interorgan metabolism
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Author(s):  
Wenliang He ◽  
Kyohei Furukawa ◽  
Masaaki Toyomizu ◽  
Tomonori Nochi ◽  
Christopher A. Bailey ◽  
...  


Author(s):  
Patrick J. Ryan ◽  
Steven E. Riechman ◽  
James D. Fluckey ◽  
Guoyao Wu


2013 ◽  
Vol 85 (1) ◽  
pp. 115-123 ◽  
Author(s):  
Sherry Dadsetan ◽  
Michael Sørensen ◽  
Lasse K. Bak ◽  
Hendrik Vilstrup ◽  
Peter Ott ◽  
...  


Life Sciences ◽  
1996 ◽  
Vol 58 (11) ◽  
pp. 935-944 ◽  
Author(s):  
Ming-ta Huang ◽  
Jui-feng Lin ◽  
Chin-fang Lee


Amino Acids ◽  
1991 ◽  
Vol 1 (1) ◽  
pp. 29-35 ◽  
Author(s):  
M. E. Brosnan ◽  
J. Letto


1986 ◽  
Vol 240 (3) ◽  
pp. 829-836 ◽  
Author(s):  
D A Tinker ◽  
J T Brosnan ◽  
G R Herzberg

Arterial-venous differences for metabolites across liver, kidney and hindquarters were measured in fed or starved, artificially ventilated chickens. The results indicate that the liver takes up amino acids under both conditions. Urate and glucose are released by the liver in both the fed and the starved state. Lactate and amino acids are extracted from blood by the kidneys, and this increases in the starved chicken. Urate is removed from the circulation by the kidney in the fed and starved state and excreted. In the fed bird there is no significant arteriovenous difference of glucose across the kidney, but in the starved state the kidney releases glucose into the circulation. The hindquarters take up glucose in the fed but not in the starved state. The branched-chain amino acids valine and leucine were taken up by the hindquarters in the fed, but not the starved, chicken. Glycerol is released by the hindquarter of fed and starved chickens. In the starved state, alanine and glutamine represent 57% of the amino acids released by the hindquarter. Lactate is released by the hindquarter of starved chickens and represents the major gluconeogenic carbon source released by the hindquarter and taken up by kidney and liver. Although the liver is the major gluconeogenic organ in the starved chicken, the kidney accounts for approx. 30% of the glucose produced.



1983 ◽  
Vol 245 (1) ◽  
pp. E94-E101 ◽  
Author(s):  
R. Park ◽  
P. R. Radosevich ◽  
W. J. Leach ◽  
P. Seto ◽  
A. I. Arieff

In fasted, diabetic dogs treated with dichloroacetate (DCA) (300 mg X kg-1 X h-1 iv), we determined the relative contributions by skeletal muscle and gut to the supply of precursors used for hepatic gluconeogenesis. The total production of lactate and alanine by skeletal muscle and gut decreased from 2,370 to 1,160 mumol X kg-1 X h-1 during treatment with DCA. Hepatic uptake of these substrates decreased from 1,040 to 435 mumol X kg-1 X h-1, and blood glucose decreased from 370 +/- 18 to 279 +/- 22 mg/dl (P less than 0.001). DCA treatment decreased the skeletal muscle production of both lactate and alanine to 40% of control, whereas gut production was decreased to only 72% of control levels. Hepatic uptake of the two substrates decreased in proportion to the change in blood levels because fractional hepatic extraction was unaltered. The effects of DCA on the interorgan metabolism of plasma amino acids showed that diminished availability of alanine for hepatic gluconeogenesis was compensated in part by increased release of other gluconeogenic amino acids from muscle and gut. Gut uptake of glutamine appeared unchanged, but most of its metabolic end products were released in greater amounts by DCA treatment, suggesting enhanced glutamine degradation. These results in fasted, diabetic dogs indicate that 1) DCA treatment lowers blood glucose in part by limitation of gluconeogenic substrate supply from skeletal muscle and gut, and 2) DCA has complex and diverse effects on the interorgan metabolism of plasma amino acids.



1980 ◽  
Vol 12 (4) ◽  
pp. 545-551 ◽  
Author(s):  
Thomas M. McIntyre ◽  
Norman P. Curthoys


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