Metabolic Syndrome: Adenosine Monophosphate‐activated Protein Kinase and Malonyl Coenzyme A
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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).”
From Hypoglycemic effects of brassinosteroid in diet-induced obese mice (2012) · cites this paper as [31]
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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
- hybrid
- doi.org
- 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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