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Citations to this article

SGLT2 inhibition reprograms systemic metabolism via FGF21-dependent and -independent mechanisms
Soravis Osataphan, … , Robert Gerszten, Mary-Elizabeth Patti
Soravis Osataphan, … , Robert Gerszten, Mary-Elizabeth Patti
Published March 7, 2019
Citation Information: JCI Insight. 2019;4(5):e123130. https://doi.org/10.1172/jci.insight.123130.
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Research Article Hepatology Metabolism Article has an altmetric score of 57

SGLT2 inhibition reprograms systemic metabolism via FGF21-dependent and -independent mechanisms

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Abstract

Pharmacologic inhibition of the renal sodium/glucose cotransporter-2 induces glycosuria and reduces glycemia. Given that SGLT2 inhibitors (SGLT2i) reduce mortality and cardiovascular risk in type 2 diabetes, improved understanding of molecular mechanisms mediating these metabolic effects is required. Treatment of obese but nondiabetic mice with the SGLT2i canagliflozin (CANA) reduces adiposity, improves glucose tolerance despite reduced plasma insulin, increases plasma ketones, and improves plasma lipid profiles. Utilizing an integrated transcriptomic-metabolomics approach, we demonstrate that CANA modulates key nutrient-sensing pathways, with activation of 5′ AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin (mTOR), independent of insulin or glucagon sensitivity or signaling. Moreover, CANA induces transcriptional reprogramming to activate catabolic pathways, increase fatty acid oxidation, reduce hepatic steatosis and diacylglycerol content, and increase hepatic and plasma levels of FGF21. Given that these phenotypes mirror the effects of FGF21 to promote lipid oxidation, ketogenesis, and reduction in adiposity, we hypothesized that FGF21 is required for CANA action. Using FGF21-null mice, we demonstrate that FGF21 is not required for SGLT2i-mediated induction of lipid oxidation and ketogenesis but is required for reduction in fat mass and activation of lipolysis. Taken together, these data demonstrate that SGLT2 inhibition triggers a fasting-like transcriptional and metabolic paradigm but requires FGF21 for reduction in adiposity.

Authors

Soravis Osataphan, Chiara Macchi, Garima Singhal, Jeremy Chimene-Weiss, Vicencia Sales, Chisayo Kozuka, Jonathan M. Dreyfuss, Hui Pan, Yanin Tangcharoenpaisan, Jordan Morningstar, Robert Gerszten, Mary-Elizabeth Patti

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Year: 2025 2024 2023 2022 2021 2020 2019 Total
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BS Kadosh, MS Garshick, J Gaztanaga, KJ Moore, JD Newman, M Pillinger, R Ramasamy, HR Reynolds, B Shah, J Hochman, GI Fishman, SD Katz
Arteriosclerosis, thrombosis, and vascular biology 2020
A metabolomics‐based molecular pathway analysis of how the sodium‐glucose co‐transporter‐2 inhibitor dapagliflozin may slow kidney function decline in patients with diabetes
S Mulder, A Hammarstedt, SB Nagaraj, V Nair, W Ju, J Hedberg, PJ Greasley, JW Eriksson, J Oscarsson, HJ Heerspink
Diabetes, obesity & metabolism 2020
Effects of canagliflozin on growth and metabolic reprograming in hepatocellular carcinoma cells: Multi-omics analysis of metabolomics and absolute quantification proteomics (iMPAQT)
D Nakano, T Kawaguchi, H Iwamoto, M Hayakawa, H Koga, T Torimura, T Kanda
PloS one 2020
Effects of Secretome from Fat Tissues on Ion Currents of Cardiomyocyte Modulated by Sodium-Glucose Transporter 2 Inhibitor
SJ Jhuo, IH Liu, WC Tsai, TW Chou, YH Lin, BN Wu, KT Lee, WT Lai
Molecules (Basel, Switzerland) 2020
Empagliflozin reverses obesity and insulin resistance through fat browning and alternative macrophage activation in mice fed a high-fat diet
L Xu, N Nagata, G Chen, M Nagashimada, F Zhuge, Y Ni, Y Sakai, S Kaneko, T Ota
BMJ Open Diabetes Research & Care 2019
Paternal Nongenetic Intergenerational Transmission of Metabolic Disease Risk
L Su, ME Patti
Current Diabetes Reports 2019
Advances in Research on Diabetes by Human Nutriomics
X Ren, X Li
International journal of molecular sciences 2019

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