Glucose disposal during insulinopenia in somatostatin-treated dogs. The roles of glucose and glucagon.
Glucose disposal during insulinopenia in somatostatin-treated dogs. The roles of glucose and glucagon.
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生长抑素治疗犬胰岛素减少期间的葡萄糖处理。
DOI：
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发表时间：
1978
影响因子：
15.9
通讯作者：
A. Cherrington
中科院分区：
文献类型：
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作者：
G. Shulman;J. Liljenquist;P. Williams;W. Lacy;A. Cherrington
本研究的第一个目的是确定血浆葡萄糖水平是否可以在体内调节肝脏葡萄糖平衡，而不依赖于其对胰岛素和胰高血糖素分泌的影响。为了实现这一点，将葡萄糖输注到清醒的狗中，这些狗的基础胰岛素和胰高血糖素分泌在生长抑素抑制内源性胰腺激素释放后被外源性门静脉内胰岛素和胰高血糖素输注所取代。在基础水平胰岛素（7+/-1 muU/ml）和胰高血糖素（76+/-3 pg/ml）存在的情况下，急性诱导高血糖症（平均增量为121 mg/dl）导致净肝葡萄糖产生减少56%，但不引起净肝葡萄糖摄取。研究的第二个目的是确定血浆胰高血糖素水平的降低是否会改变葡萄糖对肝脏的影响。重复上述方案，除了在诱导高血糖症的同时停用胰高血糖素（血浆胰高血糖素降低83%）。在这种情况下，随着胰岛素水平基础（7+/-1 μ U/ml）和胰高血糖素水平降低（16+/-2 pg/ml），高血糖症（平均增加130 mg/dl）促进显著的净肝葡萄糖摄取（1.5+/-0.2 mg/kg/min）和糖原沉积。总之，（a）血浆葡萄糖浓度的生理增量，与其对胰岛素和胰高血糖素分泌的影响无关，可以显著降低体内净肝葡萄糖产生，但在高达230 mg/dl的水平下不能诱导净肝葡萄糖储存，和（B）在存在基础胰岛素的情况下，高血糖刺激净肝葡萄糖储存的能力受到血浆胰高血糖素的影响，浓度.
The first aim of this study was to determine whether the plasma glucose level can regulate hepatic glucose balance in vivo independent of its effects on insulin and glucagon secretion. To accomplish this, glucose was infused into conscious dogs whose basal insulin and glucagon secretion had been replaced by exogenous intraportal insulin and glucagon infusion after somatostatin inhibition of endogenous pancreatic hormone release. The acute induction of hyperglycemia (mean increment of 121 mg/dl) in the presence of basal levels of insulin (7+/-1 muU/ml) and glucagon (76+/-3 pg/ml) resulted in a 56% decrease in net hepatic glucose production but did not cause net hepatic glucose uptake. The second aim of the study was to determine whether a decrease in the plasma glucagon level would modify the effect of glucose on the liver. The above protocol was repeated with the exception that glucagon was withdrawn (83% decrease in plasma glucagon) coincident with the induction of hyperglycemia. Under this circumstance, with the insulin level basal (7+/-1 muU/ml) and the glucagon levels reduced (16+/-2 pg/ml), hyperglycemia (mean increment of 130 mg/dl) promoted marked net hepatic glucose uptake (1.5+/-0.2 mg/kg per min) and glycogen deposition. In conclusion, (a) physiological increments in the plasma glucose concentration, independent of their effects on insulin and glucagon secretion, can significantly reduce net hepatic glucose production in vivo but at levels as high as 230 mg/dl cannot induce net hepatic glucose storage and (b) in the presence of basal insulin the ability of hyperglycemia to stimulate net hepatic glucose storage is influenced by the plasma glucagon concentration.