US scientists have decoded why obesity increases the risk of type 2 diabetes by targeting the fat cells.
The study, published in Cell Reports, may advance new treatments for type 2 diabetes and other chronic diseases that work by helping fat stem cells differentiate and make new, smaller fat cells. In a first, the team from the University of California-Los Angeles (UCLA) showed that obesity can make it difficult for the body to produce key cellular building blocks called ribosomal factors. Without sufficient ribosomal factors, fat stem cells cannot produce functioning fat cells.
Their energy gets trapped and they become enlarged and play a crucial role in diabetes development. While fat tissue has been blamed for long, it's "actually essential for maintaining normal glucose metabolism," said Dr. Claudio Villanueva, Associate Professor of integrative biology and physiology at the University of California-Los Angeles. Villanueva explained that people with obesity carry "too much fat tissue which is also not functioning optimally".
Fat tissue stores energy from food. However, when not functioning properly, the excess energy gets rerouted to be stored elsewhere in the body like in the liver -- leading to fatty liver disease; or in the heart -- leading to atherosclerosis or stroke. The study included obese and diabetic mice. The fat cells of these mice were four to five times larger than those found in lean mice.
The team administered them with rosiglitazone. The results showed that their ribosomal factors increased to normal levels, which triggered their fat stem cells to differentiate to produce new, smaller fat cells. Further, this enabled the mice's fat tissue to function properly in storing energy. These also generate key hormones that regulate metabolism. However, the scientists found that although the mice remained obese after taking the drug, their "type 2 diabetes essentially disappeared,"
