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Reversing obesity

Obesity reversed by manipulating Tyk2 enzyme

Tyk2 helps regulate obesity through the differentiation BAT
Dr Andrew Larner, lead researcher of the international study

An international team of scientists has successfully reversed obesity in mice by manipulating the production of an enzyme known as tyrosine-protein kinase-2 (Tyk2).

Published online in the journal Cell Metabolism, the researchers report that Tyk2 helps regulate obesity in mice and humans through the differentiation of brown adipose tissue (BAT).

"We discovered that Tyk2 levels in mice are regulated by diet. We then tested tissue samples from humans and found that levels of Tyk2 were more than 50% lower in obese humans," said Dr Andrew Larner, Virginia Commonwealth University Massey Cancer Center. "Our findings open new potential avenues for research and development of new pharmacological and nutritional treatments for obesity."

The study is the first to provide evidence of the relationship between Tyk2 and BAT. Previous studies by Larner and his team discovered that Tyk2 helps suppress the growth and metastasis of breast cancer. This current study suggests this same enzyme could help protect against and even reverse obesity.

The researchers were able to reverse obesity in mice that do not express Tyk2 by expressing a protein known as signal transducer and activator of transcription-3 (Stat3). Stat3 mediates the expression of a variety of genes that regulate a host of cellular processes. The researchers found that Stat3 formed a complex with a protein known as PR domain containing 16 (PRDM16) to restore the development of BAT and decrease obesity.

"We have made some very interesting observations in this study, but there are many questions left unanswered," said Larner. "We plan to further investigate the actions of Tyk2 and Stat3 in order to better understand the mechanisms involved in the development of brown adipose tissue. We're hopeful this research will help lead to new targets to treat a variety of obesity-related diseases such as cancer, cardiovascular disease and diabetes."

Larner collaborated on this study with Marta Derecka, Magdalena Morgan, Vidisha Raje, Jennifer Sisler and Quifang Zhang, all from the Department of Biochemistry and Molecular Biology at VCU School of Medicine; Dr Tomasz Kordula, Cancer Cell Signaling program member at VCU Massey; Agnieszka Gornicka, Cleveland Clinic Foundation; Dr Sergei B. Koralov, New York University Medical School; Dr Dennis Otero, University of California; Dr Joanna Cichy, Jagiellonian University in Krakow, Poland; Dr Klaus Rajewsky, Harvard Medical School; Dr Kazuya Shimoda, Miyazaki University Japan; Dr Valeria Poli, University of Turin in Torino, Italy; Dr Brigit Strobl, University of Veterinary Medicine in Vienna, Austria; Dr Sandra Pellegrini, Institut Pasteur in Paris, France; Drs Thurl E Harris and Susanna R Keller, University of Virginia School of Medicine; Dr Patrick Seale, University of Pennsylvania School of Medicine; Dr Aaron P Russell, Deakin University in Burwood, Australia; Dr Andrew J McAinch, Victoria University St Albans, Australia; Dr Paul E O'Brien, M Monash University Melbourne, Australia; and Dr Colleen M Croniger, Case Western University School of Medicine.

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