NDLI: Enhanced muscle fat oxidation and glucose transport by ACRP30 globular domain: Acetyl–CoA carboxylase inhibition and AMP-activated protein kinase activation

Content Provider	PubMed Central
Author	Tomas, Eva Tsao, Tsu-shuen Saha, Asish K. Murrey, Heather E. Zhang, Cheng Cheng Itani, Samar I. Lodish, Harvey F. Ruderman, Neil B.
Copyright Year	2002
Abstract	gACRP30, the globular subunit of adipocyte complement-related protein of 30 kDa (ACRP30), improves insulin sensitivity and increases fatty acid oxidation. The mechanism by which gACRP30 exerts these effects is unknown. Here, we examined if gACRP30 activates AMP-activated protein kinase (AMPK), an enzyme that has been shown to increase muscle fatty acid oxidation and insulin sensitivity. Incubation of rat extensor digitorum longus (EDL), a predominantly fast twitch muscle, with gACRP30 (2.5 μg/ml) for 30 min led to 2-fold increases in AMPK activity and phosphorylation of both AMPK on Thr-172 and acetyl CoA carboxylase (ACC) on Ser-79. Accordingly, concentration of malonyl CoA was diminished by 30%. In addition, gACRP30 caused a 1.5-fold increase in 2-deoxyglucose uptake. Similar changes in malonyl CoA and ACC were observed in soleus muscle incubated with gACRP30 (2.5 μg/ml), although no significant changes in AMPK activity or 2-deoxyglucose uptake were detected. When EDL was incubated with full-length hexameric ACRP30 (10 μg/ml), AMPK activity and ACC phosphorylation were not altered. Administration of gACRP30 (75 μg) to C57 BL/6J mice in vivo led to increased AMPK activity and ACC phosphorylation and decreased malonyl CoA concentration in gastrocnemius muscle within 15–30 min. Both in vivo and in vitro, activation of AMPK was the first effect of gACRP30 and was transient, whereas alterations in malonyl CoA and ACC occurred later and were more sustained. Thus, gACRP30 most likely exerts its actions on muscle fatty acid oxidation by inactivating ACC via activation of AMPK and perhaps other signal transduction proteins.
Related Links	http://dx.doi.org/10.1073/pnas.222657499
Ending Page	16313
Page Count	5
Starting Page	16309
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	25
Volume Number	99
Language	English
Publisher	National Academy of Sciences
Publisher Date	2002-12-10
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Enhanced muscle fat oxidation and glucose transport by ACRP30 globular domain: acetyl-CoA carboxylase inhibition and AMP-activated protein kinase activation.

CTRP1 Protein Enhances Fatty Acid Oxidation via AMP-activated Protein Kinase (AMPK) Activation and Acetyl-CoA Carboxylase (ACC) Inhibition

Insulin activation of acetyl-CoA carboxylase accompanied by inhibition of the 5'-AMP-activated protein kinase.

CTRP1 Protein Enhances Fatty Acid Oxidation via AMP-activated Protein Kinase (AMPK) Activation and Acetyl-CoA Carboxylase (ACC) Inhibition*

AMP-activated protein kinase control of fat metabolism in skeletal muscle.

Glucose Autoregulates Its Uptake in Skeletal Muscle: Involvement of AMP-Activated Protein Kinase

AMP-Activated Protein Kinase Activation by Adrenoceptors in L6 Skeletal Muscle Cells: Mediation by α1-Adrenoceptors Causing Glucose Uptake

Continuous fat oxidation in acetyl-CoA carboxylase 2 knockout mice increases total energy expenditure, reduces fat mass, and improves insulin sensitivity.

Leptin Activates Cardiac Fatty Acid Oxidation Independent of Changes in the AMP-activated Protein Kinase-Acetyl-CoA Carboxylase-Malonyl-CoA Axis

Enhanced muscle fat oxidation and glucose transport by ACRP30 globular domain: Acetyl–CoA carboxylase inhibition and AMP-activated protein kinase activation

Similar Documents

Enhanced muscle fat oxidation and glucose transport by ACRP30 globular domain: acetyl-CoA carboxylase inhibition and AMP-activated protein kinase activation.

CTRP1 Protein Enhances Fatty Acid Oxidation via AMP-activated Protein Kinase (AMPK) Activation and Acetyl-CoA Carboxylase (ACC) Inhibition

Insulin activation of acetyl-CoA carboxylase accompanied by inhibition of the 5'-AMP-activated protein kinase.

CTRP1 Protein Enhances Fatty Acid Oxidation via AMP-activated Protein Kinase (AMPK) Activation and Acetyl-CoA Carboxylase (ACC) Inhibition*

AMP-activated protein kinase control of fat metabolism in skeletal muscle.

Glucose Autoregulates Its Uptake in Skeletal Muscle: Involvement of AMP-Activated Protein Kinase

AMP-Activated Protein Kinase Activation by Adrenoceptors in L6 Skeletal Muscle Cells: Mediation by α1-Adrenoceptors Causing Glucose Uptake

Continuous fat oxidation in acetyl-CoA carboxylase 2 knockout mice increases total energy expenditure, reduces fat mass, and improves insulin sensitivity.

Leptin Activates Cardiac Fatty Acid Oxidation Independent of Changes in the AMP-activated Protein Kinase-Acetyl-CoA Carboxylase-Malonyl-CoA Axis

Enhanced muscle fat oxidation and glucose transport by ACRP30 globular domain: Acetyl–CoA carboxylase inhibition and AMP-activated protein kinase activation