Structural characterization and tartary buckwheat polysaccharides alleviate insulin resistance by suppressing SOCS3-induced IRS1 protein degradation

Tartary buckwheat is an alternative cereal crop. This study sought to establish the mechanisms whereby tartary buckwheat root polysaccharide (TBRP-1) treatment can alleviate diabetes mellitus. TBRP-1 was extracted and purified by hot water and gel permeation column chromatography. Its structure was determined by Fourier transform-infrared spectroscopy (FT-IR), monosaccharide analysis, and nuclear magnetic resonance (NMR) spectroscopy. TBRP-1 was composed of fucose, arabinose, rhamnose, galactose, glucose, xylose, mannose, galacturonic acid, and glucuronic acid. The molecular weight was 2.731 x 104 Da. In addition, for in vitro, HepG2 cells were treated with high insulin concentrations to establish a model of insulin resistance. For in vivo modeling, diabetic mice were established by injecting with streptozotocin (STZ). Body weight, blood glucose levels, glycosylated hemoglobin (HbA1c) levels, and changes in hepatic lipids were analyzed. The expression of suppressor of cytokine signaling 3 (SOCS3), insulin receptor substrate 1 (IRS1), and glucose transporter type 4 (GLUT4) was assessed via qPCR and western blotting. TBRP-1 treatment was sufficient to enhance the ability of insulin resistant HepG2 cells to take up glucose. TBRP-1 also lowered levels of blood glucose, HbA1c, and hepatic lipids in diabetic mice. The underlying molecular mechanisms suggested that TBRP-1 was able to suppress SOCS3 expression to thereby enhance IRS1 expression, thus alleviating insulin resistance.

Automated summary

This study investigated the mechanisms by which tartary buckwheat root polysaccharide (TBRP-1) treatment can alleviate diabetes mellitus. The results showed that TBRP-1 treatment enhanced glucose uptake in insulin resistant cells and lowered blood glucose levels and hepatic lipids in diabetic mice. The underlying molecular mechanisms involved the suppression of SOCS3 expression and enhancement of IRS1 expression, thus alleviating insulin resistance.