科研之友
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摘要
Context: Total pancreatectomy and intrahepatic islet autotransplantation (TP/IAT) is performed to alleviate severe abdominal pain, avoid narcotic use, maintain islet function, and avoid diabetes in patients with chronic pancreatitis. However, many TP/IAT recipients complain of postprandial hypoglycemia.
Objective: This study was designed to discover the mechanisms of this problem.
Design: Participants consumed a triple-isotope mixed meal.
Setting: This study was performed in a hospital research unit.
Participants: We studied 10 TP/IAT recipients and 10 age-and body mass index-matched control subjects. Seven of 10 recipients had a history of postprandial hypoglycemia.
Interventions: Participants were given a [1-C-13]-labeled mixed meal and two tracer infusions ([6,6-(2)H2]-and [6-H-3]-glucose).
Main Outcome Measures: Glucose kinetics and concentrations of regulatory hormones were determined.
Results: Immediately after the meal, peak glucose was elevated in recipients compared with control subjects [266 +/- 20 mg/dL (14.8 +/- 1.1 mmol/L) vs 185 +/- 13 mg/dL (10.3 +/- 0.7 mmol/L); P = 0.01]. However, mean Delta glucose for TP/IAT recipients betweenminutes 240 and 360 postprandially was significantly lower than for control subjects (P, 0.05); six of the seven recipients with a history of hypoglycemia experienced abnormally low postprandial Delta glucose. Delta Glucagon remained unchanged (minutes 240 to 360; P = 0.58) in TP/IAT recipients despite abnormal decreases in postprandial glucose. Radioisotopic studies revealed that meal appearance, glucose disappearance, and endogenous glucose production in TP/IAT recipients were not different from control subjects.
Conclusion: Initially high glucose levels followed by hypoglycemia with an absent glucagon response is a mechanistic sequence that contributes to postprandial hypoglycemia after TP/IAT.
- 出版日期2018-4
