Cited by 62Metabolism, Diabetes, and CancerPeroxisome Proliferator-Activated ReceptorsAdipose Tissue and Metabolism

Metabolic Syndrome: Adenosine Monophosphate‐activated Protein Kinase and Malonyl Coenzyme A

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Ruderman, Neil B., Saha, Asish K.·2006·Obesity

Abstract

The metabolic syndrome can be defined as a state of metabolic dysregulation characterized by insulin resistance, central obesity, and a predisposition to type 2 diabetes, dyslipidemia, premature atherosclerosis, and other diseases. An increasing body of evidence has linked the metabolic syndrome to abnormalities in lipid metabolism that ultimately lead to cellular dysfunction. We review here the hypothesis that, in many instances, the cause of these lipid abnormalities could be a dysregulation of the adenosine monophosphate‐activated protein kinase (AMPK)/malonyl coenzyme A (CoA) fuel‐sensing and signaling mechanism. Such dysregulation could be reflected by isolated increases in malonyl CoA or by concurrent changes in malonyl CoA and AMPK, both of which would alter intracellular fatty acid partitioning. The possibility is also raised that pharmacological agents and other factors that activate AMPK and/or decrease malonyl CoA could be therapeutic targets.

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  • Activation of AMPK improves insulin sensitivity by stimulating glucose uptake and lowering blood glucose, whereas AMPK activity is suppressed in disorders associated with insulin resistance.

    “The activation of AMPK improves insulin sensitivity by stimulating glucose uptake and lowering blood glucose, whereas the activity of AMPK is suppressed in disorders associated with insulin resistance (31).”

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Research works printed but not linked: 4

  1. Ruderman NB. The metabolic syndrome. In: DeGroot LJ, Jameson JL, eds. Endocrinology, 5th edition. Philadelphia, PA: Elsevier; 2006, pp. 1149 -66.
  2. Kraegen EW, Saha AK, Preston E, Wilks D, Cooney GJ, Ruderman NB. Insulin resistance induced by glucose infu- sion is associated temporally with reduced muscle and liver AMPK activity. Am J Physiol. 2006 (in press).
  3. AMPK and Malonyl CoA, Ruderman and Saha 32S OBESITY Vol. 14 Supplement February 2006
  4. 1930739x, 2006, S2, Downloaded from https://onlinelibrary.wiley.com/doi/10.1038/oby.2006.279, Wiley Online Library on [26/06/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License

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Authors
Ruderman, N. B., & Saha, A. K.
Affiliations
Boston University (US)
Corresponding author
Ruderman, Neil B.
Venue
Obesity
Publisher
Wiley
Published
2006-02
Volume
14
Issue
S2
Pages
25S-33S
ISSN
  • 1930-7381 (ISSN-L)
  • 1930-739X
OpenAlex
W1970528355
Cited by
62
References
71
Citations by year
2025: 1 · 2023: 2 · 2022: 3 · 2021: 1 · 2018: 2 · 2017: 4 · 2016: 2 · 2015: 2 · 2014: 2 · 2013: 3 · 2012: 13
FWCI
0.42
Type
journal article
Language
en
Open access
Locations
  • Obesity (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • American Diabetes Association
  • National Institutes of Health (5r01dk019514-35)
  • U.S. Public Health Service
  • National Heart, Lung, and Blood Institute (P01-HL 08758-01)
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK 19417, DK-19514)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
Keywords
metabolic syndrome, AMPK, lipid metabolism, insulin resistance, type 2 diabetes, dyslipidemia, abdominal obesity, fatty acid partitioning, AMPK activators, therapeutic target
MeSH terms
Animals, Energy Metabolism, Humans, Insulin Resistance, Malonyl Coenzyme A, Multienzyme Complexes, Signal Transduction, Protein Serine-Threonine Kinases, Metabolic Syndrome, Lipid Metabolism, AMP-Activated Protein Kinases

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