Abstract: Objective To determine the expression levels of SOCS2 in the mouse livers under fasted, diabetes and obese conditions and to study the effect of SOCS2 on gluconeogenesis. Methods Animal were divided into 3 groups: C57BL/6J mice, the control group was fed ad libtum and the experimental group was fasted for 24 h. Diabetes model db/db and the control db/m mice were fed ad libitum. Obese model ob/ob and the control C57BL/6J mice were fed ad libitum. All the mice above were sacrificed and total RNA was isolated from mouse livers and reverse transcribed to cDNA. The expression levels of SOCS2 and gluconeogenesis genes in the mouse livers in the 3 groups above were detected by real-time quantitative PCR. SOCS2 was overexpressed in the primary C57BL/6J mouse hepatocytes by the adenovirus system. The effect of SOCS2 on glucose production was measured by glucose output assay. Results C57BL/6J mouse hepatic SOCS2 expression was suppressed by fasted status. The expression levels of SOCS2 were decreased in the livers of db/db and ob/ob mice. In contrast, the key regulators of gluconeogenesis, PGC-1α, PEPCK and G6Pase exhibited the opposite expression pattern as SOCS2 in the livers under identical fasted, diabetes and obese conditions. The protein was Mr 23 000 and glucose production was inhibited after SOCS2 was overexpressed in the primary C57BL/6J mouse hepatocytes by adenovirus system. Conclusions SOCS2 is speculated to inhibit gluconeogenesis in the C57BL/6J mouse primary hepatocytes, and SOCS2 may be a new target for the treatment of type II diabetes.

Key words: SOCS2, fasted, gluconeogenesis