The experimental protocol of the perfused rat pancreas is commonly used to evaluate beta-cell function. In this context mathematical models become useful tools through the determination of indexes that allow the assessment of beta-cell function in different experimental groups, and the quantification of the effects of anti-diabetic drugs, secretagogues, or treatments. However, a minimal model applicable to the isolated perfused rat pancreas was unavailable so far. In this work, we adapt the C-peptide minimal model, previously applied to the intravenous glucose tolerance test, to obtain a specific model for the experimental settings of the perfused pancreas. Using the model, it is possible to estimate indexes describing beta-cell responsivity for first (_D) and second phase (_S, T) of insulin secretion. The model was initially applied to untreated pancreata, and afterwards used for the assessment of pharmacologically relevant agents (the gut hormone GLP1, the potent GLP1-receptor agonist, lixisenatide, and a GPR40/FFAR1 agonist, SAR1), to quantify and differentiate their effect on insulin secretion. Model fit was satisfactory and parameters were estimated with good precision for both untreated and treated pancreata. Model application showed that lixisenatide reaches improvement of beta-cell function similar to GLP1 (11.7 vs 13.1 fold increase in _D and 2.3 vs 2.8 fold increase in _S) and demonstrated that SAR1 leads to an additional improvement of beta-cell function even in the presence of postprandial GLP1 levels.