The kidneys play an important role in glucose homeostasis in three ways: Via endogenous glucose production from non-carbohydrate precursors (e.g. glutamine, lactate, alanine, glycerol) during both postprandial and post-absorptive states; via glucose filtration and reabsorption by the glomerulus and proximal tubule, respectively; and via glucose utilization and the elimination of its excess in the urine when glucose levels exceed $180\mathit{mg}/\mathit{dl}$. The renal release of glucose into the circulation occurs mainly in the renal cortex and results from the glucose phosphorylating capacity of those renal cells, meaning that, cells in the renal cortex can form glucose-6-phosphate. Considering glucose filtration and reabsorption, the kidneys filtrate and reabsorb all circulating glucose, rendering the urine virtually glucose-free in a healthy person. Finally, the kidneys take up glucose from the circulation for energetic self-supply. Besides their role in glucose metabolism, the kidneys are the major site of insulin clearance from the systemic circulation, removing approximately 50% of peripheral insulin. In this regard, insulin clearance by kidneys occurs by degradation in the proximal tubule after being filtered in the glomerulus. All the aforementioned mechanisms affect the glucose concentration levels in the blood, preventing the parametrization of a mathematical model for patients with diabetes mellitus, in the implementation of an artificial pancreas. Aiming for a complete physiological model of the glucose homeostasis, a physiological submodel of the kidneys is presented in a way not described in the literature so far. This submodel is a phenomenological-based semi-physical model with a basic structure rooted in the conservation law and for which the parameters are interpretable. The model’s results coincide well with the available clinical data reported for kidney functions associated with glucose and insulin.

肾脏通过三种方式在葡萄糖稳态中发挥重要作用：在餐后和吸收后状态下，通过非碳水化合物前体（例如谷氨酰胺，乳酸，丙氨酸，甘油）产生内源性葡萄糖；分别通过葡萄糖过滤和肾小球和近端小管的重吸收；以及通过葡萄糖利用，并在葡萄糖水平超过$180\mathit{毫克}/\mathit{dl}$。肾脏向循环中释放的葡萄糖主要发生在肾皮质中，并且是由这些肾细胞的葡萄糖磷酸化能力导致的，这意味着肾皮质中的细胞可以形成6-磷酸葡萄糖。考虑到葡萄糖过滤和重吸收，肾脏会过滤并重吸收所有循环的葡萄糖，从而使健康人的尿液几乎不含葡萄糖。最后，肾脏从循环中吸收葡萄糖，以实现能量自给。除了其在葡萄糖代谢中的作用外，肾脏还是胰岛素从体循环中清除的主要部位，可去除约50％的外周胰岛素。在这方面，肾脏的胰岛素清除作用是在肾小球滤过后，近端小管的降解引起的。所有上述机制均会影响血液中的葡萄糖浓度水平，从而在实施人工胰腺时阻止糖尿病患者数学模型的参数化。为了获得葡萄糖稳态的完整生理模型，以迄今为止文献中未描述的方式呈现了肾脏的生理子模型。该子模型是基于现象学的半物理模型，具有基于守恒定律的基本结构，并且其参数可解释。该模型的结果与报道的与葡萄糖和胰岛素相关的肾功能的可用临床数据非常吻合。在实施人工胰腺。为了建立葡萄糖稳态的完整生理模型，以迄今为止文献中未描述的方式提出了肾脏的生理子模型。该子模型是基于现象学的半物理模型，其基本结构植根于守恒定律，并且其参数可解释。该模型的结果与报道的与葡萄糖和胰岛素相关的肾功能的可用临床数据非常吻合。在实施人工胰腺。为了获得葡萄糖稳态的完整生理模型，以迄今为止文献中未描述的方式呈现了肾脏的生理子模型。该子模型是基于现象学的半物理模型，具有基于守恒定律的基本结构，并且其参数可解释。该模型的结果与报道的与葡萄糖和胰岛素相关的肾功能的可用临床数据非常吻合。