Type II diabetes may affect stem cell niche resulting in down regulation of glucose transporters and insulin receptors in cells
- Published
- Accepted
- Subject Areas
- Biochemistry, Cell Biology, Diabetes and Endocrinology, Internal Medicine, Metabolic Sciences
- Keywords
- epigenetics, Type II diabetes, high blood glucose, gene expression, muscle cells, homeostasis, reduced glucose uptake, weight gain, stem cell niche, impaired insulin sensitivity
- Copyright
- © 2018 Ng
- Licence
- This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ Preprints) and either DOI or URL of the article must be cited.
- Cite this article
- 2018. Type II diabetes may affect stem cell niche resulting in down regulation of glucose transporters and insulin receptors in cells. PeerJ Preprints 6:e27024v1 https://doi.org/10.7287/peerj.preprints.27024v1
Abstract
Characterized by high blood glucose concentration, resistance of cells to glucose uptake and reduced insulin sensitivity, Type II diabetes is a major health problem afflicting both developing and developed countries in increasing extent as populations around the world increasing adopt high energy diets. Given that, in Type II diabetes, successive generations of various cell types in the body ranging from muscles, tissues, blood, and organs are resistant to glucose uptake and exhibited reduced sensitivity to insulin, the underlying aetiology of Type II diabetes might involve the altered gene expression of stem cells in stem cell niches that adapted to a high glucose diet through an evolutionary conserved mechanism that aimed at homeostasis. Specifically, faced with a high energy and high sugar diet, stem cells in stem cell niches around the body possibly activated an evolutionary conserved mechanism aimed at reducing glucose uptake by cells for reducing weight gain by the body. Thus, successive generations of cells generated from the stem cell niche would exhibit an epigenetically controlled programme of gene expression that exhibited down regulation of genes for glucose transporters and insulin receptors. Such cells would display a phenotype of reduced glucose uptake together with reduced sensitivity to insulin; thereby, resulting in a high blood glucose concentration characteristic of Type II diabetes. The above hypothesis helped explain why high sugar intake by the body could result in impaired sensitivity to insulin and reduced glucose uptake by cells, and more importantly, the widespread nature in which many cell types (principally muscle cells) are affected by a possible epigenetically controlled gene expression programme which hitherto appeared clinically irreversible. Specifically, the most important clinical question for diabetes treatment and care remains the reasons underlying the clinically observed irreversible nature of the disease that progressively, with age and poor glucose control, worsens with complications to many organs of the body such as the eyes, kidneys, cardiovascular system and brain (stroke). Interested readers are invited to expand on the ideas presented in this abstract preprint.
Author Comment
This is an abstract preprint.