title: 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.
authors.affiliation: Department of Food Science and Nutrition, The Catholic University of Korea, Bucheon, Republic of Korea.
authors.forename: Jin Nam
authors.initials: JN
authors.lastname: Kim
authors.affiliation: Department of Food & Nutrition, Seoul National University, Seoul, Republic of Korea.
authors.forename: Sung Nim
authors.initials: SN
authors.lastname: Han
authors.affiliation: Department of Food Science and Nutrition, The Catholic University of Korea, Bucheon, Republic of Korea. Electronic address: hkyeong@catholic.ac.kr.
authors.forename: Hye-Kyeong
authors.initials: HK
authors.lastname: Kim
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D002454:Cell Differentiation / Q000187:drug effects; D051275:Glucose Transporter Type 4 / Q000235:genetics / Q000378:metabolism; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007294:Inositol / Q000494:pharmacology*; D007328:Insulin / Q000097:blood*; D055504:Insulin Receptor Substrate Proteins / Q000378:metabolism; D007333:Insulin Resistance; D050356:Lipid Metabolism / Q000187:drug effects*; D051379:Mice; D047495:PPAR gamma / Q000378:metabolism; D010833:Phytic Acid / Q000494:pharmacology*; D012333:RNA, Messenger / Q000378:metabolism; D014443:Tyrosine / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D051275:Glucose Transporter Type 4; D007004:Hypoglycemic Agents; D007328:Insulin; D055504:Insulin Receptor Substrate Proteins; D047495:PPAR gamma; D012333:RNA, Messenger; C495693:Slc2a4 protein, mouse; D014443:Tyrosine; D007294:Inositol; D010833:Phytic Acid
keywords: 3T3-L1 cells; Adipogenesis; Glucose uptake; Insulin sensitivity; Myo-inositol; Phytic acid