Response to glucose infusion in humans: role of changes in insulin concentration.
We have used the primed-constant infusion of stable isotopes of glucose ([6,6-d2]glucose), alanine([3-13C] alanine), and urea ([15N2]urea) to investigate their kinetic interrelationships in normal volunteers in the postabsorptive state and during the infusion of unlabeled glucose at two rates. Each glucose infusion was tested with and without the simultaneous infusion of somatostatin (S), insulin (I), and glucagon (G) to clamp those hormonal levels. When glucose was infused at 1 mg X kg-1 X min-1, endogenous glucose production was suppressed almost exactly 1 mg X kg-1 X min-1, regardless of whether S plus I plus G were infused. The 4 mg X kg-1 X min-1 glucose infusion suppressed endogenous glucose production, both with and without hormonal control. The plasma concentration of glucose also increased to the same extent during the 4 mg X kg-1 X min-1 infusion in both protocols, which indicated that the spontaneous insulin response to the glucose infusion (an increase from 11 +/- 2 to 24 +/- 3 microU/ml) did not stimulate the peripheral clearance of glucose. The high rate of glucose infusion, both with or without hormonal control, stimulated alanine flux and inhibited urea production. These results indicate that glucose, per se, is an important direct controller of normal metabolic interactions of endogenous alanine, glucose, and urea kinetics.
Wolfe
R R
RR
Shaw
J H
JH
Jahoor
F
F
Herndon
D N
DN
Wolfe
M H
MH
D000328:Adult; D000409:Alanine / Q000378:metabolism; D005934:Glucagon; D005947:Glucose / Q000378:metabolism; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D007700:Kinetics; D013004:Somatostatin; D014508:Urea / Q000378:metabolism
D007328:Insulin; D013004:Somatostatin; D014508:Urea; D005934:Glucagon; D005947:Glucose; D000409:Alanine