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Diabetes, Vol 34, Issue 6 580-588, Copyright © 1985 by American Diabetes Association
The disposal of an oral glucose load in healthy subjects. A quantitative study
E Ferrannini, O Bjorkman, GA Reichard, A Pilo, M Olsson, J Wahren and RA DeFronzo
Although it is an established concept that the liver is important in the
disposition of glucose, the quantitative contribution of the splanchnic and
peripheral tissues, respectively, to the disposal of an oral glucose load
is still controversial. In the present investigation, we have employed the
hepatic venous catheter technique in combination with a double-tracer
approach (in which the glucose pool is labeled with 3H-glucose and the oral
glucose load is labeled with 14C-glucose) to quantitate the four
determinants of oral glucose tolerance: rate of oral glucose appearance,
splanchnic glucose uptake, peripheral glucose uptake, and suppression of
hepatic glucose production. Studies were carried out in 11 normal
volunteers in the overnight-fasted state and for 3.5 h after the ingestion
of glucose (1 g/kg body wt; range, 55-93 g). In the postabsorptive state,
the rate of endogenous (hepatic) glucose production, evaluated from the
3H-glucose infusion, was 2.34 +/- 0.06 mg/min X kg. Glucose ingestion was
accompanied by a prompt reduction of endogenous glucose output, which
reached a nadir of 0.62 +/- 0.23 mg/min X kg at 45 min and remained
suppressed after 3.5 h (0.85 +/- 0.22 mg/min X kg). The average inhibition
of hepatic glucose output during the absorptive period was 53 +/- 5%. The
appearance of ingested glucose in arterial blood, as derived from the
14C-glucose measurements after correction for recycling 14-C radioactivity,
reached a peak after 15-30 min, and 14C-glucose continued to enter the
systemic circulation throughout the observation period. The rate of
appearance of ingested glucose was 2.47 +/- 0.45 mg/min X kg at 3.5 h. A
total of 73 +/- 4% of the oral load was recovered in the systemic
circulation within 3.5 h.(ABSTRACT TRUNCATED AT 250 WORDS)

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275(4):
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August 1, 1998;
275(2):
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[Abstract]
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Am J Physiol Endocrinol Metab,
July 1, 1998;
275(1):
E101 - E111.
[Abstract]
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Copyright © 1985 by the American Diabetes Association.
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