Objective: To explore the relationship among gastrin, somatostatin and pathogenesis of spleen deficiency syndrome (SDS). Methods: The changes of gastrin and somatostatin in body fluid and tissues were measured by radioimmunoassay. G cells (gastrin cells) and D cells (somatostatin cells) of gastroduodenal mucosa were analyzed with polyclonal antibody to gastrin and somatostatin, immunohistochemical technique and Quantimet 500 image analysis system. Sijunzi decoction (四君子汤, SJZD) was chosen for counter confirmation of syndrome. Results: The levels of gastrin in plasma, gastric juice, intestinal juice, gastric antrum, duodenum and hypothalamus of experimental SDS were significantly lowered and somatostatin markedly higher than the control group, which was improved and even better than spontaneous recovery group after prevention and treatment with SJZD ( P <0.05). The count of G cells and D cells reduced ( P <0.05), the area of D cells declined ( P <0.05), but mean grey of G cells elevated ( P <0.05) and ratio of the count and area on G/D also increased ( P <0.05) in experimental SDS, which was improved and even better than spontaneous recovery group after prevention and treatment with SJZD ( P <0.05). Conclusion: The study confirmed that disturbance of relationship between gastrin and somatostatin would lead to gastrointestinal disorder, which was one of important causes for pathogenesis of SDS. Objective: To explore the relationship among gastrin, somatostatin and pathogenesis of spleen deficiency syndrome (SDS). Methods: The changes of gastrin and somatostatin in body fluid and tissues were measured by radioimmunoassay. G cells (gastrin cells) and D cells ) of gastroduodenal mucosa were analyzed with polyclonal antibody to gastrin and somatostatin, immunohistochemical technique and Quantimet 500 image analysis system. Sijunzi decoction was selected for counter confirmation of syndrome. Results: The levels of gastrin in plasma, gastric juice , intestinal juice, gastric antrum, duodenum and hypothalamus of experimental SDS were significantly lowered and somatostatin markedly higher than the control group, which was improved and even better than spontaneous recovery group after prevention and treatment with SJZD (P <0.05). The count of G cells and D cells reduced (P <0.05), the area of ​​D cells declined (P <0.05), but mean gray o (P <0.05) in experimental SDS, which was improved and even better than spontaneous recovery group after prevention and treatment with SJZD (P <0.05) and ratio of the count and area on G / D also increased Conclusion: The study of that disturbance of relationship between gastrin and somatostatin would lead to gastrointestinal disorder, which was one of important causes for pathogenesis of SDS.