Cardiovascular
How might dapagliflozin ease diabetic stiff hearts?
Open access · cc by · source: Europe PMC
In 30 rabbits, dapagliflozin lessened diabetes-related diastolic dysfunction and fibrosis by downregulating SGK1 and ENaC, with matching H9C2 cell results.
Study at a glance
- Design
- Animal / in-vitro — Alloxan-diabetic rabbits randomized to dapagliflozin vs diabetes vs control, plus fibrotic H9C2 SGK1 mechanistic assays
- N
- N=30 · 30 male New Zealand white rabbits, n=10 per control/diabetes/diabetes+dapagliflozin group; plus H9C2 cells
- Population
- Male New Zealand white rabbits with alloxan-induced diabetes and fibrosis-induced H9C2 cardiomyoblasts
- Outcome
- LV diastolic function, myocardial fibrosis, SGK1/ENaC/NHE1 signaling, inflammation, and mitochondrial structure
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Key findings
Diabetes+dapagliflozin attenuated diastolic dysfunction vs diabetes alone. Fibrosis fell via SGK1 and ENaC inhibition in tissue and H9C2 cells. Dapagliflozin was anti-inflammatory and eased mitochondrial disruption; siSGK1 reduced ENaC and NHE1 similarly to the drug.
Methodology
Randomized 30 male NZ white rabbits to control, diabetes (IV alloxan), or diabetes+dapagliflozin (n=10 each); assessed echo, histology, and molecules, and probed SGK1 with siRNA in fibrotic H9C2 cells.
Limitations
Alloxan-rabbit and H9C2 data do not prove SGK1 is the only human mechanism or replace large SGLT2i outcome trials.
How this study connects
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