In the basal state, approx. 60–70% of the insulin released from the pancreas is extracted by the liver; the remaining 30–40% is extracted by extrasplanchnic organs. Carbohydrate ingestion is known to stimulate pancreatic insulin release and to inhibit whole-body insulin extraction. The present study was undertaken to obtain a quantitative assessment of the degree to which early postprandial insulinaemia in peripheral blood is due to the inhibition of splanchnic as opposed to extrasplanchnic insulin extraction. By means of catheterization, which allowed frequent analyses of insulin and C-peptide in arterial and hepatic venous blood and estimates of splanchnic plasma flow (indocyanine), insulin extraction by splanchnic and extrasplanchnic tissues was studied in 16 healthy volunteers at timed intervals before and after or during oral (n = 8) and intravenous (n = 8) isoglycaemic glucose loads. Splanchnic insulin extraction (66±2% in the basal state) fell significantly during the 10 min after oral glucose to a minimum of 45±8%; during 5–20 min of intravenous glucose administration it rose significantly to a maximum of 72±2%. Extrasplanchnic extraction of insulin fell from 90–100% in the basal state to a minimum of 3±6% (P< 0.001) after oral glucose; during the first 5 min of intravenous glucose infusion it fell in relative but not in absolute terms. It is concluded that the early postprandial increase in peripheral insulinaemia largely (> 85% during the first 30 min) reflects a marked inhibition of insulin extraction. It is suggested that intestinal hormones and/or splanchnic blood flow may be involved in the mechanisms governing the postprandial inhibition of insulin extraction.

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