The glucose and urea production and the uptake of gluconeogenic precursors by the liver were measured with the liver vein catheterization technique in two series of healthy subjects after 4 days on a well-defined normo-caloric diet. After a normal mixed diet the net splanchnic glucose production was 0.87 mmol/min. The glucose derived from maximum gluconeogenesis was 0.31 mmol/min. By using a liver biopsy technique in a similar series, the glycogenolysis was found to be 0.54 mmol glucoselmin. After a carbohydratepoor diet the splanchnic glucose production had decreased to 0.30 mmol/min. In this situation the liver was deprived of most of its glycogen, as shown earlier by direct determination of glycogen in liver biopsy specimens. The uptake of gluconeogenic substrates corresponded to the net glucose production. The decreased glucose production during carbohydrate-poor diet did not result in any significant change of the blood glucose level. This indicates a considerable decrease of the peripheral uptake of glucose. Scand J Clin Lab Invest Downloaded from informahealthcare.com by University of Newcastle on 01/02/15 For personal use only. 15. Havel, R. J., Kane, I. P., Balasse, E. O., Segel, N. & Basso, L. V. Splanchnic metabolism of free fatty acids and production of triglycerides of very low density lipoproteins in normotri-Scand J Clin Lab Invest Downloaded from informahealthcare.com by University of Newcastle on 01/02/15 For personal use only.
Of 120 patients who were investigated for moderately elevated liver function tests as the only sign of liver disease, 6 young persons had alpha-1-antitrypsin (AAT) deficiency. Three had a homozygous (Pi ZZ) and three had a heterozygous (Pi MZ) AAT deficiency as measured with isoelectric focusing. An extensive investigation ruled out all other causes of liver disease. The three homozygous patients showed typical periodic acid-Schiff (PAS)-positive globules in their liver biopsies and slight fibrosis, whereas none of the heterozygous patients showed these features. Electron microscopical investigation also showed typical findings in the homozygous but not in the heterozygous patients. Further development of liver disease in these young and apparently healthy AAT-deficient patients with early signs of liver damage is not known. It is possible that these patients will develop severe liver disease later in life. It was possible to detect only the three homozygous patients by histochemical examination of liver tissue, since the heterozygous patients did not show PAS-positive globules in their liver.
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