What is Tricaprin?
Tricaprin is a triglyceride obtained by the formal acylation of the three hydroxyl groups of glycerol with capric acid. Tricaprin is an oral precursor of decanoic acid (DA), which can be hydrolyzed to DA. Tricaprin is the main component of medium-chain triglycerides (MCT) and has anti-androgenic and anti-hyperglycemic properties. Tridecanoic acid has safe uses as an additive in foods, preparations, and cosmetics.
What are Tricaprin Uses?
Tricaprin is a commercially available supplement that promotes lipid breakdown in heart muscle cells. In addition to relieving troublesome and painful symptoms in these patients, tricaprin also caused significant regression of triglyceride buildup in the heart blood vessels. After oral administration, tricaprin is hydrolyzed to DA, which binds to and partially activates peroxisome proliferator-activated receptor (PPAR)-γ, as well as PPARα and PPARβ/δ without inducing lipogenesis. In addition, Tricarpiline may improve insulin sensitivity and reduce androgen production.
Secondly, Tricaprin can be used in cosmetics. When used as Tricaprin as a masking agent, it is used to reduce or suppress the odor or basic taste of a product. It can also be used as a skin conditioner to keep skin in good condition. Tricaprin can also be added to perfumes and used in perfumes and aromatic raw materials.
What are the Research and Development of Tricaprin?
Tricaprin has attracted the attention of researchers in biomedicine and drug therapy. In a study of medical treatment options for ruptured abdominal aortic aneurysm (AAA), researchers studied the effects of tricaprin on a rat model of hypoperfusion-induced AAA. Study results show that tricaprin significantly inhibits AAA development and completely prevents rupture. And tricaprin can prevent the development and rupture of AAA. Furthermore, regression in AAA diameter was observed in the tricaprin group. Pathological analysis showed that tricaprin ameliorated hypoperfusion-induced increases in hypoxia-inducible factor 1α levels, medial smooth muscle cell (SMC) loss, aortic elastin and collagen fiber degeneration, and aortic wall elasticity loss. Tricaprin administered after AAA formation ameliorates AAA wall degeneration, including degradation of aortic elastin and collagen fibers, stenosis of the vasa vasorum, and loss of medial SMC. These data suggest that tricaprin may prevent AAA by attenuating aortic hypoperfusion and degeneration. Considering the clinical safety profile of tricaprin, tricaprin can be a promising drug candidate for AAA.
Another report investigated the effect of tricaprin incorporation on the physicochemical properties of small or large hydrophilic model drug-encapsulated liposomes. Experimental results demonstrate that the incorporation of tricaprin provides multiple benefits by improving membrane properties and acting as a membrane permeability regulator.
