J Appl Biomed 22:74-80, 2024 | DOI: 10.32725/jab.2024.009
Myo-inositol rescued insulin resistance and dyslipidemia in db/db mice
- 1 Hunan Provincial People's Hospital (The First-affiliated Hospital of Hunan Normal University), Department of Pharmacy, Changsha, China
- 2 Central South University, Xiangya Hospital, Department of Neurosurgery, Changsha, China
- 3 The Second Xiangya Hospital of Central South University, Department of Metabolism and Endocrinology, National Clinical Research Center for Metabolic Diseases, Changsha, China
Myo-inositol (MI), present in a variety of foods, is essential in several important processes of cell physiology. In this study, we explored the protective effects of MI against hyperglycemia and dyslipidemia in db/db mice, a typical animal model of type 2 diabetes mellitus (T2DM). MI supplement effectively suppressed the high plasma glucose and insulin levels and markedly relieved the insulin resistance (IR) in the db/db mice, comparable to metformin's effects. In MIN6 pancreatic β cells, MI also restrained the upsurge of insulin secretion stimulated by high-concentration glucose but had no impact on the promoted cell proliferation. Moreover, MI abated the enhanced plasma triglyceride and total cholesterol levels in the db/db mice. Notably, the lipid droplet formation of mesenchymal stem cells (MSCs) from db/db mice was significantly diminished after the treatment of MI, indicating that MI could effectively inhibit the differentiation of db/db mouse MSCs into adipocytes. However, MI regretfully failed to control obesity in db/db mice. This work proved that MI significantly helped db/db mice's metabolic disorders, indicating that MI has potential as an effective adjunctive treatment for hyperglycemia and dyslipidemia in T2DM patients.
Keywords: db, db mice; Dyslipidemia; Hyperglycemia; Insulin resistance; Myo-inositol
Grants and funding:
This project was supported by Hunan Provincial Natural Science Foundation of China (No. 2022JJ70134, 2022JJ80120).
Conflicts of interest:
The authors have no conflict of interest to declare.
Received: October 11, 2023; Revised: May 3, 2024; Accepted: June 12, 2024; Prepublished online: June 14, 2024; Published: June 24, 2024 Show citation
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