Σάββατο 20 Ιανουαρίου 2018

Deficient glucagon response to hypoglycemia during a mixed meal in total pancreatectomy/islet autotransplantation recipients.

Deficient glucagon response to hypoglycemia during a mixed meal in total pancreatectomy/islet autotransplantation recipients.

J Clin Endocrinol Metab. 2018 Jan 17;:

Authors: Bogachus LD, Bellin MD, Vella A, Robertson RP

Abstract
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 post-prandial hypoglycemia.
Objective: This study was designed to discover mechanisms of this problem.
Design: Participants consumed a triple-isotope mixed meal.
Setting: Hospital research unit.
Patients or Other Participants: We studied 10 TP/IAT and 10 age and BMI-matched control subjects. 7 of 10 recipients had a history of post-prandial hypoglycemia.
Interventions: Participants were given a [1-13C]-labeled mixed meal and two tracer infusions ([6,6-2H2]- and [6-3H]-glucose).
Main Outcome Measure(s): Glucose kinetics and concentrations of regulatory hormones were determined.
Results: Peak glucose immediately after the meal was elevated in recipients compared to controls (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 between minutes 240 to 360 post-prandially was significantly lower than control (p<0.05); 6 of the 7 recipients with a history of hypoglycemia experienced abnormally low postprandial delta glucose. Importantly, delta glucagon remained unchanged (min 240-360; p=0.58) in TP/IAT despite abnormal decreases in post-prandial glucose. Radioisotopic studies revealed that meal appearance, glucose disappearance, and endogenous glucose production in TP/IAT recipients were not different than controls.
Conclusion: Initially high glucose levels followed by hypoglycemia with an absent glucagon response is a mechanistic sequence that contributes to post-prandial hypoglycemia after TP/IAT.

PMID: 29351616 [PubMed - as supplied by publisher]



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