A molecule known as adipocyte adhesion molecule (ACAM) protects from obesity and type 2 diabetes, Okayama researchers find.
Scientists from the University of Okayama have found a strong correlation between the overexpression of ACAM, which is also known as the receptor-like membrane protein CLMP, and the molecular regulation of fat tissue accumulation.
CLMP plays a role in the binding activity of fat. When abundantly expressed in mature adipocytes, it forms an element of the cell junction called F-acti, which is responsible for anchoring the cell junctions.
F-actin determines the molecular architecture of a variety of cell types. The combined action of ACAM and F-actin in epithelial cells can remodel their junctions to preferentially inhibit adipocyte hypertrophy – the expansion of fat cells – and improve insulin sensitivity.
In this study study/findings – published in the journal Diabetes, March 2016 – the lead author of the report Jun Wada and his co-workers monitored how ACAM behaved and interacted with other molecules involved in fat metabolism inside the body.
ACAM is present on the surface of fat cells in rats, mice and humans. Part of the experiment consisted in following three groups of mice that each expressed varying levels of ACAM – induced by another promoter adipocyte fatty acid binding protein known as – ap2 – and were fed a high fat, high sugar diet.
When the mice with the highest levels of ACAM expression were bound to ACAM-driven fatty acid, it revealed a prominent reduction of adipose tissue mass and smaller size of adipocytes from an alteration in the volume of intercellular space between epithelial cells.
Tighter cellular adherence (10-20 nm) was observed through fluorescent tagging over the distances of plasma membranes activated by ACAM and F-acti, conferring an anti-obesity action to the cells.
Until now, limited information has existed regarding the role of cell surface proteins in fat tissues and the extent of their involvement in the build-up of excess fat leading to obesity.
The Japanese team is confident that the protection from developing obesity and diabetes shown in mice engineered to express high levels of ACAM will translate to new therapies targeting these diseases in humans.
