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Review
. 2022 Mar 7:13:805837.
doi: 10.3389/fendo.2022.805837. eCollection 2022.

Underestimated Prediabetic Biomarkers: Are We Blind to Their Strategy?

Carla Luís  1   2   3 , Raquel Soares  2   3 , Pilar Baylina  1   3   4 , Rúben Fernandes  1   3   4
Affiliations
Review

Underestimated Prediabetic Biomarkers: Are We Blind to Their Strategy?

Carla Luís et al. Front Endocrinol (Lausanne). .

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.

Keywords: biomarkers; diabetes; early diagnosis; fetuin-A; galectin-3; ophthalmate; prediabetes.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Brief description of Gal3’s functions. Gal3 exerts different functions depending on its location. Intracellularly, Gal3 can act as a Pre-mRNA splicing factor, regulating the cell cycle, promoting proliferation, and protecting from apoptosis. Extracellularly, Gal3 is able to regulate cell adhesion (either cell-to-cell or cell-to-matrix) and mediate features of T2D pathophysiology like binding to AGEs, regulating inflammatory and immune pathways (emphasized by the boxes) [20]. (Created with BioRender.com).
Figure 2
Figure 2
Glutathione and ophthalmate shared pathways via transsulfuration in conjugation with methionine metabolism. The increase in OPH levels works as a rather compensatory mechanism when glutathione depletion occurs. MS, methionine synthase; BHMT, Betaine homocysteine methyltransferase; MTs, methyltransferases; CBS, cystathionine β-synthase; CTH, cystathionase; GCS, glutamyl-cysteine synthase; GS, Glutathione synthetase. (Created with BioRender.com).
Figure 3
Figure 3
Mechanisms of Fetuin-A in order to promote insulin resistance. The association of Fetuin-A with the insulin receptor inhibits IRS1 and, therefore, the cascade that will block GLUT4. Via TLR4, Fetuin-A will activate the NF-kB genes, which will promote the secretion of inflammatory cytokines and lead to insulin resistance. FFA, Free Fatty Acids; NF-kB, Nuclear Factor Kappa-light-chain-enhancer of activated B cells; IRS1, Insulin Receptor Substrate 1; PI3K, Phosphoinositide 3-Kinases; AKT, Protein kinase B; GLUT4, Glucose transporter type 4. (Created with BioRender.com).
See this image and copyright information in PMC

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