Abstract
Diabetes results from the inability of pancreatic islets to maintain blood glucose concentrations within a normal physiological range. Clinical features are usually not observed until islets begin to fail and irreversible damage has occurred. Diabetes is generally diagnosed based on elevated glucose, which does not distinguish between type 1 and 2 diabetes. Thus, new diagnostic approaches are needed to detect different modes of diabetes before manifestation of disease. During prediabetes (pre-DM), islets undergo stress and release micro (mi) RNAs. Here, we review studies that have measured and tracked miRNAs in the blood for those with recent-onset or longstanding type 1 diabetes, obesity, pre-diabetes, type 2 diabetes, and gestational diabetes. We summarize the findings on miRNA signatures with the potential to stage progression of different modes of diabetes. Advances in identifying selective biomarker signatures may aid in early detection and classification of diabetic conditions and treatments to prevent and reverse diabetes.
Highlights
Pancreatic islets regulate glucose homeostasis through insulin and glucagon, which are central to key biological processes and energy homeostasis
Immune cell infiltration is the first event that leads to significant reduction in beta-cell mass and eventual hyperglycemia, followed by changes in blood glucose, autoimmunity, beta-cell mass, beta-cell death, islet compensation, and corresponding circulating miRNA profiles (Figure 1)
For recent-onset and longstanding type 1 diabetes (T1D) groups, only those miRNAs that were identified independently in at least 2 studies are provided in the figure
Summary
Pancreatic islets regulate glucose homeostasis through insulin and glucagon, which are central to key biological processes and energy homeostasis. Loss or impairment of islet function results in dysregulated blood glucose, which gives rise to multiple life-threatening complications including cardiovascular disease, neuropathy, nephropathy, blindness, and stroke. The most common clinical sign of diabetes, is usually observed only when islet beta cells are already deficient or exhausted. In the case of type 1 diabetes (T1D), clinical symptoms manifest when >80% of islet beta cells are already lost to autoimmunity. During the progression of type 2 diabetes (T2D), islet compensation maintains normoglycemia for years without symptoms before progressing to a state of detectable impaired glucose tolerance (IGT) and impaired fasting glucose (IFG). During pregnancy, lack of islet compensation leads to gestational diabetes (GDM), which increases risk for
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