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The Role of Tyk2 in Regulating Energy Expenditure and Preventing Obesity
Author(s) -
Raje Vidisha B,
Derecka Marta,
Gornicka Agnieszka,
Sczepanek Karol,
Sisler Jennifer,
Croniger Colleen M,
Larner Andrew
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.570.10
Subject(s) - thermogenesis , skeletal muscle , prdm16 , endocrinology , biology , medicine , brown adipose tissue , thermogenin , adipose tissue , microbiology and biotechnology
Brown adipose tissue(BAT) and skeletal muscle(SKM) are the two major tissues involved in energy expenditure, mediated by thermogenesis. We have observed that mice that do not express the JAK kinase‐ Tyk2 become spontaneously obese and exhibit the metabolic syndrome. Tyk2−/− mice show defects in BAT and SKM, which arise from the same lineage of Myf5+ progenitors of the mesenchymal lineage. Tyk2−/− mice exhibit decreased expression of BAT specific genes like UCP1 and PRDM16. The expression of SKM specific transcription factors is elevated in Tyk2−/− BAT. Tyk2−/− mice also have more muscle mass compared to the wild type controls. However, the skeletal muscle is functionally impaired as shown by decreased mitochondria respiration capacity, decreased expression of mRNAs involved in muscle contraction, exercise intolerence and a defect in maintaining the core‐body temperature upon cold exposure. Taken together, these findings suggest a novel role for Tyk2 kinase in regulation of energy expenditure and preventing the obese phenotype.