06:19am Monday 23 October 2017

Loss of key estrogen regulator may lead to metabolic syndrome, atherosclerosis

The protein, known as estrogen receptor alpha, is critical in regulating immune system activity, including helping cells suppress inflammation and gobble up debris. 
                                   
This early pre-clinical study in female mice demonstrated that removing estrogen receptor alpha was alone enough to reduce the immune system’s protective process, promote increased fat accumulation and accelerate atherosclerosis development. Without this protein, mice developed additional aspects of metabolic syndrome, such as glucose intolerance, insulin resistance and inflammation.
 
This estrogen receptor is also expressed in non-reproductive tissues such as fat, muscle and liver and can act independently of the hormone estrogen. However, little is known about the receptor’s actions in these tissues involved in blood-sugar regulation, which plays an integral role in metabolic syndrome.
 
In further research, the team plans to study the status of this estrogen receptor in pre- and post-menopausal women.
 
IMPACT      
Researchers hope the early findings may provide insight into the development of metabolic syndrome, which affects millions of people worldwide. A better understanding of the activity of this receptor may lead to improved future therapies.
 
Impairment of the receptor’s function could also play a role in the increased incidence of metabolic syndrome seen in younger women, the researchers said. It may be, they said, that the action of this estrogen receptor is just as important as that of circulating estrogen, which is key to therapies such as hormone-replacement therapy.
 
AUTHORS:  
Senior author Andrea Hevener, a UCLA associate professor of endocrinology, diabetes and hypertension, is available for interviews.
 
FUNDING:   
The research was funded by the National Institutes of Health–National Institute of Diabetes and Digestive and Kidney Disorders; the Iris Cantor–UCLA Women’s Health Foundation; and the UCLA Department of Medicine. 
 
JOURNAL:  
The study appears in the early edition of the journal Proceedings of the National Academy of Sciences (PNAS), published the week of Sept. 5.
Contact: Rachel Champeau

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