ArticleDiabetes therapy : research, treatment and education of diabetes and related disorders2024
Dapagliflozin-Induced Myocardial Flow Reserve Improvement is not Associated with HDL Ability to Stimulate Endothelial Nitric Oxide Production.
Article in Diabetes therapy : research, treatment and education of diabetes and related disorders, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It reports registered trial NCT03313752. Cited by 7 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Study on the Effect of Dapagliflozin on Myocardial Insulin Sensitivity and Perfusion
Open the trial in the graphWho cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Dapagliflozin treatment is associated with a reduction of epicardial adipose tissue thickness and epicardial glucose uptake in human type 2 diabetes.Cardiovascular diabetology · 2023Trial
- Sodium-glucose Co-transporter 2 (SGLT2) inhibitor dapagliflozin acutely activates cardiomyocyte HIF-1α signaling via succinate, a signaling metabolite.Journal of pharmacological sciences · 2026Article
- Insulin or Dapagliflozin Potentially Improves Microcirculatory Dysfunction or INOCA Related to Culprit Vessels in Diabetic Patients With STEMI After DCB Therapy During Long-Term Follow-Up.Journal of diabetes · 2026Observational
- Coronary microvascular disease in heart failure with preserved ejection fraction.Physiological reports · 2025Review
- Impact of SGLT2 Inhibitors on Lipoproteins in Type 2 Diabetes.Current diabetes reports · 2025Review
- SGLT2 inhibition and adipose tissue metabolism: current outlook and perspectives.Cardiovascular diabetology · 2024Review
- Antioxidant and Anti-Inflammatory Functions of High-Density Lipoprotein in Type 1 and Type 2 Diabetes.Antioxidants (Basel, Switzerland) · 2023Review
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSodium-glucose cotransporter-2 (SGLT2) inhibitors have shown controversial results in modulating plasma lipids in clinical trials. Most studies found slight increases in high-density lipoprotein (HDL) cholesterol but few have provided evidence on HDL functionality with disappointing results. However, there is broad agreement that these drugs provide cardiovascular protection through several mechanisms. Our group demonstrated that dapagliflozin improves myocardial flow reserve (MFR) in patients with type 2 diabetes (T2D) with coronary artery disease (CAD). The underlying mechanisms are still unknown, although in vitro studies have suggested the involvement of nitric oxide (NO).
aimTo investigate changes in HDL-mediated modulation of NO production with dapagliflozin and whether there is an association with MFR.
methodsSixteen patients with CAD-T2D were enrolled and randomized 1:1 to dapagliflozin or placebo for 4 weeks. Blood samples were collected before and after treatment for each group. The ability of HDL to stimulate NO production in endothelial cells was tested in vitro by incubating human umbilical vein endothelial cells (HUVEC) with apoB-depleted (apoB-D) serum of these patients. The production of NO was assessed by fluorescent assay, and results were expressed as fold versus untreated cells.
resultsChange in HDL-mediated NO production remained similar in dapagliflozin and placebo group, even after adjustment for confounders. There were no significant correlations between HDL-mediated NO production and MFR either at baseline or after treatment. No changes were found in HDL cholesterol in either group, while low-density lipoprotein cholesterol (LDL cholesterol) significantly decreased compared to baseline only in treatment group (p = 0.043).
conclusionsIn patients with T2D-CAD, beneficial effects of dapagliflozin on coronary microcirculation seem to be unrelated to HDL functions. However, HDL capacity to stimulate NO production is not impaired at baseline; thus, the effect of drug treatments would be negligible. To conclude, we can assume that HDL-independent molecular pathways are involved in the improvement of MFR in this population.
trial registrationEudraCT No. 2016-003614-27; ClinicalTrials.gov Identifier: NCT03313752.
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