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식물 노화·수명 연구단
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Loss of the E3 ubiquitin ligase MKRN1 represses diet-induced metabolic syndrome through AMPK activation

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Title
Loss of the E3 ubiquitin ligase MKRN1 represses diet-induced metabolic syndrome through AMPK activation
Author(s)
Min-Sik Lee; Hyun-Ji Han; Su Yeon Han; Il Young Kim; Sehyun Chae; Choong-Sil Lee; Sung Eun Kim; Seul Gi Yoon; Jun-Won Park; Jung-Hoon Kim; Soyeon Shin; Manhyung Jeong; Aram Ko; Ho-Young Lee; Kyoung-Jin Oh; Yun-Hee Lee; Kwang-Hee Bae; Seung-Hoi Koo; Jea-woo Kim; Je Kyung Seong; Daehee Hwang; Jaewhan Song
Publication Date
2018-08
Journal
NATURE COMMUNICATIONS, v.9, no.1, pp.3404 -
Publisher
NATURE PUBLISHING GROUP
Abstract
AMP-activated protein kinase (AMPK) plays a key role in controlling energy metabolism in response to physiological and nutritional status. Although AMPK activation has been proposed as a promising molecular target for treating obesity and its related comorbidities, the use of pharmacological AMPK activators has been met with contradictory therapeutic challenges. Here we show a regulatory mechanism for AMPK through its ubiquitination and degradation by the E3 ubiquitin ligase makorin ring finger protein 1 (MKRN1). MKRN1 depletion promotes glucose consumption and suppresses lipid accumulation due to AMPK stabilisation and activation. Accordingly, MKRN1-null mice show chronic AMPK activation in both liver and adipose tissue, resulting in significant suppression of diet-induced metabolic syndrome. We demonstrate also its therapeutic effect by administering shRNA targeting MKRN1 into obese mice that reverses non-alcoholic fatty liver disease. We suggest that ubiquitin-dependent AMPK degradation represents a target therapeutic strategy for metabolic disorders.© The Author(s) 2018
URI
https://pr.ibs.re.kr/handle/8788114/5231
ISSN
2041-1723
Appears in Collections:
Center for Plant Aging Research (식물 노화·수명 연구단) > Journal Papers (저널논문)
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Nat Commun. 9, 3404.pdfDownload

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