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About:
Sodium–glucose cotransporter 2 inhibition suppresses HIF-1α-mediated metabolic switch from lipid oxidation to glycolysis in kidney tubule cells of diabetic mice
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research paper
schema:ScholarlyArticle
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Academic Article
research paper
schema:ScholarlyArticle
isDefinedBy
Covid-on-the-Web dataset
has title
Sodium–glucose cotransporter 2 inhibition suppresses HIF-1α-mediated metabolic switch from lipid oxidation to glycolysis in kidney tubule cells of diabetic mice
Creator
Cai, Ting
Zhang, Yu
Jiang, Lei
Zhou, Yang
Luo, Jing
Fang, Yi
Sun, Qi
Chen, Hanzhi
Ke, Qingqing
Lv, Yunhui
Wen, Ping
Yang, Junwei
Zen, Ke
Yuan, Qi
Source
PMC
abstract
Inhibition of sodium–glucose cotransporter 2 (SGLT2) in the proximal tubule of the kidney has emerged as an effective antihyperglycemic treatment. The potential protective role of SGLT2 inhibition on diabetic kidney disease (DKD) and underlying mechanism, however, remains unknown. In this study, metabolic switch was examined using kidney samples from human with diabetes and streptozocin (STZ)-induced experimental mouse model of diabetes treated with or without SGLT2 inhibitor dapagliflozin. Results were further validated using primarily cultured proximal tubule epithelial cells. We found that DKD development and progression to renal fibrosis entailed profound changes in proximal tubule metabolism, characterized by a switch from fatty acid utilization to glycolysis and lipid accumulation, which is associated with the increased expression of HIF-1α. Diabetes-induced tubulointerstitial damage, such as macrophage infiltration and fibrosis, was significantly improved by dapagliflozin. Consistent with the effects of these beneficial interventions, the metabolic disorder was almost completely eliminated by dapagliflozin. The increased level of HIF-1α in renal proximal tubule was nearly nullified by dapagliflozin. Moreover, dapagliflozin protects against glucose-induced metabolic shift in PTCs via inhibiting HIF-1α. It suggests that SGLT2 inhibition is efficient in rectifying the metabolic disorder and may be a novel prevention and treatment strategy for kidney tubule in DKD.
has issue date
2020-05-22
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bibo:doi
10.1038/s41419-020-2544-7
bibo:pmid
32444604
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549a4dfb8aa2e783cbf59f004211552a515e5f60
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https://doi.org/10.1038/s41419-020-2544-7
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Sodium–glucose cotransporter 2 inhibition suppresses HIF-1α-mediated metabolic switch from lipid oxidation to glycolysis in kidney tubule cells of diabetic mice
has PubMed Central identifier
PMC7242894
has PubMed identifier
32444604
schema:publication
Cell Death Dis
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covid:549a4dfb8aa2e783cbf59f004211552a515e5f60#body_text
is
schema:about
of
named entity 'kidney'
named entity 'metabolic disorder'
named entity 'proximal tubule'
named entity 'diabetic kidney disease'
named entity 'SGLT2'
named entity 'streptozocin'
named entity 'accumulation'
named entity 'inhibition'
named entity 'diabetic'
named entity 'TREATMENT'
named entity 'DEVELOPMENT'
named entity 'COMPLETELY'
named entity 'UNDERLYING'
named entity 'CONSISTENT WITH'
named entity 'PROXIMAL TUBULE'
named entity 'EPITHELIAL CELLS'
named entity 'NULLIFIED'
named entity 'ALMOST'
named entity 'level'
named entity 'strategy'
named entity 'metabolism'
named entity 'beneficial'
named entity 'fibrosis'
named entity 'dapagliflozin'
named entity 'macrophage'
named entity 'kidney tubule'
named entity 'lipid accumulation'
named entity 'mouse model'
named entity 'diabetic kidney disease'
named entity 'glycolysis'
named entity 'epithelial cells'
named entity 'SGLT2'
named entity 'metabolic disorder'
named entity 'DKD'
named entity 'glucose'
named entity 'HIF-1α'
named entity 'fibrosis'
named entity 'diabetic'
named entity 'lipid oxidation'
named entity 'HIF-1α'
named entity 'dapagliflozin'
named entity 'fatty acid'
named entity 'mice'
named entity 'diabetes'
named entity 'renal proximal tubule'
named entity 'SGLT2'
named entity 'Diabetes'
named entity 'sodium-glucose cotransporter 2'
named entity 'proximal tubule'
named entity 'dapagliflozin'
named entity 'metabolic'
named entity 'renal'
named entity 'proximal tubule of the kidney'
named entity 'Sodium-glucose cotransporter 2'
named entity 'BENEFICIAL'
named entity 'CULTURED'
named entity 'HIF-1'
named entity 'UTILIZATION'
named entity 'SGLT2 INHIBITOR'
named entity 'KIDNEY TUBULE'
named entity 'GLYCOLYSIS'
named entity 'INHIBITION'
named entity 'FOUND'
named entity 'MODEL OF'
named entity 'IMPROVED BY'
named entity 'TREATMENT STRATEGY'
named entity 'PROGRESSION'
named entity 'DAPAGLIFLOZIN'
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