Reversal of abnormal glucose production after pancreatic resection by pancreatic polypeptide administration in man

N. E. Seymour, C. Brunicardi, R. L. Chaiken, H. E. Lebovitz, R. E. Chance, R. L. Gingerich, D. Elahi, D. K. Andersen

Research output: Contribution to journalArticle

Abstract

Pancreatic polypeptide (PP) deficiency has been associated with impaired hepatic sensitivity to insulin and pancreatogenic diabetes in chronic pancreatitis. Since pancreatic resection might also result in PP deficiency, hepatic responses to insulin infusion (0.25 mU/kg/min) were determined by the euglycemic glucose clamp technique in 10 patients who had previously undergone pancreatic resection for trauma and in eight healthy control subjects. Six resection patients (RES-PP) demonstrated deficient PP levels, with a mean increase of plasma immunoreactive PP of 20 ± 7 pg/ml above basal rate after a test meal compared with 232 ± 82 pg/ml in control subjects (p <0.01) and 353 ± 133 pg/ml in four other patients undergoing resection with normal levels of immunoreactive PP (RES + PP) (p <0.03). Three identical insulin infusion studies were performed in each subject, the second of which was performed during the final 2 hours of an 8-hour infusion of bovine PP (2.0 pmol/kg/min). Whereas hepatic glucose production (HGP) in control subjects fell 74% ± 4% from a basal rate of 2.0 ± 0.1 mg/kg/min to a 60- to 120-minute value of 0.5 ± 0.1 mg/kg/min during insulin infusion, HGP was suppressed only 58% ± 5% in RES-PP subjects, from 1.9 ± 0.1 to 0.8 ± 0.1 mg/kg/min (p <0.05 vs controls). Intravenous infusion of PP corrected the hepatic resistance to insulin seen in the PP-deficient group. During PP infusion, HGP was suppressed 74% ± 5% in RES-PP subjects, from 2.1 ± 0.2 to 0.5 ± 0.1 mg/kg/min (p <0.04 compared with initial study). PP infusion produced no significant change in glucose metabolism in control and RES + PP subjects. Overall glucose disposal rates were not altered by PP infusion in any group. These findings support a role of PP as a glucoregulatory hormone and suggest that PP deficiency may serve as a reversible pathophysiologic factor in the abnormal glucose metabolism seen after pancreatic resection.

Original languageEnglish (US)
Pages (from-to)119-129
Number of pages11
JournalSurgery
Volume104
Issue number2
StatePublished - 1988
Externally publishedYes

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Pancreatic Polypeptide
Glucose
Liver
Glucose Clamp Technique
Insulin
Insulin Resistance

ASJC Scopus subject areas

  • Surgery

Cite this

Seymour, N. E., Brunicardi, C., Chaiken, R. L., Lebovitz, H. E., Chance, R. E., Gingerich, R. L., ... Andersen, D. K. (1988). Reversal of abnormal glucose production after pancreatic resection by pancreatic polypeptide administration in man. Surgery, 104(2), 119-129.

Reversal of abnormal glucose production after pancreatic resection by pancreatic polypeptide administration in man. / Seymour, N. E.; Brunicardi, C.; Chaiken, R. L.; Lebovitz, H. E.; Chance, R. E.; Gingerich, R. L.; Elahi, D.; Andersen, D. K.

In: Surgery, Vol. 104, No. 2, 1988, p. 119-129.

Research output: Contribution to journalArticle

Seymour, NE, Brunicardi, C, Chaiken, RL, Lebovitz, HE, Chance, RE, Gingerich, RL, Elahi, D & Andersen, DK 1988, 'Reversal of abnormal glucose production after pancreatic resection by pancreatic polypeptide administration in man', Surgery, vol. 104, no. 2, pp. 119-129.
Seymour NE, Brunicardi C, Chaiken RL, Lebovitz HE, Chance RE, Gingerich RL et al. Reversal of abnormal glucose production after pancreatic resection by pancreatic polypeptide administration in man. Surgery. 1988;104(2):119-129.
Seymour, N. E. ; Brunicardi, C. ; Chaiken, R. L. ; Lebovitz, H. E. ; Chance, R. E. ; Gingerich, R. L. ; Elahi, D. ; Andersen, D. K. / Reversal of abnormal glucose production after pancreatic resection by pancreatic polypeptide administration in man. In: Surgery. 1988 ; Vol. 104, No. 2. pp. 119-129.
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abstract = "Pancreatic polypeptide (PP) deficiency has been associated with impaired hepatic sensitivity to insulin and pancreatogenic diabetes in chronic pancreatitis. Since pancreatic resection might also result in PP deficiency, hepatic responses to insulin infusion (0.25 mU/kg/min) were determined by the euglycemic glucose clamp technique in 10 patients who had previously undergone pancreatic resection for trauma and in eight healthy control subjects. Six resection patients (RES-PP) demonstrated deficient PP levels, with a mean increase of plasma immunoreactive PP of 20 ± 7 pg/ml above basal rate after a test meal compared with 232 ± 82 pg/ml in control subjects (p <0.01) and 353 ± 133 pg/ml in four other patients undergoing resection with normal levels of immunoreactive PP (RES + PP) (p <0.03). Three identical insulin infusion studies were performed in each subject, the second of which was performed during the final 2 hours of an 8-hour infusion of bovine PP (2.0 pmol/kg/min). Whereas hepatic glucose production (HGP) in control subjects fell 74{\%} ± 4{\%} from a basal rate of 2.0 ± 0.1 mg/kg/min to a 60- to 120-minute value of 0.5 ± 0.1 mg/kg/min during insulin infusion, HGP was suppressed only 58{\%} ± 5{\%} in RES-PP subjects, from 1.9 ± 0.1 to 0.8 ± 0.1 mg/kg/min (p <0.05 vs controls). Intravenous infusion of PP corrected the hepatic resistance to insulin seen in the PP-deficient group. During PP infusion, HGP was suppressed 74{\%} ± 5{\%} in RES-PP subjects, from 2.1 ± 0.2 to 0.5 ± 0.1 mg/kg/min (p <0.04 compared with initial study). PP infusion produced no significant change in glucose metabolism in control and RES + PP subjects. Overall glucose disposal rates were not altered by PP infusion in any group. These findings support a role of PP as a glucoregulatory hormone and suggest that PP deficiency may serve as a reversible pathophysiologic factor in the abnormal glucose metabolism seen after pancreatic resection.",
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AU - Seymour, N. E.

