Role of the Liver in Endotoxin‐Induced Hyperinsulinemia and Hyperglucagonemia in Rats

Robert P. Cornell – 1 January 1983 – The intravenous administration of bacterial endotoxin to fasted rats elicited basal portal and systemic venous hyperinsulinemia and hyperglucagonemia. Enhanced pancreatic secretion of insulin and glucagon was implied by the elevated portal venous hormonal levels. Elevated insulin and glucagon levels were present at 4 hr after a 33 m̈g/100 gm intravenous endotoxin dose despite no fluctuation of the plasma glucose concentration.

Lipolysosomes in Human Hepatocytes: Their Increase in Number Associated with Serum Level of Cholesterol in Chronic Liver Diseases

Hisao Hayashi, Yoichi Sameshima, Michio Lee, Yasuhiro Hotta, Toshihiko Kosaka – 1 January 1983 – The clinical significance of hepatocellular lipolysosomes in patients with various liver diseases was investigated. Of the 102 cases studied, lipolysosomes were found in 78 cases or 76%. In patients with fatty change of the liver, hepatocellular lipolysosomes were found in 62 of 68 or 91%. In patients without fatty change, lipolysosomes were found in 16 of 34 or 47%. The lipolysosome:.lipido ratio in the hepatocytes ranged from 0 to 10%.

Galactosamine Hepatitis, Endotoxemia, and Lactulose

Hendrina Van Vugt, Jacobus Van Gool, Lambert L. M. Thomas – 1 January 1983 – Studies by Liehr et al. suggest that endotoxins are important in the pathogenesis of galactosamine hepatitis (Gal‐N hepatitis) in rats. Lactulose (9.1 gm per kg per day) prevents hepatic lesions induced by Gal‐N; an antiendotoxin effect of lactulose is postulated. However, commercial preparations of lactulose are contaminated with galactose, which shows a competitive action to Gal‐N.

Spironolactone‐ and Canrenone‐Induced Changes in Hepatic (Na+, K+)ATPase Activity, Surface Membrane Cholesterol and Phospholipid, and Fluorescence Polarization in the Rat

Philip B. Miner, Michael Sneller, Synda S. Crawford – 1 January 1983 – We studied changes in hepatic membrane (Na+,K+)ATPase activity and membrane lipids induced by canrenoate, the water‐soluble congener of canrenone, the active metabolite of spironolactone. (Na+,K+)ATPase activity was decreased after canrenoate in a dose‐ and time‐dependent manner.

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