Underestimated Prediabetic Biomarkers: Are We Blind to Their Strategy?

Raquel Soares,Rúben Fernandes,Pilar Baylina,Carla Luís

doi:10.3389/fendo.2022.805837

Abstract

Type 2 Diabetes (T2D) is currently one of the fastest growing health challenging, a non-communicable disease result of the XXI century lifestyle. Given its growing incidence and prevalence, it became increasingly imperative to develop new technologies and implement new biomarkers for early diagnosis in order to promote lifestyle changes and thus cause a setback of the disease. Promising biomarkers have been identified as predictive of T2D development; however, none of them have yet been implemented in clinical practice routine. Moreover, many prediabetic biomarkers can also represent potential therapeutical targets in disease management. Previous studies have identified the most popular biomarkers, which are being thoroughly investigated. However, there are some biomarkers with promising preliminary results with limited associated studies; hence there is still much to be understood about its mechanisms and associations in T2D pathophysiology. This work identifies and discusses the promising results of Galectin-3, Ophthalmate and Fetuin-A.

Highlights

Type 2 Diabetes (T2D) is already considered a worldwide pandemic, no longer restricted to developed countries [1], responsible for more than 4.2 million deaths in 2019 [2] and a trigger for other non‐communicable diseases like cancer and cardiovascular diseases
Our aim is to identify promising biomarkers able to represent the metabolic alterations that occur during the pathophysiological transformation of prediabetes to the clinical stage of T2D
We identify Galectin-3, Ophthalmate and Fetuin-a, as encouraging metabolites to address, which have been neglected in the last 10 years

Summary

Introduction

Type 2 Diabetes (T2D) is already considered a worldwide pandemic, no longer restricted to developed countries [1], responsible for more than 4.2 million deaths in 2019 [2] and a trigger for other non‐communicable diseases like cancer and cardiovascular diseases. It is a complex disease with different pathophysiology profiles concomitant with inflammation, adiposity/obesity, lipid oxidation, hyperglycemia, glycation/glycosylation, and oxidative stress, further discussed. Such mechanisms can lead to insulin secretion deficiency from pancreatic beta cells, tissue insulin resistance, and impaired compensatory response to insulin [3].

Objectives

Conclusion