Potentiation of insulin-stimulated glucose transport by the AMP-activated protein kinase
Open accessAbstract
Data from the use of activators and inhibitors of the AMP-activated protein kinase (AMPK) suggest that AMPK increases sensitivity of glucose transport to stimulation by insulin in muscle cells. We assayed insulin action after adenoviral (Ad) transduction of constitutively active (CA; a truncated form of AMPKα 1) and dominant-negative (DN; which depletes endogenous AMPKα) forms of AMPKα (Ad-AMPKα-CA and Ad-AMPKα-DN, respectively) into C 2 C 12 myotubes. Compared with control (Ad-green fluorescent protein), Ad-AMPK-CA increased the ability of insulin to stimulate glucose transport. The increased insulin action in cells expressing AMPK-CA was suppressed by compound C (an AMPK inhibitor). Exposure of cells to 5-aminoimidazole-4-carboxamide-1β-d-ribofuranoside (an AMPK activator) increased insulin action in uninfected myotubes and myotubes transduced with green fluorescent protein but not in Ad-AMPK-DN-infected myotubes. In Ad-AMPK-CA-transduced cells, serine phosphorylation of insulin receptor substrate 1 was decreased at a mammalian target of rapamycin (or p70 S6 kinase) target site that has been reported to be associated with insulin resistance. These data suggest that, in myotubes, activated AMPKα 1 is sufficient to increase insulin action and that the presence of functional AMPKα is required for 5-aminoimidazole-4-carboxamide-1β,d-ribofuranoside-related increases in insulin action.
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Incubation with AICAR in C2C12 myotubes transfected with constitutively active or KD AMPKα revealed that serine phosphorylation of IRS1 was decreased at a target site of mTOR/p70 S6K.
“Similarly, incubation with AICAR in C2C12 myotubes transfected with an adenovirus of a constitutively active (truncated form of AMPKα1) or KD form of AMPKα revealed that serine phosphorylation of IRS1 was decreased at a target site of mTOR/p70 S6K, which has been associated with insulin resistance [158].”
From AMPK and Exercise: Glucose Uptake and Insulin Sensitivity (2013) · cites this paper as [158]
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References 44 · Cited by 47
- Authors
- Ju, J.-S., Gitcho, M. A., Casmaer, C. A., Patil, P. B., Han, D.-G., Spencer, S. A., & Fisher, J. S.
- Affiliations
- Saint Louis University (US)
- Venue
- American Journal of Physiology-Cell Physiology
- Publisher
- American Physiological Society
- Published
- 2007-01
- Volume
- 292
- Issue
- 1
- Pages
- C564-C572
- ISSN
- 0363-6143 (ISSN-L)
- 1522-1563
- PMC
- PMC1868576
- OpenAlex
- W2107627105
- Cited by
- 47
- References
- 44
- Citations by year
- 2026: 1 · 2020: 5 · 2019: 1 · 2018: 1 · 2016: 1 · 2015: 1 · 2014: 5 · 2013: 3 · 2012: 5
- FWCI
- 2.18
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Physiology-Cell Physiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- University of Pennsylvania
- National Institute of Diabetes and Digestive and Kidney Diseases (K01DK066330)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Natural Antidiabetic Agents Studies
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- AMPK, insulin-stimulated glucose transport, insulin sensitivity, muscle cells, C2C12 myotubes, AMPKα1, compound C, IRS-1, serine phosphorylation, mTOR, p70 S6 kinase, insulin resistance, adenoviral transduction
- MeSH terms
- Aminoimidazole Carboxamide, Animals, Biological Transport, Cells, Cultured, Drug Synergism, Genes, Dominant, Glucose, Hypoglycemic Agents, Insulin, Isoenzymes, Multienzyme Complexes, Phosphoproteins, Phosphorylation, Protein Kinases, Ribonucleotides, Signal Transduction, Protein Serine-Threonine Kinases, Muscle Fibers, Skeletal, Enzyme Activators, Luminescent Agents, Green Fluorescent Proteins, Mice, AMP-Activated Protein Kinases, Insulin Receptor Substrate Proteins, TOR Serine-Threonine Kinases
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