Vella A, Shah P, Basu R, Basu A, Camilleri M, Schwenk W F, Rizza R A
Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA.
Diabetologia. 2001 Jun;44(6):729-37. doi: 10.1007/s001250051682.
AIMS/HYPOTHESIS: Our aim was to determine whether an alteration in splanchnic glucose metabolism could contribute to postprandial hyperglycaemia in people with Type I (insulin-dependent) diabetes mellitus.
Splanchnic glucose extraction, hepatic glycogen synthesis and endogenous glucose production were compared in 8 Type I diabetic patients and in 11 control subjects. Endogenous hormone secretion was inhibited with somatostatin while insulin (approximately 550 pmol/l) and glucagon (approximately 130 ng/l) concentrations were matched with exogenous hormone infusions. Glucose containing [3-3H] glucose was infused into the duodenum at a rate of 20 micromol.kg(-1).min(-1). Plasma glucose concentrations were maintained at about 8.5 mmol/l in both groups by means of a separate variable intravenous glucose infusion.
Initial splanchnic glucose uptake, calculated by subtracting the systemic rate of appearance of [3-3H] glucose from the rate of infusion of [3-3H] glucose into the duodenum, did not differ in the diabetic and non-diabetic patients (4.1 +/- 0.8 vs 3.0 +/- 1.0 micromol/kg/min). In addition, hepatic glycogen synthesis, measured using the acetaminophen glucuronide method did not differ (10.7 +/- 2.4 vs 10.1 +/- 2.7 micromol.kg(-1).min(-1)). On the other hand, suppression of endogenous glucose production, measured by an intravenous infusion of [6,6-2H2] glucose, was greater (p < 0.05) in the diabetic than in the non-diabetic subjects (1.7 +/- 1.6 vs 5.8 +/- 1.9 micromol.kg(-1).min(-1)).
CONCLUSION/INTERPRETATION: When glucose, insulin and glucagon concentrations are matched in individuals with relatively good chronic glycaemic control, Type I diabetes does not alter initial splanchnic glucose uptake of enterally delivered glucose or hepatic glycogen synthesis. Alterations in splanchnic glucose metabolism are not likely to contribute to postprandial hyperglycaemia in people with well controlled Type I diabetes.
目的/假设：我们的目的是确定内脏葡萄糖代谢的改变是否会导致I型（胰岛素依赖型）糖尿病患者的餐后高血糖。
比较了8例I型糖尿病患者和11例对照者的内脏葡萄糖摄取、肝糖原合成及内源性葡萄糖生成。使用生长抑素抑制内源性激素分泌，同时通过外源性激素输注使胰岛素（约550 pmol/l）和胰高血糖素（约130 ng/l）浓度相匹配。以20 μmol·kg⁻¹·min⁻¹的速率将含[3-³H]葡萄糖的葡萄糖注入十二指肠。通过单独的可变静脉葡萄糖输注使两组的血浆葡萄糖浓度维持在约8.5 mmol/l。
通过从十二指肠注入[3-³H]葡萄糖的速率中减去[3-³H]葡萄糖的全身出现速率计算得出的初始内脏葡萄糖摄取，在糖尿病患者和非糖尿病患者中无差异（4.1±0.8对3.0±1.0 μmol/kg/min）。此外，使用对乙酰氨基酚葡糖醛酸苷法测量的肝糖原合成也无差异（10.7±2.4对10.1±2.7 μmol·kg⁻¹·min⁻¹）。另一方面，通过静脉输注[6,6-²H₂]葡萄糖测量的内源性葡萄糖生成抑制，在糖尿病患者中比非糖尿病患者更大（p<0.05）（1.7±1.6对5.8±1.9 μmol·kg⁻¹·min⁻¹）。
结论/解读：当血糖、胰岛素和胰高血糖素浓度在慢性血糖控制相对良好的个体中相匹配时，I型糖尿病不会改变经肠道给予葡萄糖的初始内脏葡萄糖摄取或肝糖原合成。内脏葡萄糖代谢的改变不太可能导致血糖控制良好的I型糖尿病患者出现餐后高血糖。
