ArticleFrontiers in pharmacology2020
Effects of D-Chiro-Inositol on Glucose Metabolism in db/db Mice and the Associated Underlying Mechanisms.
Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.
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Who cites it
17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 53 citations in OpenAlex.
- Effects of different supplements on Hashimoto's thyroiditis: a systematic review and network meta-analysis.Frontiers in endocrinology · 2024Pooled it
- Pooled it
- Trial
- Effects of Different Nutritional Strategies on the Prevention and Management of Gestational Diabetes Mellitus: A Systematic Review and Network Meta-Analysis.Healthcare (Basel, Switzerland) · 2026Review
- Mitigation of Hepatic and Pancreatic Injury byFood science & nutrition · 2026Article
- cTnIR193H restrictive cardiomyopathy mice satisfy high-energy metabolic demands through regulating glucose metabolism.Genes & diseases · 2026Article
- Article
- Highland Barley Alleviates High-Fat Diet-Induced Obesity and Liver Injury Through the IRS2/PI3K/AKT Signaling Pathway in Rats.Nutrients · 2024Article
- Study of the molecular interaction of a phosphonium-based ionic liquid within myo-inositol and non-steroidal anti-inflammatory drugs.RSC advances · 2024Article
- Indoleacrylic acid produced by Parabacteroides distasonis alleviates type 2 diabetes via activation of AhR to repair intestinal barrier.BMC biology · 2023Article
- Myo-Inositol and D-Chiro-Inositol as Modulators of Ovary Steroidogenesis: A Narrative Review.Nutrients · 2023Review
- The Role of Inositols in the Hyperandrogenic Phenotypes of PCOS: A Re-Reading of Larner's Results.International journal of molecular sciences · 2023Review
- Synthesis, molecular docking, and pharmacological evaluation of 5-(4-(2-(5-ethyl pyridine-2-yl) ethoxy) benzyl)-3-(phenylsulfonyl) thiazolidine-2, 4-dione against HFD-induced diabesity via interaction with the CB1 receptor.Iranian journal of basic medical sciences · 2022Article
- Inositols: From Established Knowledge to Novel Approaches.International journal of molecular sciences · 2021Review
- D-Chiro-Inositol Regulates Insulin Signaling in Human Adipocytes.Frontiers in endocrinology · 2021Article
- Role of Inositols and Inositol Phosphates in Energy Metabolism.Molecules (Basel, Switzerland) · 2020Review
- Direct Effects of D-Chiro-Inositol on Insulin Signaling and Glucagon Secretion of Pancreatic Alpha Cells.Biomolecules · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we observed the effect of D-chiro-inositol (DCI) on glucose consumption in type 2 diabetic db/db mice, and investigated the relevant mechanism. We discovered that the stability of 24-h blood glucose under the nonfasting condition and decreased glucose tolerance were both alleviated after treatment with DCI. Moreover, the content of glycosylated protein and advanced glycation end products in the serum was reduced, the damage in the liver tissue was alleviated, and the synthesis of liver glycogen was significantly promoted. In addition, DCI increased the expression of insulin receptor substrate 2 (IRS2), phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT), glucose transporters 4 (GLUT4), and phospho-AKT (S473) protein. In contrast, DCI decreased the expression level of glycogen synthase kinase 3β (GSK3β) protein in liver tissue to various degrees, as shown by immunohistochemistry and western blotting. Furthermore, DCI increased the mRNA expression of IRS2, PI3K, AKT, and GLUT4, and reduced that of GSK3β in liver tissue, as demonstrated by polymerase chain reaction. Finally, DCI promoted glucose consumption in high glucose-stimulating HepG2 cells and increased the expression of IRS2 protein in HepG2 cells, as revealed by fluorescence staining and flow cytometry. Our results indicate that DCI can significantly improve glucose metabolism in diabetic mice and HepG2 cells. This effect may be associated with the upregulation of IRS2, PI3K, AKT, and GLUT4 and downregulation of GSK3β.
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