GLUCAGON DEFICIENCY AND HYPERAMINOACIDEMIA AFTER TOTAL PANCREATECTOMY
GLUCAGON DEFICIENCY AND HYPERAMINOACIDEMIA AFTER TOTAL PANCREATECTOMY
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DOI:
10.1172/jci109717
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发表时间:
1980-01-01
影响因子:
15.9
通讯作者:
OWEN, OE
中科院分区:
文献类型:
--
作者:
BODEN, G;MASTER, RW;OWEN, OE
The first goal of this study was to investigate whether totally pancreatectomized patients are glucagon [G] deficient and if so, to what degree. Immunoreactive glucagon (IRG) concentrations in peripheral plasma of 9 pancreatectomized patients were not significantly different from those of 10 normal controls as measured by 2 antisera (30-K and RCS-5) both detecting the COOH-terminal portion of the molecule and one (RCS-5) postulated to be specific for pancreatic G. Plasma from 6 of 9 pancreatectomized patients were fractionated over Sephadex G-50 and IRG was measured with both antisera in the column eluates. Using 30-K, 80.8 .+-. 9% of the IRG eluted within the void volume. This material was rechromatographed on Sephadex G-200 and had an apparent MW of .apprx. 200,000. Only 18.3 .+-. 9% eluted in the IRG3500 region. IRG3500 was significantly reduced in pancreatectomized patients as compared to normal controls (49 .+-. 9 vs. 18 .+-. 9 pg/ml, P < 0.05). Using RCS-5, all IRG (corresponding to 20 .+-. 6 pg/ml of plasma) eluted in the IRG3500 region. The second goal of this study was to investigate the effects of chronic G deficiency on plasma amino acids. In the 9 pancreatectomized patients studied, postabsorptive plasma concentrations of Ser, Ala, Arg, Gly, Thr, citrulline, .alpha.-aminobutyrate and Tyr were significantly elevated compared to values obtained from 20 normal controls. Physiological G increments produced in 2 pancreatectomized patients by G infusion (6.25 and 8.0 .mu.g/h, respectively) resulted in normalization of the hyperaminoacidemia within 22 h. Apparently pancreatectomized patients are partially G deficient because of diminished basal as well as diminished stimulated G secretion; fasting concentrations of certain glucogenic amino acids are elevated in pancreatectomized patients probably as a result of reduced hepatic gluconeogenesis; and the RCS-5 antiserum is not pancreatic G specific.