Phytic acid and myo -inositol support adipocyte differentiation and improve insulin sensitivity in 3T3-L1 cells

Abstract Phytic acid, also known as myo -inositol hexaphosphate, has been shown to lower blood glucose levels and to improve insulin sensitivity in rodents. We investigated the effects of phytic acid and myo -inositol on differentiation, insulin-stimulated glucose uptake, and lipolysis of adipocytes to test the hypothesis that the antidiabetic properties of phytic acid and myo -inositol are mediated directly through adipocytes. 3T3-L1 cells were treated with 10, 50, or 200 μmol/L of phytic acid or myo -inositol. Oil Red O staining and an intracellular triacylglycerol assay were used to determine lipid accumulation during adipocyte differentiation. Immunoblotting and real-time polymerase chain reaction (PCR) were performed to evaluate expression of transcription factors, a target protein, and insulin signaling molecules. Phytic acid and myo -inositol exposures increased lipid accumulation in a dose-dependent manner ( P < .01). The expression of key transcription factors associated with adipocyte differentiation, such as peroxisome proliferator-activated receptor γ (PPARγ) and sterol regulatory element-binding protein 1c, and the expression of fatty acid synthase increased upon treatments with phytic acid and myo -inositol ( P < .05). Insulin-stimulated glucose uptake in mature adipocytes increased with phytic acid and myo -inositol treatments ( P < .01). In addition, mRNA levels of insulin receptor substrate 1 (IRS1), mRNA levels of glucose transporter 4, and phosphorylation of tyrosine in IRS1 increased upon phytic acid and myo -inositol treatments. In fully differentiated adipocytes, phytic acid and myo -inositol reduced basal lipolysis dose dependently ( P < .01). These results suggest that phytic acid and myo -inositol increase insulin sensitivity in adipocytes by increasing lipid storage capacity, improving glucose uptake, and inhibiting lipolysis.