(-)-Epicatechin Is a Biased Ligand of Apelin Receptor
This paper identifies (-)-epicatechin as a biased ligand of the apelin receptor, supporting a receptor-mediated signaling mechanism that may help explain some of its vascular and metabolic effects.
(-)-epicatechin activation of endothelial cell endothelial nitric oxide synthase, nitric oxide, and related signaling pathways
This study found that (-)-epicatechin activates endothelial nitric oxide synthase and increases nitric oxide signaling in endothelial cells, helping define a plausible endothelial mechanism for vascular benefit.
The effects of (−)-epicatechin on endothelial cells involve the G protein-coupled estrogen receptor (GPER)
The authors report that the effects of (-)-epicatechin in endothelial cells involve GPER, adding a specific receptor-linked explanation for observed vascular signaling responses.
Influence of the AT(2) receptor on the L-arginine-nitric oxide pathway and effects of (-)-epicatechin on HUVECs from women with preeclampsia
This study examined nitric oxide biology and arginase activity in plasma and endothelial cells from women with preeclampsia. It found altered L-arginine/NO signaling and showed that (-)-epicatechin reduced arginase and superoxide-related activity in HUVECs.
Acute effects of an oral supplement of (-)-epicatechin on postprandial fat and carbohydrate metabolism in normal and overweight subjects
This human study assessed short-term metabolic effects of an oral (-)-epicatechin supplement after meals, reporting changes in postprandial fat and carbohydrate handling in normal and overweight participants.
Is it possible to treat nonalcoholic liver disease using a flavanol-based nutraceutical approach? Basic and clinical data
This article reviews and discusses basic and clinical evidence relevant to using a flavanol-based nutraceutical strategy for nonalcoholic liver disease, summarizing translational evidence rather than making a single-trial claim.
Effects of (−)-epicatechin on the time course of the expression of perilipins in a diet-induced model of nonalcoholic steatohepatitis
Using a diet-induced NASH model, this study tracked the time course of perilipin expression and assessed how (-)-epicatechin altered those lipid-droplet–related responses over time.
(−)-Epicatechin induced reversal of endothelial cell aging and improved vascular function: underlying mechanisms
This paper reports that (-)-epicatechin reversed several features of endothelial cell aging and improved vascular function, while also exploring the mechanisms behind those changes.
Beneficial effects of dark chocolate on exercise capacity in sedentary subjects: underlying mechanisms. A double blind, randomized, placebo controlled trial†
In sedentary adults, dark chocolate intake improved exercise-related performance measures, including work achieved and VO2 max trends, with mechanistic data pointing toward mitochondrial efficiency and upstream signaling changes.
Cell membrane mediated (−)-epicatechin effects on upstream endothelial cell signaling: Evidence for a surface receptor
This paper provides evidence that (-)-epicatechin can trigger endothelial signaling through a cell-surface receptor mechanism, supporting membrane-initiated signaling rather than only intracellular antioxidant activity.
Browning effects of (-)-epicatechin on adipocytes and white adipose tissue
This study found that (-)-epicatechin promoted browning-related changes in adipocytes and white adipose tissue, with associated improvements in mitochondrial function and thermogenic markers.
Arginase inhibition by (−)-Epicatechin reverses endothelial cell aging
This study identifies arginase inhibition as a key mechanism by which (-)-epicatechin reverses endothelial cell aging, tying vascular anti-aging effects to a defined enzymatic pathway.