Impact of Glucose Ingestion on Hepatic and Peripheral Glucose Metabolism in Man: An Analysis Based on Simultaneous Use of the Forearm and Double Isotope Techniques*

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Abstract
The metabolic response to glucose ingestion was studied in 10 normalmen (aged 21–23 yr) by the simultaneous application of the forearm and double isotope techniques. The latterconsisted of a primed constant infusion of [3-3H[glucose, followedby the administration of an oral glucose load (mean ± SE, 90.7 ± 0.7 g) containing [l-14C]glucose. Most (80.6 ± 8.1%) of the ingested glucose appeared systemically within 270 min, suggesting that initial splanchnic glucose extraction accounted for 19.4±3.1% (17.7 ± 2.8 g) of the oral load. Basal hepatic glucose output (2.22±0.12 mg/kg-min) was reduced (P <0.005) within 30 min after glucose loading and remained suppressed throughout the study; its mean reduction from 0–270 min was 54.9 ± 9.9%, thereby accounting for the conservation of 26.5 ± 4.9 g glucose. Suprabasal glucose appearance from 0–270 min was 46.6 ± 4.3 g. Forearm glucose uptake rose 8.5–fold to 0664±0.083 mg⁄100 ml forearm–min at 45 min, but basal forearm oxygen uptake (6.1 ± 0.4 µxmol/100 ml forearm·min) did not change.The increment in glucose disappearance from 0–270 min was 46.4 ± 3.8 g, of which increased glucose uptake by muscle, determined from the forearm glucose uptake data, accounted for 37.7 ± 5.1 g (81%). If uptake of the remaining 8.7 g was shared equally by the liver and peripheral tissues, the splanchnic bed and periphery would account, respectively, for 47.1 g (52%) and 43.5 g (48%) of the ingested load. We conclude that 1) s lanchnic and peripheral tissues contribute almost equally to the total homeostatic response; 2) in kinetic terms,decreased hepatic glucose output and increased glucose uptake (splanchnic plusperipheral) constitute 29% and 71% of the total response, respectively; 3) restoration of basal glucose kinetics after glucose ingestion requires more than 270 min; and 4) increased peripheral oxygen uptake is not the mechanism of glucose–induced thermogenesis which, instead, may reflect increased splanchnic oxygenconsumption.

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