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. 2021 Apr 12:6:e57-e78.
doi: 10.5114/amsad.2021.105314. eCollection 2021.

Empagliflozin therapy and insulin resistance-associated disorders: effects and promises beyond a diabetic state

Affiliations

Empagliflozin therapy and insulin resistance-associated disorders: effects and promises beyond a diabetic state

Georgios S Papaetis. Arch Med Sci Atheroscler Dis. .

Abstract

Empagliflozin is a SGLT2 inhibitor that has shown remarkable cardiovascular and renal activities in patients with type 2 diabetes (T2D). Preclinical and clinical studies of empagliflozin in T2D population have demonstrated significant improvements in body weight, waist circumference, insulin sensitivity, and blood pressure - effects beyond its antihyperglycaemic control. Moreover, several studies suggested that this drug possesses significant anti-inflammatory and antioxidative stress properties. This paper explores extensively the main preclinical and clinical evidence of empagliflozin administration in insulin resistance-related disorders beyond a diabetic state. It also discusses its future perspectives, as a therapeutic approach, in this high cardiovascular-risk population.

Keywords: empagliflozin; insulin resistance; metabolic syndrome; obesity.

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Conflict of interest statement

The author declares no conflict of interest.

Figures

Figure 1
Figure 1
Empagliflozin and WAT: possible mechanisms to suppress an overweight/obese non-diabetic insulin-resistant state. M – macrophages, CYT – cytokines, CHEM – chemokines, T – T lymphocytes, NLRP-3 – nucleotide-binding domain, leucine-rich repeat containing protein, mTOR – mammalian target of rapamycin, NEFAs – non-esterified fatty acids, WAT – white adipose tissue.

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References

    1. Lebovitz HE. Insulin resistance: definition and consequences. Exp Clin Endocrinol Diabetes. 2001;109(Suppl 2):S135–48. - PubMed
    1. Papaetis GS, Papakyriakou P, Panagiotou TN. Central obesity, type 2 diabetes and insulIn: exploring a pathway full of thorns. Arch Med Sci. 2015;11:463–82. - PMC - PubMed
    1. Papaetis GS, Orphanidou D, Panagiotou TN. Thiazolidinediones and type 2 diabetes: from cellular targets to cardiovascular benefit. Curr Drug Targets. 2011;12:1498–512. - PubMed
    1. Ferrannini E. Is insulin resistance the cause of the metabolic syndrome? Ann Med. 2006;38:42–51. - PubMed
    1. Mirzaalian Y, Nourian M, Gholamalizadeh M, et al. The association of quantitative insulin sensitivity indices (HOMA-IR and QUICKI) with anthropometric and cardiometabolic indicators in adolescents. Arch Med Sci Atheroscler Dis. 2019;4:e32–7. - PMC - PubMed

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