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Unveiling the Connection Obesity-Related Dysfunction and Endotrophin

Dysfunction and Endotrophin

Connection Between Obesity-Related Metabolic Dysfunction and Endotrophin

As global obesity rates continue to surge, there’s an urgent imperative to decode the intricate mechanisms underlying metabolic ailments, such as diabetes. Taking this challenge head-on, Professor Jiyoung Park and her team from the Department of Biological Sciences at UNIST have spearheaded a groundbreaking investigation into endotrophin—an extracellular matrix protein with a pivotal role in maintaining adipose tissue equilibrium.

The outcomes of this research shed illuminating insights into the impact of intracellular endotrophin levels on autophagy, a natural cellular process responsible for purging unnecessary or dysfunctional components. In individuals grappling with obesity, heightened endotrophin levels set in motion deleterious effects within adipose cells by disrupting the autophagic flow, thereby fostering inflammation and the insulin resistance associated with diabetes.

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Unraveling the relationship between obesity-related metabolic dysfunction and endotrophin holds profound implications for crafting precisely targeted treatments for metabolic disorders.

Professor Jiyoung Park, Department of Biological Sciences at UNIST

Professor Park initially unearthed the significance of endotrophin in 2012 as a central player in responding to metabolic stress in obese individuals. The recent study embarked on a more profound exploration, seeking to understand how endotrophin permeates and influences fat cells under both lean and obese conditions through meticulous comparative analysis.

In the context of obesity, the study observed that endocytosis, the process by which extracellular substances are internalized into cells, facilitates the accumulation of endotrophin within adipocytes. This accumulation not only encourages the formation of autophagosomes, key players in the autophagy process, but also disrupts their degradation process, ultimately leading to cellular demise, inflammation, and insulin resistance.

Moreover, the research squad unveiled specific interactions between proteins governing protein transport (SEC13) and autophagy (ATG7), pivotal in driving excessive autophagosome formation triggered by endotrophin within adipose cells. This dysregulation of autophagy further compounds the adverse impacts on adipocyte well-being.

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Notably, the study demonstrated that inhibiting ATG7 protein function or neutralizing endotrophin using the siRNA system, designed explicitly to interfere with gene expression, markedly ameliorated metabolic disorders associated with obesity.

These findings lay the groundwork for potential future therapies aimed at mitigating endotrophin-mediated impairment of autophagic flow in obesity-related conditions. “The buildup of endotrophin in cells could serve as an indicator of an imbalance in extracellular matrix homeostasis,” noted Professor Park.

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The study’s findings have been released in advance of their official publication in the online version of Metabolism: Clinical and Experimental, a prestigious international scholarly journal specializing in endocrine metabolism, on June 10, 2023. This research was made possible with support from the National Research Foundation (NRF) of Korea, funded by the Ministry of Science and ICT (MSIT).