Called estrogen receptor alpha, this protein is critical in regulating immune system activity such as helping cells suppress inflammation and gobble-up debris.
This early preclinical study in female mice demonstrated that removing estrogen regulator alpha alone was enough to reduce the immune system's protective process and promote increased fat accumulation and accelerate atherosclerosis development.
Without this protein, the mice developed additional aspects of metabolic syndrome such as glucose intolerance, insulin resistance and inflammation.
Researchers hope that a better understanding of the activity of this receptor may lead to improved therapies in future.
"Impairment of this receptor's function could also play a role in the heightened incidence of metabolic syndrome being seen in younger women," said senior author Andrea Hevener, Ph.D., associate professor of endocrinology, diabetes and hypertension, David Geffen School of Medicine at UCLA.
"We may find that action of this estrogen receptor is just as important as that of circulating estrogen, which is key in multiple therapies such as HRT," she added.