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STK25 regulates oxidative capacity and metabolic efficiency in adipose tissue

Journal article
Authors Silva Sütt
Emmelie Cansby
A. Paul
M. Amrutkar
Esther Nuñez Durán
Nagaraj M. Kulkarni
M. Ståhlman
J. Borén
J. Laurencikiene
B. W. Howell
Sven Enerbäck
Margit Mahlapuu
Published in Journal of Endocrinology
Volume 238
Issue 3
Pages 187-202
Publication year 2018
Published at Institute of Biomedicine, Department of Medical and Clinical Genetics
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 187-202
Language en
Keywords Brown adipose tissue, Lipid metabolism, Oxidative stress, White adipose tissue
Subject categories Endocrinology and Diabetes


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. © 2018 Society for Endocrinology.

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