Effects of starvation, diabetesand obese conditions on mouse hepatic SOCS2 gene expression
- VernacularTitle:饥饿、糖尿病和肥胖状态对小鼠肝脏SOCS2基因表达的影响
- Author:
Anfang CUI
;
Xiaolei MA
;
Yanhong HUANG
;
Xiangyang ZHANG
- Keywords:
SOCS2;
fasted;
gluconeogenesis
- From:
Basic & Clinical Medicine
2017;37(6):855-859
- CountryChina
- Language:Chinese
-
Abstract:
Objective To determine the expression levels of SOCS2 in the mouse livers under starvation, diabetes and obese conditions and to study the effect of SOCS2 on gluconeogenesis.Methods Animals 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 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 starvation status.The expression of SOCS2 was 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 underidentical starvation, diabetes and obese conditions.The protein was Mr 23 000 and glucose production was inhibited after SOCS2 being overexpressed in the primary C57BL/6J mouse hepatocytes by adenovirus system.Conclusions SOCS2 may inhibit gluconeogenesis in the C57BL/6J mouse primary hepatocytes, and SOCS2 may be a potential target for the treatment of type Ⅱ diabetes.
