Improvement of insulin resistance

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Buckwheat contains D-chiro-inositol (Figure 13.3), which can lower the concentration of blood glucose in streptozotocin-diabetic rats (Kawa, Taylor, et al., 2003) and type 2 diabetic mice (KK-Ay) (Yao et al., 2008). D-chiro-Inositol can be incorporated into mammalian cells as the free form and exists in cells as inositol phosphates and inositol phospholipids. Women with polycystic ovary syndrome have insulin resistance and hyperinsulinemia, and these symptoms are considered to be due to the deficiency of D-chiro-inositol containing phosphoglycan (see Figure 13.3), which mediates the action of insulin. The administration of D-chiro-inositol increases the action of insulin in patients with polycystic ovary syndrome, improving the function of ovaries and decreasing the blood pressure and the concentrations of androgen and triacylglycerol in blood (Cheang et al., 2004; Nestler et al., 1999). These data suggest that products containing buckwheat flour may be used to treat diabetes and polycystic ovary syndrome.

Insulin delivers its signal through a cell membrane receptor, which is formed by two a and two b subunits. The binding of insulin to the extracellular domain of the a subunits leads to the activation of the intracellular tyrosine kinase domain of the b subunits. The activated tyrosine

FIGURE 13.3

Glycosylphosphatidylinositol lipid and its hydrolysis by phospholipase.

FIGURE 13.3

Glycosylphosphatidylinositol lipid and its hydrolysis by phospholipase.

Phospholipase Insulin

kinase initiates a multitude of downstream signals leading to the uptake of glucose, the synthesis of glycogen, and so forth. This mechanism of action of insulin is insufficient to explain type 2 diabetes or insulin resistance. In 1986, water-soluble components derived from glycolipids were suggested to mediate the cellular responses to insulin, and one of the components was D-chiro-inositol phosphoglycan (see Figure 13.3).

Figure 13.4 summarizes the mechanism of the improvement of insulin resistance by D-chiro-inositol. In patients with insulin resistance, there is a low concentration of glycosyl-phosphatidylinositol lipids at the outer leaflet of the cell membrane, which may be due to the enhanced loss of D-chiro-inositol from the urine (Kawa, Przybylski, et al., 2003). In the presence of a low concentration of glycosylphosphatidylinositol lipids in the cell membrane, the hydrolysis rate of the lipids may be slow, even when phospholipases are fully activated by insulin, because the reaction rate between the lipases and the substrate is limited by the concentration of the substrate when the substrate concentration is not much higher than the substrate affinity. The slow hydrolysis results in the slow uptake of D-chiro-inositol phosphoglycan, lowering its concentration in the cytosol. The administration of D-chiro-inositol may increase the concentration of cytosolic inositol, leading to an increased concentration of glycosylphosphatidylinositol lipids in the cell membrane. Therefore, the activated phospho-lipases can hydrolyze the phospholipids, rapidly increasing the concentration of D-chiro-inositol phosphoglycan in the cytosol. The increase in the concentration of D-chiro-inositol phosphoglycan can enhance various activities related to glucose metabolism, such as the transportation of glucose into cells and the synthesis of glycogen. The enhancement of cellular glucose metabolism can result in a decreased concentration of glucose in the bloodstream.

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