Journal
JOURNAL OF ENDOCRINOLOGY
Volume 238, Issue 3, Pages 187-202Publisher
BIOSCIENTIFICA LTD
DOI: 10.1530/JOE-18-0182
Keywords
brown adipose tissue; white adipose tissue; lipid metabolism; oxidative stress
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Funding
- Swedish Research Council
- Novo Nordisk Foundation
- Swedish Heart and Lung Foundation
- Diabetes Wellness Network Sweden
- Estonian Research Council
- Swedish Diabetes Foundation
- Royal Society of Arts and Sciences in Gothenburg
- Wiberg Foundation
- Adlerbert Research Foundation
- I. Hultman Foundation
- S. and E. Goljes Foundation
- West Sweden ALF Program
- F. Neubergh Foundation
- I.-B. and A. Lundbergs Research Foundation
- Swedish Innovation Agency Vinnova
- Torsten Soderbergs Foundation
- European Foundation for the Study of Diabetes/Lilly European Diabetes Research Programme
- L. och J. Gronbergs Foundation
- European Foundation for the Study of Diabetes and Novo Nordisk Partnership for Diabetes Research in Europe
- European Union [607842]
- Prof. Nanna Svartz Foundation
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Whole-body energy homeostasis at over-nutrition critically depends on how well adipose tissue remodels in response to excess calories. We recently identified serine/threonine protein kinase (STK) 25 as a critical regulator of ectopic lipid storage in non-adipose tissue and systemic insulin resistance in the context of nutritional stress. Here, we investigated the role of STK25 in regulation of adipose tissue dysfunction in mice challenged with a high-fat diet. We found that overexpression of STK25 in high-fat-fed mice resulted in impaired mitochondrial function and aggravated hypertrophy, inflammatory infiltration and fibrosis in adipose depots. Reciprocally, Stk25-knockout mice displayed improved mitochondrial function and were protected against diet-induced excessive fat storage, meta-inflammation and fibrosis in brown and white adipose tissues. Furthermore, in rodent HIB-1B cell line, STK25 depletion resulted in enhanced mitochondrial activity and consequently, reduced lipid droplet size, demonstrating an autonomous action for STK25 within adipocytes. In summary, we provide the first evidence for a key function of STK25 in controlling the metabolic balance of lipid utilization vs lipid storage in brown and white adipose depots, suggesting that repression of STK25 activity offers a potential strategy for establishing healthier adipose tissue in the context of chronic exposure to dietary lipids.
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