The 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,".
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