Clinically validated, enhanced Oleoylethanolamide [OEA] to support metabolic health, microbiome balance and satiety.

Trpti™ is Oleoylethanolamide [ OEA ] powered by the LipiSperse® technology by Pharmako Biotechnologies Pty Ltd, Australia. The LipiSperse shepherds OEA through the GI tract and delivers OEA efficiently to the intestines, where it best enhances the production of the body’s own GLP-1. This ensures no side effects, unlike the synthetic GLP-1 agonists, which have a myriad side effects.

The physiological actions of OEA stem largely from high-affinity binding to the nuclear receptor PPAR-α (Stahel et al., 2008). Through this pathway, OEA promotes satiety, stimulates lipolysis, drives ketone production ], and even facilitates memory consolidation . In addition, OEA engages GPR119 , enhancing release of the incretin hormone GLP-1, which supports metabolic regulation (Overton et al., 2006; Lauffer et al., 2009). At pharmacological- but not physiological – concentrations, OEA can also activate the TRPV1 channel (Christie et al., 2018; De Petrocellis et al., 2017).

The gut microbiota plays a critical role in metabolic health, and dysbiosis is linked to obesity and insulin resistance. OEA administration alters microbial composition, notably shifting the Firmicutes-to-Bacteroidetes ratio toward the latter, which is generally associated with leaner phenotypes (Di Paola et al., 2018).

A randomized, double-blind, placebo-controlled trial to determine whether 12 weeks of TRPTI supplementation at a dose of 300 mg / day could alter gut microbiota composition and related functional outcomes in overweight adults. Fifty-seven participants were enrolled, with 44 completing all assessments. Groups were well matched at baseline with no significant demographic differences. The primary endpoint, change in microbiome/metagenomic profile, revealed that while overall diversity was preserved across both arms, TRPTI supplementation led to distinct microbial shifts. The TRPTI group showed enrichment of beneficial species, notably Akkermansia muciniphila and Faecalibacterium prausnitzii, linked to improved gut barrier function, metabolic health, and anti-inflammatory activity. In contrast, the placebo group exhibited increases in taxa associated with microbial dysbiosis and potential antibiotic resistance.

Functional metagenomic analysis demonstrated upregulation of several microbial pathways in the TRPTI group, including enhanced detoxification (4-hydroxybenzoyl-CoA reductase activity), energy metabolism (gluconate 5-dehydrogenase, carbamate kinase), amino acid/nitrogen metabolism (acetylornithine deacetylase), and mucosal integrity (N-acylglucosamine-6-phosphate 2-epimerase). These changes suggest improved microbial efficiency in carbohydrate utilization, redox balance, and barrier support. The only downregulated pathway was telomere maintenance. Anthropometric data showed modest weight and BMI reductions in participants with baseline BMI <35 on TRPI, while placebo users gained weight over the same period. Quality-of-life, stress, and sleep scores were stable across groups.

In summary, TRPTI supplementation promoted a more favorable gut microbiome signature and microbial functional capacity, with trends toward modest metabolic benefits, while maintaining safety and tolerability.

A clinical trial evaluated the metabolic effects of two doses of TRPTI 150 mg and 300 mg versus placebo in overweight but otherwise healthy adults. Thirty-six participants completed the crossover study, with the primary endpoint being GLP-1 secretion over 8 hours. In this study, high-dose TRPTI 300 mg produced a clear dose-dependent enhancement of GLP-1. Compared to placebo, it induced a rapid rise within 30 minutes and sustained elevations after both breakfast and lunch, yielding a ~3.5-fold greater AUC and 1.7-fold higher Cmax. In contrast, the low dose suppressed GLP-1 below baseline, while placebo induced only minor increases. The GLP-1 enhancing effect was strongly correlated with marked suppression of DPP-4, the GLP-1–degrading enzyme. High-dose TRPTI reduced DPP-4 activity by up to 87% shortly after dosing and maintained partial inhibition throughout the study period, whereas placebo produced a robust rise in DPP-4 and the low dose yielded only modest reductions. These findings suggest that Trpti’s enhances GLP-1 levels via DPP-4 inhibition, rather than direct stimulation of secretion. Other incretin responses were unaffected: GIP showed typical meal-driven biphasic peaks across all groups, with only a small early rise unique to high-dose Trpti. Glucagon concentrations remained stable, indicating preservation of counter-regulatory responses. Satiety ratings were unchanged, but participants consumed slightly less food in both Trpti arms. All treatments were well tolerated, with only mild, infrequent gastrointestinal effects.

Overall, in this study TRPTI demonstrated dose-dependent, selective enhancement of GLP-1 signaling, with the 300 mg dose achieving robust metabolic effects while maintaining safety.

References:

1.] Christie et al 2018 : https://doi.org/10.3389/fendo.2018.00420

2.] De Petrocellis et. al 2017 : https://doi.org/10.1016/bs.apha.2017.04.001

3.] Di Paola et. al. 2018 : https://doi.org/10.1038/s41598-018-32925-x

4.] Lauffer et. al. 2009 : https://doi.org/10.2337/db08-1237

5.] Overton et. al. 2006 : https://doi.org/10.1016/j.cmet.2006.02.004

6.] Stahel et. al. 2008 : https://doi.org/10.1155/2008/538141

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