Radioimmunoassay of Gastric Inhibitory Polypeptide (GIP) and the Effect of Intraduodenal Acidification on Glucose-Stimulated and Unstimulated GIP Release in Humans

Abstract

GIP was measured by a radioimmunoassay with an antiserum specific for a site within the sequence GIP 15–43. Plasma was precipitated with acetic acid alcohol, and bound and free antigen were separated with polyethylene glycol. The sensitivity (ID 50) was 9.2 pM, corresponding to 46.0 pM in plasma and expressed as the detection limit 2.26 pM and 11.3 pM, respectively. Dilutions of human plasma extracts were parallel to the standard curve, and 80% of the GIP immunoreactivity eluted corresponding to standard GIP by gel chromatography. The effect of duodenal acidification on the glucose-stimulated GIP and insulin release was investigated in man by intraduodenal infusion of glucose with a pH of 6.5 or 1.5 (no. = 7). The GIP concentration in plasma increased from 36.7 (27.5–62.2) to 134 (78.9–215) pM after infusion of glucose with a pH of 6.5 and from 44.6 (23.4–60.5) to 141 (74.0–246) pM after pH 1.5 glucose. Peak values of insulin were 52 (28–73) and 58 (46–122) mU/1, respectively. Infusion of 50 ml 0.1 M HCl intraduodenally (no. = 6) or aspiration of the gastric secretion (no. = 9) for 150 min did not alter the unstimulated GIP concentration in plasma. It is concluded that an acid environment in the duodenum neither potentiates the glucose-induced GIP and insulin release nor influences the unstimulated GIP concentration.

Key-words:

• Acidification, duodenal
• entero-insular axis
• gastric aspiration
• gastric inhibitory polypeptide (GIP)
• glucose
• human
• incretin
• insulin
• precipitation, plasma
• polyethylene glycol
• radioimmunoassay