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Current molecular aspects in the development and treatment of diabetes

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Abstract

Diabetes mellitus (DM) leads to microvascular, macrovascular, and neurological complications. Less is understood about the mechanisms of this disease that give rise to weak bones. The many molecular mechanisms proposed to explain the damage caused by chronic hyperglycemia are organ and tissue dependent. Since all the different treatments for DM involve therapeutic activity combined with side effects and each patient represents a unique condition, there is no generalized therapy. The alterations stemming from hyperglycemia affect metabolism, osmotic pressure, oxidative stress, and inflammation. In part, hemodynamic modifications are linked to the osmotic potential of the excess of carbohydrates implicated in the disease. The change in osmotic balance increases as the disease progresses because hyperglycemia becomes chronic. The aim of the current contribution is to provide an updated overview of the molecular mechanisms that participate in the development and treatment of diabetes.

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Acknowledgments

The authors thank the Secretaría de Investigación y Posgrado, Instituto Politécnico Nacional (SIP20195079/SIP20195185). Samuel Álvarez-Almazán is grateful for the scholarship from CONACyT (No. 434986).

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Correspondence to Feliciano Tamay-Cach or Jessica Elena Mendieta-Wejebe.

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Key points

• Most molecular alterations of diabetes are based on the overactivation of the protein kinase C pathway.

• Since every diabetes treatment has beneficial and adverse effects, there is no general therapy for all patients.

• Bone weakening is now recognized as a complication of diabetes that also requires attention for treatment.

DM treatments are based on decrease of oxidative stress, inflammation, cardiovascular disorders, and/or bone damage.

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Álvarez-Almazán, S., Filisola-Villaseñor, J.G., Alemán-González-Duhart, D. et al. Current molecular aspects in the development and treatment of diabetes. J Physiol Biochem 76, 13–35 (2020). https://doi.org/10.1007/s13105-019-00717-0

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  • DOI: https://doi.org/10.1007/s13105-019-00717-0

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