Stem cell therapy for obesity-induced metabolic disorders
doi:10.1038/nindia.2019.141 Published online 21 October 2019
Fat-tissue-derived specific stem cells could be used to alleviate obesity-induced metabolic disorders, a study reveals1.
Stem cells have the potential to grow into other tissue types such as bone, cartilage and muscle, making them suitable for treating metabolic disorders such as diabetes, insulin resistance and high levels of blood lipids.
A combination of high food intake and lack of physical activity increases fat storage in the body that puts stress on the metabolic pathways, eventually leading to metabolic dysfunction and disorders. Long-term use of drugs such as metformin, used to manage diabetes, cause adverse effects.
In search of a safer alternative, scientists from the Manipal Academy of Higher Education and Jain University in Bangalore, India, prepared three different stem-cell-based formulations. They then injected separate groups of obese mice with the different formulations and compared their efficacy with that of metformin.
All the formulations significantly lowered glucose and serum triglyceride levels in the mice. Besides, the formulations significantly reduced serum insulin levels. Of all the formulations, stem cell suspension remarkably reduced inflammation and triglycerides in the liver.
The cell suspension also dramatically increased protein content in the skeletal muscle and enhanced the expression of the GLUT4 gene, which encodes GLUT4 protein. This protein transports glucose and make the muscle tissue sensitive to insulin.
The same treatment also decreased the activity of specific marker genes that signal inflammation in the liver. The stem cells easily migrated to other major organs such as the heart, the kidneys and the brain, suggesting their potential to correct metabolic dysfunctions in these organs.
1. Shree, N. et al. Human adipose tissue mesenchymal stem cells as a novel treatment modality for correcting obesity induced metabolic dysregulation. Int. J. Obes. 43, 2107-2118 (2019)