PDK4 Augments ER–Mitochondria Contact to Dampen Skeletal Muscle Insulin Signaling During Obesity-Reference-Cited by-同舟云学术

PDK4 Augments ER–Mitochondria Contact to Dampen Skeletal Muscle Insulin Signaling During Obesity

Published:2018-12-06 Issue:3 Volume:68 Page:571-586
ISSN:0012-1797
Container-title:Diabetes
language:en
Short-container-title:Diabetes

Author:

Thoudam Themis,Ha Chae-Myeong,Leem Jaechan,Chanda Dipanjan,Park Jong-Seok,Kim Hyo-Jeong,Jeon Jae-Han,Choi Yeon-Kyung,Liangpunsakul Suthat,Huh Yang Hoon,Kwon Tae-Hwan,Park Keun-Gyu^ORCID,Harris Robert A.,Park Kyu-Sang,Rhee Hyun-Woo,Lee In-Kyu^ORCID

Funder

Ministry of Science, ICT and Future Planning

Ministry of Health & Welfare

Korea Basic Science Institute

VA Merit Award

National Institutes of Health

U.S. Department of Defense

Publisher

American Diabetes Association

Subject

Endocrinology, Diabetes and Metabolism,Internal Medicine

Reference50 articles.

1. Calcium Homeostasis and Organelle Function in the Pathogenesis of Obesity and Diabetes

2. Chaperone-mediated coupling of endoplasmic reticulum and mitochondrial Ca2+ channels

3. Mitochondria-Associated Endoplasmic Reticulum Membrane (MAM) Integrity Is Required for Insulin Signaling and Is Implicated in Hepatic Insulin Resistance

4. Chronic enrichment of hepatic endoplasmic reticulum–mitochondria contact leads to mitochondrial dysfunction in obesity

5. Disruption of calcium transfer from ER to mitochondria links alterations of mitochondria-associated ER membrane integrity to hepatic insulin resistance

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