AI Article Synopsis
- Brown adipose tissue (BAT) and brite/beige adipose tissue are key for nonshivering thermogenesis in mammals, primarily driven by mitochondrial uncoupling protein 1 (UCP1), which plays a crucial role in heat production.
- Recent studies on UCP1 suggest it operates through a fatty acid cycling model where it expels fatty acid anions while allowing protonated fatty acids to return, facilitating uncoupling and supporting heat generation.
- There is ongoing research into how modifications of UCP1, like sulfenylation, may enhance its activity and how mitochondrial pro-oxidant states relate to BAT development and thermogenesis, indicating potential future areas of study regarding UCP1's function.
Article Abstract
Brown adipose tissue (BAT) and brown in white (brite) adipose tissue, termed also beige adipose tissue, are major sites of mammalian nonshivering thermogenesis. Mitochondrial uncoupling protein 1 (UCP1), specific for these tissues, is the key factor for heat production. Recent molecular aspects of UCP1 structure provide support for the fatty acid cycling model of coupling, i.e. when UCP1 expels fatty acid anions in a uniport mode from the matrix, while uncoupling. Protonophoretic function is ensured by return of the protonated fatty acid to the matrix independent of UCP1. This mechanism is advantageous for mitochondrial uncoupling and compatible with heat production in a pro-thermogenic environment, such as BAT. It must still be verified whether posttranslational modification of UCP1, such as sulfenylation of Cys253, linked to redox activity, promotes UCP1 activity. BAT biogenesis and UCP1 expression, has also been linked to the pro-oxidant state of mitochondria, further endorsing a redox signalling link promoting an establishment of pro-thermogenic state. We discuss circumstances under which promotion of superoxide formation exceeds its attenuation by uncoupling in mitochondria and throughout point out areas of future research into UCP1 function.
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| http://dx.doi.org/10.1016/j.bbabio.2018.11.007 | DOI Listing |
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