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Review
. 2018 Dec 15;9(12):209-219.
doi: 10.4239/wjd.v9.i12.209.

Treatment approach to type 2 diabetes: Past, present and future

Affiliations
Review

Treatment approach to type 2 diabetes: Past, present and future

Kristina Blaslov et al. World J Diabetes. .

Abstract

Type 2 diabetes mellitus (DM) is a lifelong metabolic disease, characterized by hyperglycaemia which gradually leads to the development and progression of vascular complications. It is recognized as a global burden disease, with substantial consequences on human health (fatality) as well as on health-care system costs. This review focuses on the topic of historical discovery and understanding the complexity of the disease in the field of pathophysiology, as well as development of the pharmacotherapy beyond insulin. The complex interplay of insulin secretion and insulin resistance developed from previously known "ominous triumvirate" to "ominous octet" indicate the implication of multiple organs in glucose metabolism. The pharmacological approach has progressed from biguanides to a wide spectrum of medications that seem to provide a beneficial effect on the cardiovascular system. Despite this, we are still not achieving the target treatment goals. Thus, the future should bring novel antidiabetic drug classes capable of acting on several levels simultaneously. In conclusion, given the raising burden of type 2 DM, the best present strategy that could contribute the most to the reduction of morbidity and mortality should be focused on primary prevention.

Keywords: Hyperglycaemia; Hypoglycaemic agents; Insulin resistance; Physical activity; Type 2 diabetes mellitus.

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Conflict of interest statement

Conflict-of-interest statement: No potential conflicts of interest.

Figures

Figure 1
Figure 1
The molecular mechanism of insulin resistance. In insulin resistance, the binding of insulin to its receptor does not result in serine phosphorylation of insulin receptor substrate-1 and activation of the cascade of intracellular substrates’ activation which result in glucose influx, glucagon and protein synthesis, and lipolysis inhibition. IRS: Insulin receptor substrate; Ser/Thr: Serine/threonine protein kinase; Tyr: Tyrosine kinase; PI-3: Phosphatidylinositol 3; PDK-1: Phosphoinositide-dependent protein kinase-1; Akt/PBK: AKT serine/threonine kinase 1 (protein kinase B family); PDE: Phosphodiesterase; cAMP: Cyclic adenosine monophosphate; PKA: Protein kinase A; GLUT4: Glucose transporter type 4.

References

    1. Powers AC. Diabetes Mellitus. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, et al., editors. Harrison’s Principles of Internal Medicine, 18th ed. New York: McGraw-Hill; 2012.
    1. International Diabetes Federation. IDF Diabetes Atlas, 8th ed. Brussels: International Diabetes Federation; 2017.
    1. Guthrie DW, Humphreys SS. Diabetes urine testing: an historical perspective. Diabetes Educ. 1988;14:521–526. - PubMed
    1. Eknoyan G, Nagy J. A history of diabetes mellitus or how a disease of the kidneys evolved into a kidney disease. Adv Chronic Kidney Dis. 2005;12:223–229. - PubMed
    1. Reece E. The history of diabetes mellitus. In: Reece E, Coustan D, et al., editors. Diabetes Mellitus in Pregnancy. New York: Churchill Livingstone; 1995.