4.7 Article

Effects of D-Pinitol on Insulin Resistance through the PI3K/Akt Signaling Pathway in Type 2 Diabetes Mellitus Rats

Journal

JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
Volume 63, Issue 26, Pages 6019-6026

Publisher

AMER CHEMICAL SOC
DOI: 10.1021/acs.jafc.5b01238

Keywords

D-pinitol; diabetes mellitus; PI3K/Akt signaling pathway

Funding

  1. National Science-Technology Pillar Program [2012BAD33B05]
  2. Program for Changjiang Scholars
  3. Innovative Research Team in University of Ministry of Education of People's Republic of China [IRT1166]

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D-Pinitol, a compound isolated from Pinaceae and Leguminosae plants, has been reported to possess insulin-like properties. Although the hypoglycemic activity of D-pinitol was recognized in recent years, the molecular mechanism of D-pinitol in the treatment of diabetes mellitus remains unclear. In this investigation, a model of type 2 diabetes mellitus (T2PM) With insulin resistance was established by feeding a high-fat diet (HFD) and injecting streptozocin (STZ) to Sprague-Dawley (SD) rats, targeting the exploration of more details of the mechanism in the therapy of T2DM. D-Pinitol was administrated to the diabetic rats as two. doses [30, 60 mg/(kg.body weight.day)]. The level of fasting blood glucose (FBG) was decreased 12.63% in the high-dosage group, and the ability of oral glucose tolerance was improved in D-pinitol-treated groups. The biochemical indices revealed that D-pinitol had a positive effect on hypoglycemic activity. Western boltting suggested that D-pinitol could promote the expression of the phosphatidylinositol-3-kinase (PI3K) p85, PI3Kp110, as well as the downstream target protein kinase B/Akt (at Ser473). Besides, D-pinitol inhibited the expression of glycogen synthesis kinase-3 beta (GSK-3 beta) protein and regulated the expression of glycogen synthesis (GS) protein and then accelerated the glycogen synthesis. Above all, D-pinitol played a positive role in regulating insulin-mediated glucose uptake in the liver through translocation and activation of the PI3K/Akt signaling pathway in T2DM rats.

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