We developed a unique virtual human model of gastric acid secretion and its regulation in which food provides a driving force. Food stimulus triggers both neural activity in central and enteric nervous systems and G cells to release gastrin, a critical stimulatory hormone. Gastrin stimulates ECL cells to release histamine that together with acetylcholine stimulates acid secretion from parietal cells. Secretion of somatostatin from antral and corpus D cells comprises a negative feedback loop. We demonstrate that while acid levels are most sensitive to food and nervous system inputs, somatostatin-associated interactions are also important in governing acidity. The importance of gastrin on acid secretion is exemplified greatest at the level of transport between the antral and corpus regions. Our model can be applied to study conditions not yet experimentally reproducible. For example, we are able to preferentially deplete either antral or corpus somatostatin. Depletion of antral somatostatin exhibits a more significant elevation of acid release as compared to corpus somatostatin depletion. This increase in acid release is likely due to elevated gastrin levels. Prolonged hypergastrinemia has significant effects in the long term (5 days) by promoting ECL cell overgrowth. Our results may be useful in the design of therapeutic strategies for acid secretory dysfunctions such as hyper- and hypo- chlorhydria.