Emerging roles of SGLT2 inhibitors in obesity and insulin resistance: Focus on fat browning and macrophage polarization

Obesity-associated low-grade inflammation underlies insulin resistance and associated metabolic comorbidities, such as type 2 diabetes (T2D) and nonalcoholic fatty liver disease. Excessive ectopic fat deposition in obesity causes disorders of energy homeostasis and low-grade chronic inflammation in...

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Bibliographic Details
Published in:Adipocyte 2018-01, Vol.7 (2), p.121-128
Main Authors: Xu, Liang, Ota, Tsuguhito
Format: Article
Language:English
Subjects:
adipose tissue macrophage
Adipose Tissue, Brown - drug effects
Adipose Tissue, Brown - metabolism
Animals
Diabetes Mellitus, Type 2 - drug therapy
Diabetes Mellitus, Type 2 - metabolism
empagliflozin
fat browning
Humans
inflammation
Insulin Resistance
Macrophage Activation - drug effects
Macrophages - drug effects
Macrophages - metabolism
Non-alcoholic Fatty Liver Disease - drug therapy
Non-alcoholic Fatty Liver Disease - metabolism
Obesity - drug therapy
Obesity - metabolism
Sodium-Glucose Transporter 2 Inhibitors - pharmacology
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Summary:Obesity-associated low-grade inflammation underlies insulin resistance and associated metabolic comorbidities, such as type 2 diabetes (T2D) and nonalcoholic fatty liver disease. Excessive ectopic fat deposition in obesity causes disorders of energy homeostasis and low-grade chronic inflammation in metabolic tissues. In particular, obesity-induced recruitment and activation of adipose tissue macrophages play a key role in the pathogenesis of insulin resistance and T2D. Therefore, treatment options for energy metabolism and macrophage polarization in obese subjects are needed. Sodium-glucose cotransporter (SGLT) 2 inhibitors increase urinary glucose excretion by inhibiting renal glucose reabsorption, thereby having subsequent anti-hyperglycemic effects and reducing body weight. We recently reported that the SGLT2 inhibitor empagliflozin increases fat utilization and browning in white adipose tissue and attenuates obesity-induced inflammation and insulin resistance by activating M2 macrophages. Thus, this review focuses on the beneficial effects of empagliflozin in energy homeostasis and obesity-related inflammation and insulin resistance.
ISSN:2162-3945
2162-397X
DOI:10.1080/21623945.2017.1413516