The JAK2 (Janus kinase-2)-STAT5 (signaling transducer and activator of transcription-5) pathway participates in the signaling of several hormones including leptin, erythropoietin and growth hormone. Leptin, erythropoietin and growth hormone are in turn known to protect cells against ischemic injury. During ischemia cell survival may depend on the ability of cells to accumulate glucose. Glucose could be taken up by Na⁺ coupled glucose transport through SGLT1 (SLC5A1), which may operate against a chemical glucose gradient and may thus be effective even at low extracellular glucose concentrations. The present study thus explored whether JAK2 activates SGLT1. To this end, SGLT1 was expressed in Xenopus oocytes with and without JAK2 and electrogenic glucose transport determined by dual electrode voltage clamp experiments. In SGLT1-expressing oocytes but not in oocyte injected with water the addition of glucose to the extracellular bath generated a current (I_g), which was significantly increased following coexpression of JAK2. In conclusion, JAK2 upregulates SGLT1 activity which may play a role in the protecting effect of JAK2 during ischemia.