 20% alkali-treated lactalbumin had elevated GPT levels, but BUN and total plasma protein were normal; replacement of half the protein content of the diet with non-nutritive cellulose caused elevation of GPT, with no change in the BUN or plasma protein values. In rats fed 20% alkali-treated soya protein, approximately 33% of the lysinoalanine ingested daily was found in the faeces and 1·2% in the urine. No lysinoalanine was detected in liver or blood, but a quantity equivalent to about 0·6% of the daily intake was found in the kidneys. Higher urinary lysinoalanine excretion (2–7% of the intake) was found in animals fed alkali-treated lactalbumin.

Biological effects of alkali-treated soya protein and lactalbumin in the rat and mouse

Diets containing 20% alkali-treated soya protein and providing 1370–2630 ppm dietary lysinoalanine produced nephrocytomegaly in the pars recta of the proximal tubule in male Sprague-Dawley and Wistar rats. The frequency of abnormally large pars recta nuclei exceeded 33% in rats fed alkali-treated soya protein providing dietary lysinoalanine levels of 2080 or 2630 ppm. There were no quantitative or qualitative differences between the renal responses of Sprague-Dawley and Wistar rats fed the same diets. Swiss-Webster mice fed alkali-treated soya protein had slightly more than twice as many enlarged pars recta nuclei as did the control group, but the shift in size distribution was not significant at the 5% level. Sprague-Dawley rats developed only minimal karyomegaly on a diet of 20% alkali-treated lactalbumin, despite a dietary lysinoalanine level of 4970 ppm. Diets containing 8 or 10% untreated lactalbumin in addition to 12% alkali-treated soya protein or 10%, alkali-treated lactalbumin did not induce nephrocytomegaly or karyomegaly, despite providing dietary lysinoalanine levels of 1753 and 2490 ppm, respectively. Sprague-Dawley and Wistar rats fed 20% alkali-treated soya protein showed elevated plasma levels of glutamic-pyruvic transaminase (GPT) and blood urea nitrogen (BUN), and had a significantly lower plasma protein content than control animals after 8 or 12 wk on the diet. Sprague-Dawley rats fed 20% alkali-treated lactalbumin had elevated GPT levels, but BUN and total plasma protein were normal; replacement of half the protein content of the diet with non-nutritive cellulose caused elevation of GPT, with no change in the BUN or plasma protein values. In rats fed 20% alkali-treated soya protein, approximately 33% of the lysinoalanine ingested daily was found in the faeces and 1·2% in the urine. No lysinoalanine was detected in liver or blood but a quantity equivalent to about 0·6% of the daily intake was found in the kidneys. Higher urinary lysinoalanine excretion (2–7% of the intake) was found in animals fed alkali-treated lactalbumin.

Diagnostic Value of Serum-transaminase Activity in Hepatic and Gastrointestinal Diseases

Glutamic-oxaloacetic transaminase is increased in the serum following damage to either liver or muscle cells. Glutamic-pyruvic transaminase is found in relatively high concentration in the liver. In this investigation of an assortment of liver and gastrointestinal diseases, it was found that both enzymes became elevated following damage to liver cells. Damage to muscle cells alone, as in myocardial infarction, did not produce a significant elevation of glutamic-pyruvic transaminase. Thus the simultaneous determinations of glutamic-oxaloacetic transaminase and glutamic-pyruvic transaminase may be of value in differentiation between diseases with damage to liver cells and diseases causing necrosis of muscle.