Abstract: In order to study the effect of mogroside on growth performance, organ indexes and muscle fiber types in mice, thirty 21-day-old male mice weighing about 26 g were selected in this experiment, 5 in each cage, 6 cages in total, 3 cages each in the control group and the test group. Mogroside was dissolved in normal saline. On the basis of the basic diet, the test group was fed with 600 mg/kg mogroside by body weight, and the control group was fed with the normal saline 0.3 mL; the test period was 12 weeks. At the end of the experiment, the mice were weighed at 12 h after fasting, and were sacrificed by cervical dislocation and the extensor digitorum longus, soleus muscle, gastrocnemius muscle, tibialis anterior muscle, heart, liver, spleen, lung, kidney and other tissues/organs were collected and weighed. Tissue/organ indexes were calculated. The expression of AdipoQ, AdipoR1, AMPK, PGC-1α in soleus muscle and extensor digitorum longus, which were related to MYHCⅠ, MYHCⅡa, MYHCⅡb and adiponectin signaling pathways, was detected by real-time fluorescent quantitative PCR. The results showed that there was no significant difference in the body weight of mice in the test group compared with the control group（P＞0.05）. The tissue/organ indexes of the mice in the test group increased, but the difference was not significant with that in the control group（P＞0.05）. The expression levels of MYHCⅠ and MYHCⅡ genes in soleus muscle and extensor digitorum longus of mice in the test group were significantly higher than those in the control group（P＜0.05）, while the expression level of MYHCⅡb gene was significantly lower than that in the control group（P＜0.05）. In addition, the expression levels of adiponectin signaling pathway genes（AdipoQ, AdipoR1, AMPK, PGC-1α） in mice were significantly higher than those in the control group（P＜0.05）. The results suggested that mogroside had no significant effect on the growth performance and tissue/organ indexes of mice, but it could promote the conversion of mouse glycolytic muscle fiber to oxidized muscle fiber through the adiponectin signaling pathway.