Downstream mechanisms of nitric oxide-mediated skeletal muscle glucose uptake during contraction.

In oher blogs, I discuss this pathway alot in reference to a number of conditions in environmental illness. In addition, I also mention how specific toxicants may "knock-out" this pathway and therefore provides clues into understanding chemical sensitivity and certain exposures. Unfortunately, it also provides evidence that some therapies that are advocated and out there in the mainstream may be counterproductive depending on the symptoms experienced. Of course, this is up to therapy doctors to determine.

"NOS-derived oxidants regulate skeletal muscle glucose uptake during ex vivo contractions via a cGMP/PKG-, AMPK-, and p38 MAPK-independent pathway. In addition, it appears that NO and ROS may regulate skeletal muscle glucose uptake during contraction through a similar pathway."



Merry, T. L., Lynch, G. S. & McConell, G. K. Downstream mechanisms of nitric oxide-mediated skeletal muscle glucose uptake during contraction. American Journal of Physiology - Regulatory, Integrative and Comparative Physiology 299, R1656-R1665 (2010). URL http://dx.doi.org/10.1152/ajpregu.00433.2010.

AMPK agonist downregulates innate and adaptive immune responses in TNBS-induced murine acute and relapsing colitis.

"AICAR-initiated AMPK activation may act as a central downregulator in ongoing innate and adaptive immune responses of murine colitis, providing a novel therapeutic approach in the treatment of IBD."

Read more: CiteULike: AMPK agonist downregulates innate and adaptive immune responses in TNBS-induced murine acute and relapsing colitis.:

For further reading: AMPK

Interdependence of AMPK and SIRT1 for Metabolic Adaptation to Fasting and Exercise in Skeletal Muscle.

"Here we demonstrate that AMPK acts as the prime initial sensor that translates this information into SIRT1-dependent deacetylation of the transcriptional regulators PGC-1alpha and FOXO1, culminating in the transcriptional modulation of mitochondrial and lipid utilization genes. Deficient AMPK activity compromises SIRT1-dependent responses to exercise and fasting, resulting in impaired PGC-1alpha deacetylation and blunted induction of mitochondrial gene expression."

Interdependence of AMPK and SIRT1 for Metabolic Adaptation to Fasting and Exercise in Skeletal Muscle.

Protein shown to be natural inhibitor of aging in fruit fly model

Protein shown to be natural inhibitor of aging in fruit fly model: "Sestrins are highly conserved small proteins that are produced in high amounts when cells experience stress. Sestrin function, however, remained puzzling until the Karin group found that these proteins function as activators of AMP-dependent protein kinase (AMPK), and inhibitors of the Target of Rapamycin (TOR). AMPK and TOR are two protein kinases that serve as key components of a signaling pathway shown to be the central regulator of aging and metabolism in a variety of model organisms, including the worm Caenorhabditis elegans, the fruit fly Drosophila melanogaster and mammals."

Note:

• Incidentally, AMPK is an important mediator of GSK-3b which is implicated in a number of mood disorders as well as, provides a mechanim for the shut-off of the antioxidant system. Because the antioxidant system, Nrf2 and it associated proteins, are important for a number of processes of cellular homeostasis, the regulation of AMPK is a very crucial step in maintaining resistance to cell stress.
• EGCG has been demonstrated to activate this same pathway. (Huang)

For further reading:

• HEIRS Research Blog Tag: AMPK ,
• HEIRS Library Tag:  Rapamycin, GSK-3b,

Huang, C.-H., Tsai, S.-J., Wang, Y.-J., Pan, M.-H., Kao, J.-Y., and Way, T.-D. (2009). Egcg inhibits protein synthesis, lipogenesis, and cell cycle progression through activation of ampk in p53 positive and negative human hepatoma cells. Molecular Nutrition & Food Research, 9999(9999):NA+. http://www.citeulike.org/user/HEIRS/article/5402238

AMPK-mediated GSK3beta inhibition by isoliquiritigenin contributes to protecting mitochondria against iron-catalyzed oxidative stress.

AMPK-mediated GSK3beta inhibition by isoliquiritigenin contributes to protecting mitochondria against iron-catalyzed oxidative stress.: "URL: AMPK-mediated GSK3beta inhibition by isoliquiritigenin contributes to protecting mitochondria against iron-catalyzed oxidative stress.

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AMPK-mediated GSK3beta inhibition by SIRT activator contributes to protecting mitochondria against iron-catalyzed oxidative stress

Choi, S. H. H., Kim, Y. W. W., and Kim, S. G. G. (2009). Ampk-mediated gsk3beta inhibition by isoliquiritigenin contributes to protecting mitochondria against iron-catalyzed oxidative stress. Biochemical pharmacology. http://www.citeulike.org/user/HEIRS/article/6436818

Caffeine Activates AMPK and Increases Glucose Transport in Skeletal Muscle

Title: Caffeine acutely activates 5′adenosine monophosphate–activated protein kinase and increases insulin-independent glucose transport in rat skeletal muscles.

 

Summary: These results suggest that caffeine has similar actions to exercise by acutely stimulating skeletal muscle AMPK activity and insulin-independent glucose transport with a reduction of the intracellular energy status.

 

Agawaa, T., Hamadab, T., Kamedac, N., Karaikea, K., Maa, X., Masudaa, S., Iwanakaa, N., and Hayash, T. (2009). Caffeine acutely activates 5′adenosine monophosphate–activated protein kinase and increases insulin-independent glucose transport in rat skeletal muscles. Metabolism Clinical and Experimental, 58(11):1609-1617. http://www.citeulike.org/user/HEIRS/article/5989180

 

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Adiponectin directly improves endothelial dysfunction in obese rats through the AMPK–eNOS Pathway

Adiponectin directly improves endothelial dysfunction in obese rats through the AMPK–eNOS Pathway