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Divisions of 1 Endocrinology, Metabolism, and Nutrition and 2 Gastroenterology, Departments of Internal Medicine and 3 Pediatrics and Adolescent Medicine, Mayo Clinic and Foundation, Rochester, Minnesota 55905
To
determine if enteral delivery of glucose influences splanchnic
glucose metabolism, 10 subjects were studied when glucose was
either infused into the duodenum at a rate of 22 µmol · kg
1 · min
1 and
supplemental glucose given intravenously or when all glucose was
infused intravenously while saline was infused intraduodenally. Hormone
secretion was inhibited with somatostatin, and glucose (~8.5 mmol/l)
and insulin (~450 pmol/l) were maintained at constant but elevated
levels. Intravenously infused
[6,6-2H2]glucose was used to trace the
systemic appearance of intraduodenally infused
[3-3H]glucose, whereas UDP-glucose flux (an index of
hepatic glycogen synthesis) was measured using the acetaminophen
glucuronide method. Despite differences in the route of glucose
delivery, glucose production (3.5 ± 1.0 vs. 3.3 ± 1.0 µmol · kg
1 · min
1) and
glucose disappearance (78.9 ± 5.7 vs. 85.0 ± 7.2 µmol · kg
1 · min
1) were
comparable on intraduodenal and intravenous study days. Initial
splanchnic glucose extraction (17.5 ± 4.4 vs. 14.5 ± 2.9%) and hepatic UDP-glucose flux (9.0 ± 2.0 vs. 10.3 ± 1.5 µmol · kg
1 · min
1) also
did not differ on the intraduodenal and intravenous study days. These
data argue against the existence of an "enteric" factor that
directly (i.e., independently of circulating hormone concentrations) enhances splanchnic glucose uptake or hepatic glycogen synthesis in
nondiabetic humans.
splanchnic glucose metabolism; postprandial hyperglycemia; acetaminophen glucuronide; hepatic glycogen synthesis; enteric signal
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