AU - Brunicardi, C.

AU - Chaiken, R. L.

AU - Lebovitz, H. E.

AU - Chance, R. E.

AU - Gingerich, R. L.

AU - Elahi, D.

AU - Andersen, D. K.

PY - 1988

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N2 - Pancreatic polypeptide (PP) deficiency has been associated with impaired hepatic sensitivity to insulin and pancreatogenic diabetes in chronic pancreatitis. Since pancreatic resection might also result in PP deficiency, hepatic responses to insulin infusion (0.25 mU/kg/min) were determined by the euglycemic glucose clamp technique in 10 patients who had previously undergone pancreatic resection for trauma and in eight healthy control subjects. Six resection patients (RES-PP) demonstrated deficient PP levels, with a mean increase of plasma immunoreactive PP of 20 ± 7 pg/ml above basal rate after a test meal compared with 232 ± 82 pg/ml in control subjects (p <0.01) and 353 ± 133 pg/ml in four other patients undergoing resection with normal levels of immunoreactive PP (RES + PP) (p <0.03). Three identical insulin infusion studies were performed in each subject, the second of which was performed during the final 2 hours of an 8-hour infusion of bovine PP (2.0 pmol/kg/min). Whereas hepatic glucose production (HGP) in control subjects fell 74% ± 4% from a basal rate of 2.0 ± 0.1 mg/kg/min to a 60- to 120-minute value of 0.5 ± 0.1 mg/kg/min during insulin infusion, HGP was suppressed only 58% ± 5% in RES-PP subjects, from 1.9 ± 0.1 to 0.8 ± 0.1 mg/kg/min (p <0.05 vs controls). Intravenous infusion of PP corrected the hepatic resistance to insulin seen in the PP-deficient group. During PP infusion, HGP was suppressed 74% ± 5% in RES-PP subjects, from 2.1 ± 0.2 to 0.5 ± 0.1 mg/kg/min (p <0.04 compared with initial study). PP infusion produced no significant change in glucose metabolism in control and RES + PP subjects. Overall glucose disposal rates were not altered by PP infusion in any group. These findings support a role of PP as a glucoregulatory hormone and suggest that PP deficiency may serve as a reversible pathophysiologic factor in the abnormal glucose metabolism seen after pancreatic resection.

AB - Pancreatic polypeptide (PP) deficiency has been associated with impaired hepatic sensitivity to insulin and pancreatogenic diabetes in chronic pancreatitis. Since pancreatic resection might also result in PP deficiency, hepatic responses to insulin infusion (0.25 mU/kg/min) were determined by the euglycemic glucose clamp technique in 10 patients who had previously undergone pancreatic resection for trauma and in eight healthy control subjects. Six resection patients (RES-PP) demonstrated deficient PP levels, with a mean increase of plasma immunoreactive PP of 20 ± 7 pg/ml above basal rate after a test meal compared with 232 ± 82 pg/ml in control subjects (p <0.01) and 353 ± 133 pg/ml in four other patients undergoing resection with normal levels of immunoreactive PP (RES + PP) (p <0.03). Three identical insulin infusion studies were performed in each subject, the second of which was performed during the final 2 hours of an 8-hour infusion of bovine PP (2.0 pmol/kg/min). Whereas hepatic glucose production (HGP) in control subjects fell 74% ± 4% from a basal rate of 2.0 ± 0.1 mg/kg/min to a 60- to 120-minute value of 0.5 ± 0.1 mg/kg/min during insulin infusion, HGP was suppressed only 58% ± 5% in RES-PP subjects, from 1.9 ± 0.1 to 0.8 ± 0.1 mg/kg/min (p <0.05 vs controls). Intravenous infusion of PP corrected the hepatic resistance to insulin seen in the PP-deficient group. During PP infusion, HGP was suppressed 74% ± 5% in RES-PP subjects, from 2.1 ± 0.2 to 0.5 ± 0.1 mg/kg/min (p <0.04 compared with initial study). PP infusion produced no significant change in glucose metabolism in control and RES + PP subjects. Overall glucose disposal rates were not altered by PP infusion in any group. These findings support a role of PP as a glucoregulatory hormone and suggest that PP deficiency may serve as a reversible pathophysiologic factor in the abnormal glucose metabolism seen after pancreatic resection.

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