Page 70 - ebook
P. 70

[A. Biochemistry/Molecular Biology] A-35



              PEX13 is required for thermogenesis of white adipose tissue


                                            in cold-exposed mice




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                           Woo Yong Park¹ , Gahee Song¹ , Ja Yeon Park¹ , Jea-Young Um¹,²*
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             ¹Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul 2447, Korea,
               ²Department of Pharmacology, College of Korean Medicine, Kyung Hee University, Seoul 2447, Korea




        Non-shivering thermogenesis (NST) is a heat generating process controlled by the mitochondria of brown adipose

        tissue (BAT). In the recent decade, ‘functionally’ acting brown adipocytes in white adipose tissue (WAT) have been
        identified as well: the so-called process of the ‘browning’ of WAT. While the importance of uncoupling protein 1

        (UCP1)-oriented mitochondrial activation has been intensely studied, the role of peroxisomes during the browning
        of  white  adipocytes  is  poorly  understood.  Here,  we  assess  the  change  in  peroxisomal  membrane  proteins,  or

        peroxins (PEXs), during cold stimulation and importantly, the role of PEX13 in the cold-exposed remodeling of white
        adipocytes. PEX13, a protein that originally functions as a docking factor and is involved in protein import into

        peroxisome matrix, was highly increased during cold-induced recruitment of beige adipocytes within the inguinal
        WAT of C57BL/6  mice. Moreover, beige-induced 3T3-L1 adipocytes  and stromal  vascular  fraction (SVF) cells by

        exposure to the peroxisome proliferator-activated  receptor  gamma  (PPARγ)  agonist  rosiglitazone  showed  a
        significant increase in mitochondrial thermogenic factors along with peroxisomal proteins including PEX13, and

        these were confirmed in SVF cells with the beta 3 adrenergic receptor (β3AR)-selective agonist CL316,243. To verify
        the relevance of PEX13, we used the RNA silencing method targeting the Pex13.
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