Obesity can turn a person’s own fat tissue into a source of toxic molecules that damage the pancreas, liver, and muscles. This matters because not everyone who is obese develops diabetes or heart disease, and researchers do not yet understand why. The project aims to uncover the molecular mechanisms that distinguish “healthy” fat expansion from the dysfunctional kind that releases harmful lipid species. It also asks whether activating brown fat—tissue that burns fat to generate heat—could prevent or reverse obesity’s metabolic complications. If successful, the work could lead to diagnostic biomarkers that identify which obese individuals are at highest risk of developing diabetes or cardiovascular problems, allowing earlier intervention. It may also reveal new drug targets for preventing or reversing lipotoxicity. The researchers will first use mouse models and cell studies, then validate the most promising findings in humans with clinical collaborators. This is fundamental science with a clear translational path: understanding how fat tissue fails could eventually change how doctors assess and treat metabolic disease.
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Obesity is associated with insulin resistance, diabetes and cardiovascular problems. We want to know why and how obesity causes these problems and what can be done to either prevent or reverse it. For this purpose, we will investigate the molecular links between this cluster of pathologies. We think that one of the mechanisms that links obesity to other metabolic diseases is related to the impaired capacity of the adipose tissue (fat) to expand and function, causing it to release toxic lipid species that accumulate and affect other organs such as pancreas, liver and skeletal muscle. Specifically we aim to: a) understand the normal mechanisms enabling the adipose tissue to grow in a “healthy” way that does not result in the metabolic problems typically associated with obesity, such as diabetes and heart attacks; b) define whether targeting brown adipose tissue, a type of fat that uses fat to make heat, can prevent or reverse obesity and its associated diseases; and c) identify diagnostic biomarkers to identify the risk of developing complications as well as pathogenic therapeutically targetable mechanisms. For this purpose, we will use mouse models and cells, advanced experimental studies and technologies to validate our most significant findings before working with our collaborators to confirm them in humans.
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