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YOGESH C. PATEL, OM. P. GANDA, ROBERT BENOIT, Pancreatic Somatostatinoma: Abundance of Somatostatin-28(1–2)-Like Immunoreactivity in Tumor and Plasma, The Journal of Clinical Endocrinology & Metabolism, Volume 57, Issue 5, 1 November 1983, Pages 1048–1053, https://doi.org/10.1210/jcem-57-5-1048
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In the present study we characterized and compared the relative amounts of the different molecular forms of somatostatin-14 like immunoreactivity (S-14 LI) and of somato-statin-28(1–2) like immunoreactivity (S-28(1–2) LI) in extracts of tumor and peripheral plasma of a patient with a pancreatic somatostatinoma. Tissue and plasma were chromatographed on Sephadex G-50 columns equilibrated with 6 m urea. Immuno-reactivity in the eluting fractions was assayed with two separate, region specific RIAs using antibodies R149 (S-14 LI) and S309 (S-28(1–2)LI). RIA R149 recognizes the 6-8 and 14 regions of the S-14 sequence and detects S-14, S-28, and prosomatostatin, an approximately 14,000 mol wt precursor for the two peptides. RIA S309 recognizes the 2–11 segment of S-28 and reacts with S-28, S-28(1–2), and higher mol wt S-28(1–2) LI but not S-14. Total tumor S-14 LI was 190 pmol/mg protein and consisted of three peaks of immunoreactivity of apparent 14,000 mol wt (14K S-14 LI), 3,200 mol wt (3.2K corresponding to S-28) and 1,600 mol wt (1.6K corresponding to S-14). The three peaks comprised, respectively, 7%, 57%, and 36% of total S-14 LI. Total tumor S-28(1–2) LI was 594 pmol/mg protein and eluted as four major peaks of immunoreactivity as follows: peak I (mol wt 15,000, 10% of total S-28(1–2) LI); peak II (mol wt 8,000, 20% of S-28(1–2) LI), peak III (corresponding to S-28,19% of S-28(1–2)LI); peak IV (corresponding to S-28(1–2), ∼50% of total S-28(1–2)LI). Total plasma concentration of S-14 LI was 714 pm, being made up of the three peaks found in tumor but in the following relative amounts (14K S-14 LI, 22%; 3.2K, 29%; 1.6 K, 49%). Plasma S-28(1–2) LI was 4 times higher (2879 pm) than S-14 LI and contained immunoreactivity corresponding to each of the four peaks found in the tumor.
Conclusions: 1) The tumor and plasma concentrations of S-28(1–2) LI were greater than that of S-14 LI. 2) Both tumor and plasma S-14 LI and S-28 LI were heterogeneous and comprised species corresponding not only to S-14 but also S-28, S-28(1–2), prosomatostatin, and other higher mol wt forms of S-28. 3) The finding of high concentrations of forms corresponding to S-28(1–2) and 8K S-28(1–2) LI (without S-14 activity) suggests the existence of two pathways for synthesis of S-14 from prosoma-tostatin, either directly (prosomatostatin → S-14 + 8K S-28(1–2) LI) or via S-28 (prosomatostatin → S-28 → S-14 + S-28(1–2). 4) The hormonal effects associated with somatostatinomas must result not only from high circulating levels of S-14 but also from S-28 and higher mol wt forms with potential biological activity.
