Turner R C, Holman R R
Lancet. 1976 Jun 12;1(7972):1272-4. doi: 10.1016/s0140-6736(76)91739-6.
Hepatic glucose efflux is very sensitive to changes in plasma-insulin and it is postulated that this provides an important feedback control of insulin secretion. In diabetes this hepatic "insulin sensor" increases the basal plasma-glucose until the impaired beta cells are sufficiently stimulated to secrete normal basal insulin concentrations. Glucose regulation thus becomes of secondary importance to the maintenance of basal insulin secretion, which is teleologically needed for the "anabolic" requirements of cell growth. This hypothesis provides an explanation for the "normal" basal plasma-insulin concentrations found in diabetes in spite of impaired beta-cell function. This maintenance of basal insulin secretion accounts for the discrepancy between the marked hyperglycaemia and minimal ketosis of maturity onset diabetic patients.
肝脏葡萄糖外流对血浆胰岛素的变化非常敏感，据推测这为胰岛素分泌提供了重要的反馈控制。在糖尿病中，这种肝脏“胰岛素传感器”会提高基础血糖水平，直到受损的β细胞受到充分刺激，分泌出正常的基础胰岛素浓度。因此，对于维持基础胰岛素分泌而言，血糖调节变得次要，而基础胰岛素分泌对于细胞生长的“合成代谢”需求在目的论上是必需的。这一假说解释了尽管β细胞功能受损，但糖尿病患者仍存在“正常”基础血浆胰岛素浓度的现象。基础胰岛素分泌的这种维持解释了成年型糖尿病患者显著高血糖与轻微酮症之间的差异。
