Carnitine palmitoyltransferase 1 increases lipolysis, UCP1 protein expression and mitochondrial activity in brown adipocytes

The discovery of active brown adipose tissue (BAT) in adult humans and the fact that it is reduced in obese and diabetic patients have put a spotlight on this tissue as a key player in obesity-induced metabolic disorders. BAT regulates energy expenditure through thermogenesis; therefore, harnessing...

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Bibliographic Details
Published in:PloS one 2016-07
Main Authors: Calderón Domínguez, María, Sebastián Muñoz, David, Fucho Salvador, Raquel, Weber Blattes, Minéia, Mir Bonnín, Joan Francesc, García-Casarrubios, Ester, Obregón, Maria Jesús, Zorzano Olarte, Antonio, Valverde, Ángela M, Serra i Cucurull, Dolors, Herrero Rodríguez, Laura
Format: Article
Language:English
Subjects:
Adipose tissues
Carnitina palmitoïl-transferasa 1
Carnitine palmitoyltransferase I
Obesitat
Obesity
Teixit adipós
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Summary:The discovery of active brown adipose tissue (BAT) in adult humans and the fact that it is reduced in obese and diabetic patients have put a spotlight on this tissue as a key player in obesity-induced metabolic disorders. BAT regulates energy expenditure through thermogenesis; therefore, harnessing its thermogenic fat-burning power is an attractive therapeutic approach. We aimed to enhance BAT thermogenesis by increasing its fatty acid oxidation (FAO) rate. Thus, we expressed carnitine palmitoyltransferase 1AM (CPT1AM), a permanently active mutant form of CPT1A (the rate-limiting enzyme in FAO), in a rat brown adipocyte (rBA) cell line through adenoviral infection. We found that CPT1AM-expressing rBA have increased FAO, lipolysis, UCP1 protein levels and mitochondrial activity. Additionally, enhanced FAO reduced the palmitate-induced increase in triglyceride content and the expression of obese and inflammatory markers. Thus, CPT1AM-expressing rBA had enhanced fat-burning capacity and improved lipid-induced derangements. This indicates that CPT1AM-mediated increase in brown adipocytes FAO may be a new approach to the treatment of obesity-induced disorders.
ISSN:1932-6203
1932-6203