Abstract
BackgroundAlpha-synuclein (SNCA) as the presynaptic protein is expressed in different tissues and prevents insulin-resistance (IR) through increasing glucose-uptake by adipocytes and muscles. However, the effect of insulin metabolism on SNCA expression has scarcely elucidated. In present study we assessed the probable effect of insulin resistance on SNCA expression in muscle C2C12 cells and also skeletal muscle tissues of type 2 diabetic mice.Materials and methodsSixteen male C57BL/6 mice were divided into two experimental groups, including control and type 2 diabetic mice with IR (induced by high-fat diet + low-dose streptozotocin). The animals of the study involved the measurements of fasting blood glucose, oral-glucose-tolerance-test, as well as fasting plasma insulin. Moreover, insulin-resistant and insulin-sensitive muscle C2C12 cells were prepared. The insulin-resistance was confirmed by the glucose-uptake assay. Comparative quantitative real time PCR was used to assess the SNCA expression.ResultsThe obtained results have showed a significant ~ 27% decrease in SNCA expression level in muscle tissue of diabetic mice (P = 0.022). Moreover, there was a significant change of SNCA expression in insulin-resistant C2C12 cells (P < 0.001).ConclusionType 2 diabetes due to insulin-resistance can decrease SNCA gene expression in muscles. In addition to the role of SNCA in cell susceptibility to insulin and glucose uptake, the SNCA expression can also be affected by insulin metabolism.
Highlights
Alpha-synuclein (SNCA) as the presynaptic protein is expressed in different tissues and prevents insulin-resistance (IR) through increasing glucose-uptake by adipocytes and muscles
There was a significant change of SNCA expression in insulin-resistant C2C12 cells (P < 0.001)
Insulin has a critical role in regulation of glucose uptake and metabolism in different tissues via activating of the tyrosine kinase signaling pathway [1]
Summary
Alpha-synuclein (SNCA) as the presynaptic protein is expressed in different tissues and prevents insulin-resistance (IR) through increasing glucose-uptake by adipocytes and muscles. The effect of insulin metabolism on SNCA expression has scarcely elucidated. In present study we assessed the probable effect of insulin resistance on SNCA expression in muscle C2C12 cells and skeletal muscle tissues of type 2 diabetic mice. Insulin has a critical role in regulation of glucose uptake and metabolism in different tissues via activating of the tyrosine kinase signaling pathway [1]. Insulin resistance (IR) as the main hyperglycemic process in non-insulin dependent diabetes mellitus (NIDDM) is observed in many tissues such as adipose and skeletal muscle [2]. The plasma level of alpha-synuclein was reversely related to body mass index (BMI) and homeostatic model assessment for insulin resistance (HOMA-IR) [1]. Since the basal expression of SNCA in the muscle cells in response to insulin has not been investigated to date, we decided to examine the expression of SNCA in insulin-resistant (IR) and insulin-sensitive (IS) models of skeletal muscle cells in both in vitro and in vivo studies
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