Study explains why obesity increases risk of diabetes
In a groundbreaking study, researchers from the University of California-Los Angeles (UCLA) have uncovered a crucial mechanism explaining why obesity significantly raises the risk of developing type 2 diabetes. Published in Cell Reports , the research offers fresh insights that could pave the way for novel treatments for type 2 diabetes and other chronic diseases by targeting fat cells.
The study reveals that obesity disrupts the body’s ability to produce vital cellular building blocks known as ribosomal factors. These factors are essential for fat stem cells to create functioning fat cells. When ribosomal factors are insufficient, the fat cells become enlarged and dysfunctional, which plays a key role in the development of type 2 diabetes.
Dr. Claudio Villanueva, an Associate Professor of Integrative Biology and Physiology at UCLA, explained that while fat tissue has long been blamed for metabolic issues, it is, in fact, essential for maintaining normal glucose metabolism. “Obesity leads to an overabundance of fat tissue that doesn’t function properly,” Villanueva said, highlighting how the dysfunction in fat cells contributes to metabolic complications.
Under normal conditions, fat tissue acts as an energy reservoir, storing energy from food. However, when fat cells are not functioning optimally, excess energy is rerouted to other parts of the body, leading to conditions such as fatty liver disease, atherosclerosis, or stroke. This, in turn, contributes to the onset of type 2 diabetes.
The study was conducted using obese and diabetic mice, whose fat cells were found to be four to five times larger than those of lean mice. The researchers then administered the drug rosiglitazone to the mice. Remarkably, the treatment resulted in an increase in ribosomal factors to normal levels, which in turn triggered the differentiation of fat stem cells into smaller, functional fat cells. This restored the fat tissue’s ability to store energy properly and produce hormones that regulate metabolism.
Although the treated mice remained obese, the most striking result was that their type 2 diabetes symptoms essentially disappeared. The research highlights a promising approach for treating type 2 diabetes by focusing on improving fat tissue function rather than solely reducing fat mass.
This discovery could have profound implications for developing new therapies aimed at restoring proper fat cell function, potentially transforming how we treat diabetes and other obesity-related diseases.
