Role of hyperglucagonemia in maintenance of increased rates of hepatic glucose output in type II diabetics

Diabetes ◽  
1987 ◽  
Vol 36 (3) ◽  
pp. 274-283 ◽  
Author(s):  
A. D. Baron ◽  
L. Schaeffer ◽  
P. Shragg ◽  
O. G. Kolterman
Diabetes ◽  
1987 ◽  
Vol 36 (3) ◽  
pp. 274-283 ◽  
Author(s):  
A. D. Baron ◽  
L. Schaeffer ◽  
P. Shragg ◽  
O. G. Kolterman

2005 ◽  
Vol 2 (5) ◽  
pp. 331-338 ◽  
Author(s):  
Gianluca Canettieri ◽  
Seung-Hoi Koo ◽  
Rebecca Berdeaux ◽  
Jose Heredia ◽  
Susan Hedrick ◽  
...  

1985 ◽  
Vol 63 (11) ◽  
pp. 1460-1464 ◽  
Author(s):  
Ronald P. Brockman

Ruminant animals, as a result of the fermentative nature of their digestion, ordinarily absorb little or no hexose sugar from the gut. Their glucose needs must be met by gluconeogenesis, even postprandially. The role of insulin in regulating hepatic gluconeogenesis in ruminants has not been assessed, in this study the effect of insulin on net hepatic removal of the major glucose precursors was determined, insulin was infused with glucose matched to maintain euglycemia. The insulin concentrations attained in plasma were within the physiological range, insulin at low concentrations reduced the hepatic removal of lactate, glutamine, and glycerol. At higher concentrations of insulin the hepatic extractions of pyruvate and alanine were also reduced. Thus, in sheep insulin at physiological concentrations may reduce hepatic glucose output by altering the uptake of glucose precursors.


1989 ◽  
Vol 257 (4) ◽  
pp. E531-E540 ◽  
Author(s):  
J. C. Levy ◽  
G. Brown ◽  
D. R. Matthews ◽  
R. C. Turner

Steele and others have suggested that minimizing changes in glucose specific activity when estimating hepatic glucose output (HGO) during glucose infusions could reduce non-steady-state errors. This approach was assessed in nondiabetic and type II diabetic subjects during constant low dose [27 mumol.kg ideal body wt (IBW)-1.min-1] glucose infusion followed by a 12 mmol/l hyperglycemic clamp. Eight subjects had paired tests with and without labeled infusions. Labeled infusion was used to compare HGO in 11 nondiabetic and 15 diabetic subjects. Whereas unlabeled infusions produced negative values for endogenous glucose output, labeled infusions largely eliminated this error and reduced the dependence of the Steele model on the pool fraction in the paired tests. By use of labeled infusions, 11 nondiabetic subjects suppressed HGO from 10.2 +/- 0.6 (SE) fasting to 0.8 +/- 0.9 mumol.kg IBW-1.min-1 after 90 min of glucose infusion and to -1.9 +/- 0.5 mumol.kg IBW-1.min-1 after 90 min of a 12 mmol/l glucose clamp, but 15 diabetic subjects suppressed only partially from 13.0 +/- 0.9 fasting to 5.7 +/- 1.2 at the end of the glucose infusion and 5.6 +/- 1.0 mumol.kg IBW-1.min-1 in the clamp (P = 0.02, 0.002, and less than 0.001, respectively).


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