Cited by 134Adipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and MetabolismDiabetes Treatment and Management

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

Open access
Xu, Liang, Ota, Tsuguhito·2017·Adipocyte

Abstract

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.

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Crossref · 10.1080/21623945.2017.1413516

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  • Dapagliflozin and empagliflozin were able to reduce liver lipid content in people with type 2 diabetes with or without MASLD.

    “whereas both dapagliflozin and empagliflozin were able to reduce liver lipid content in people with type 2 diabetes with (dapagliflozin [153,154]) or both with and without MASLD (empagliflozin [98]).”

    From Obesity and MASLD: Is weight loss the (only) key to treat metabolic liver disease? (2024) · cites this paper as [154]

    The available indexed passages contain reference DOIs and section headings, but no findings about liver lipid content in people with type 2 diabetes. Searches for empagliflozin, hepatic triglycerides, and liver content did not retrieve a passage addressing the claimed reduction or the with-versus-without-MASLD distinction. (LLM, conf=0.74)

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Authors
Xu, L., & Ota, T.
Affiliations
Kanazawa University (JP)
Corresponding author
Ota, Tsuguhito
Venue
Adipocyte
Published
2017-12-11
Volume
7
Issue
2
Pages
1-8
ISSN
  • 2162-3945 (ISSN-L)
  • 2162-397X
OpenAlex
W2775166788
Cited by
134
References
63
Citations by year
2026: 6 · 2025: 14 · 2024: 21 · 2023: 27 · 2022: 25 · 2021: 14 · 2020: 18 · 2019: 5 · 2018: 4
Type
journal article
Language
en
Open access
Locations
  • Adipocyte (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
Japan Society for the Promotion of Science (16H03035)
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Keywords
SGLT2 inhibitors, empagliflozin, obesity, insulin resistance, fat browning, white adipose tissue, macrophage polarization, M2 macrophages, low-grade inflammation, type 2 diabetes, non-alcoholic fatty liver disease, energy homeostasis, ectopic fat deposition, urinary glucose excretion
MeSH terms
Sodium-Glucose Transporter 2 Inhibitors, Animals, Adipose Tissue, Brown, Diabetes Mellitus, Type 2, Humans, Insulin Resistance, Macrophage Activation, Macrophages, Obesity, Non-alcoholic Fatty Liver Disease

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