The conversion process breaks down when disease enters
En los laboratorios de la Universidad de Talca, dos investigadoras chilenas exploran si un derivado molecular del Omega 3 —llamado Maresin 1— puede reparar el hígado dañado por la diabetes y la obesidad, enfermedades que hoy afectan a millones en todo el mundo. Su trabajo no busca confirmar lo que ya se sabe sobre los beneficios del pescado, sino identificar con precisión el mecanismo por el cual este compuesto podría interrumpir el deterioro orgánico una vez que ya ha comenzado. Es una distinción pequeña en apariencia, pero enorme en sus implicaciones: la diferencia entre prevenir el daño y revertirlo.
- La diabetes y la obesidad desencadenan una cascada inflamatoria que destruye el tejido hepático, y los tratamientos actuales apenas logran frenar el deterioro, no repararlo.
- El cuerpo humano debería producir Maresin 1 de forma natural al metabolizar el Omega 3, pero la inflamación crónica interrumpe ese proceso, dejando al organismo sin su propia defensa.
- Los modelos experimentales mostraron que la introducción de Maresin 1 normalizó marcadores bioquímicos alterados y mejoró visiblemente el tejido hepático dañado.
- Aún no existe consenso científico sobre la dosis óptima de Omega 3 para tratar enfermedades metabólicas, lo que convierte esta investigación en un paso necesario hacia terapias más precisas.
- Las investigadoras Jéssica Zúñiga y Roxana Orrego continúan sus experimentos con la vista puesta en un horizonte concreto: el desarrollo de un fármaco específico para una enfermedad específica, no un suplemento de bienestar general.
En la Facultad de Ciencias de la Salud de la Universidad de Talca, las investigadoras Jéssica Zúñiga Hernández y Roxana Orrego Castillo estudian si el Maresin 1 —un derivado del Omega 3 presente en el pescado y semillas como la chía y el lino— puede revertir el daño hepático causado por la diabetes y la obesidad. Su enfoque no es nutricional sino molecular: no les interesa si comer más pescado ayuda, sino si este compuesto específico puede interrumpir el proceso que destruye el hígado cuando la enfermedad metabólica ya se ha instalado.
El hígado es el centro de la química corporal, y cuando la diabetes y la obesidad convergen, esa química se desordena. La inflamación se expande, el tejido se degrada y el órgano que debería proteger al cuerpo se convierte en un sitio de daño progresivo. Los resultados preliminares del equipo son alentadores: al introducir Maresin 1 en modelos experimentales, los marcadores bioquímicos alterados comenzaron a normalizarse y el tejido hepático mostró signos de recuperación. Ninguno de estos hallazgos ha sido probado en pacientes humanos, pero ambos sugieren que el camino molecular que investigan podría tener consecuencias reales.
Lo que hace más urgente esta investigación es una paradoja biológica: el cuerpo humano debería producir Maresin 1 por sí solo al metabolizar el Omega 3, pero la inflamación crónica interrumpe esa conversión. La dieta puede prevenir, pero no curar lo que ya está dañado. Ahí vive exactamente este trabajo: en la frontera entre la prevención y el tratamiento.
Un obstáculo persiste: no existe aún consenso sobre la dosis óptima de Omega 3 para tratar enfermedades metabólicas. Es precisamente esa ausencia la que justifica continuar. Zúñiga y Orrego no buscan validar los beneficios conocidos del aceite de pescado, sino identificar con suficiente precisión un mecanismo molecular que permita, en el futuro, desarrollar un fármaco dirigido a una enfermedad concreta en una población concreta.
At the University of Talca's Faculty of Health Sciences, a team of researchers is pursuing a narrow but promising path: they want to understand whether a single compound derived from fish oil might help reverse liver damage in people whose bodies have been ravaged by diabetes and obesity.
The compound is called Maresin 1. It comes from Omega-3 fatty acids—the same nutrients that nutritionists have been recommending for decades, found in fish like jack mackerel and in seeds such as flax and chia. What makes this research different is not the source material but the specificity of the target. Jéssica Zúñiga Hernández and Roxana Orrego Castillo, the academics leading the work, are not studying whether eating more fish helps. They are studying whether this particular derivative can interrupt the molecular cascade that damages the liver when metabolic disease takes hold.
The liver is where the body's chemistry happens. When diabetes and obesity converge, that chemistry goes wrong. Inflammation spreads. Tissue degrades. The organ that should be protecting you becomes a site of damage. For years, doctors have had few tools to reverse this process once it begins. Most treatments manage symptoms or slow decline. They do not repair.
In their experimental models, Zúñiga and Orrego introduced Maresin 1 and watched what happened. The preliminary results were encouraging enough to warrant continued investigation. Biochemical markers that had been abnormal began to normalize. The liver tissue itself showed signs of improvement. Neither result is a cure, and neither has been tested in human patients. But both suggest that the molecular pathway they are investigating might actually matter—that this derivative could eventually become a drug for people whose metabolic disease has damaged their livers.
What complicates the picture is that the human body should already be making Maresin 1 on its own. When you eat Omega-3 fatty acids under normal conditions, your body converts them into protective compounds, including this one. The problem emerges when inflammation or metabolic disease enters the picture. The conversion process breaks down. Your body stops making what it needs. This is why a synthetic or concentrated form might work where diet alone cannot.
The researchers emphasized that nutrition remains foundational to prevention. You cannot eat your way out of established metabolic disease, but you can reduce your risk of developing it. The gap between prevention and treatment is where this research lives.
One obstacle remains unresolved: no one has yet established the optimal dose of Omega-3 compounds needed to treat these diseases. This absence of consensus is precisely why the work matters. It is why Zúñiga and Orrego continue their experiments. They are not trying to prove that fish oil is good for you—that is already established. They are trying to identify the specific molecular mechanism by which one particular derivative might help repair damage that has already been done, and to do so with enough precision that a future drug could be developed not for general wellness but for a specific disease in a specific population.
Notable Quotes
The objective is to identify a molecular pathway that explains how certain Omega-3 derivatives can improve specific diabetes conditions associated with obesity and liver damage— Jéssica Zúñiga Hernández, lead researcher
The Hearth Conversation Another angle on the story
Why focus on this one compound when Omega-3s are already well-known?
Because knowing that something is good for you is different from understanding how to use it as medicine. Maresin 1 is what your body should make from Omega-3s, but when you have metabolic disease, that process fails. We're trying to bypass that failure.
So you're replacing what the body can't make anymore?
Exactly. In a healthy person, eating fish does the job. But once inflammation and metabolic disease take over, the conversion stops working. We're asking whether giving the body this specific derivative directly might repair the damage that's already happened.
The preliminary results showed improvement. What does that actually mean in practical terms?
The liver tissue looked better under examination. The chemical markers that indicate liver function moved back toward normal ranges. It's not a reversal of disease—not yet. But it suggests the pathway is real and worth pursuing further.
Why hasn't this been tested in humans yet?
Because we need to understand the mechanism first, and we need to know the right dose. Right now there's no consensus on how much Omega-3 you need to treat these diseases. We're still in the phase of asking whether this works at all.
If it does work, how long until patients could access it?
That's years away. We're still in experimental models. But if the mechanism holds up, and if we can identify the right dose, then yes—eventually this could become a drug for people whose diabetes and obesity have already damaged their livers.