Pivotal Role of O-GlcNAc Modification in Cold-Induced Thermogenesis by Brown Adipose Tissue Through Mitochondrial Biogenesis
- Authors
- Ohashi, Natsuko; Morino, Katsutaro; Ida, Shogo; Sekine, Osamu; Lemecha, Mengistu; Kume, Shinji; Park, Shi-Young; Choi, Cheol Soo; Ugi, Satoshi; Maegawa, Hiroshi
- Issue Date
- 1-Sep-2017
- Publisher
- AMER DIABETES ASSOC
- Citation
- DIABETES, v.66, no.9, pp.2351 - 2362
- Journal Title
- DIABETES
- Volume
- 66
- Number
- 9
- Start Page
- 2351
- End Page
- 2362
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/5720
- DOI
- 10.2337/db16-1427
- ISSN
- 0012-1797
- Abstract
- Adipose tissues considerably influence metabolic homeostasis, and both white (WAT) and brown (BAT) adipose tissue play significant roles in lipid and glucose metabolism. O-linked N-acetylglucosamine (O-GlcNAc) modification is characterized by the addition of N-acetylglucosamine to various proteins by O-GlcNAc transferase (Ogt), subsequently modulating various cellular processes. However, little is known about the role of O-GlcNAc modification in adipose tissues. Here, we report the critical role of O-GlcNAc modification in cold-induced thermogenesis. Deletion of Ogt in WAT and BAT using adiponectin promoterdriven Cre recombinase resulted in severe cold intolerance with decreased uncoupling protein 1 (Ucp1) expression. Furthermore, Ogt deletion led to decreased mitochondrial protein expression in conjunction with decreased peroxisome proliferator-activated receptor gamma coactivator 1-alpha protein expression. This phenotype was further confirmed by deletion of Ogt in BAT using Ucp1 promoter-driven Cre recombinase, suggesting that O-GlcNAc modification in BAT is responsible for cold-induced thermogenesis. Hypothermia was significant under fasting conditions. This effect was mitigated after normal diet consumption but not after consumption of a fatty acid-rich ketogenic diet lacking carbohydrates, suggesting impaired diet-induced thermogenesis, particularly by fat. In conclusion, O-GlcNAc modification is essential for cold-induced thermogenesis and mitochondrial biogenesis in BAT. Glucose flux into BAT may be a signal to maintain BAT physiological responses.
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