Medizinische Universität Graz - Research portal
Selected Publication:
SHR Neuro Cancer Cardio Lipid Metab Microb
Schreiber, R; Diwoky, C; Schoiswohl, G; Feiler, U; Wongsiriroj, N; Abdellatif, M; Kolb, D; Hoeks, J; Kershaw, EE; Sedej, S; Schrauwen, P; Haemmerle, G; Zechner, R.
Cold-Induced Thermogenesis Depends on ATGL-Mediated Lipolysis in Cardiac Muscle, but Not Brown Adipose Tissue.
Cell Metab. 2017; 26(5):753-763
Doi: 10.1016/j.cmet.2017.09.004
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- Co-authors Med Uni Graz
- Abdellatif Mahmoud
- Kolb Dagmar
- Sedej Simon
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- Abstract:
- Fatty acids (FAs) activate and fuel UCP1-mediated non-shivering thermogenesis (NST) in brown adipose tissue (BAT). Release of FAs from intracellular fat stores by adipose triglyceride lipase (ATGL) is considered a key step in NST. Accordingly, the severe cold intolerance of global ATGL knockout (AKO) mice has been attributed to defective BAT lipolysis. Here we show that this conclusion is incorrect. We demonstrate that although the BAT-specific loss of ATGL impairs BAT lipolysis and alters BAT morphology, it does not compromise the β3-adrenergic thermogenic response or cold-induced NST. Instead, NST depends on nutrient supply or lipolysis in white adipose tissue during fasting, suggesting that circulating energy substrates are sufficient to fuel NST. Cold intolerance in AKO mice is not caused by BAT dysfunction as previously suspected but by severe cardiomyopathy. We conclude that functional NST requires adequate substrate supply and cardiac function, but does not depend on ATGL-mediated lipolysis in BAT. Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.
- Find related publications in this database (using NLM MeSH Indexing)
- Adipose Tissue, Brown - metabolism
- Adipose Tissue, White - metabolism
- Animals -
- Cold Temperature -
- Eating -
- Electrocardiography -
- Fasting -
- Lipase - genetics
- Lipase - physiology
- Lipolysis - physiology
- Mice -
- Mice, Inbred C57BL -
- Mice, Knockout -
- Myocardium - metabolism
- Thermogenesis - physiology
- Uncoupling Protein 1 - genetics
- Uncoupling Protein 1 - metabolism