Page 39 - N. Metabolism and metabolic diseases

MKRN1 deficiency attenuates metabolic syndrome via AMPK stabilization and activation

Seungyeon Kim, Jaewhan Song
Department of Biochemistry, College of Life science and Biotechnology,
Yonsei University, Seoul, Korea
ABSTRACT
The 5' adenosine monophosphate-activated protein kinase (AMPK) is an essential cellular energy sensing enzyme, which
maintains ATP to restore energy homeostasis. The activation of AMPK is associated with various cellular metabolic processes,
including suppression of gluconeogenesis, lipogenesis, promotion of glucose consumption, and fatty acid oxidation. Therefore,
AMPK activation is significant to prevent and ameliorate metabolic disorders such as type II diabetes (T2D), non-alcoholic fatty
liver disease (NAFLD) and cardiovascular diseases. Although regulation of AMPK stability in energy metabolism is considerable,
an E3 ubiquitin ligase for AMPK that controls systemic metabolism is yet to be reported. Here, we investigated that makorin ring
finger protein 1 (MKRN1) acts as an E3 ubiquitin ligase for AMPK. MKRN1 deficiency reduced high-fat diet (HFD)- induced
obesity and reversed NAFLD by stabilizing and activating AMPK. Moreover, MKRN1 ablation altered lipid and glucose
metabolism in the liver and adipose tissues. Taken together, our findings suggest that MKRN1 may serve as a possible
therapeutic target for metabolic syndromes.
RESULTS

CONCLUSION REFERENCES ACKNOWLEDGEMENTS

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by stabilizing and activating AMPK. cherry0313@yonsei.ac.kr