AMPK Activation Impaired in CFS.


AMPK, what? o_O

AMP Kinase is an enzyme that is responsible, basically, for maintaining cellular homeostasis. And those of us with MECFS have abnormalities in this area as determined by this recent study.

Post exertional muscle fatigue is a key feature in Chronic Fatigue Syndrome (CFS). Abnormalities of skeletal muscle function have been identified in some but not all patients with CFS. To try to limit potential confounders that might contribute to this clinical heterogeneity, we developed a novel in vitro system that allows comparison of AMP kinase (AMPK) activation and metabolic responses to exercise in cultured skeletal muscle cells from CFS patients and control subjects.

There are things that can be done to help activate AMPK though. Metformin is an example of a prescription drug that can help to activate AMPK. Life Extension makes a supplement that purports to do the same thing without a prescription using gynostemma and rose hips. Other natural products may increase the level of AMPK as well, such as resveratrol, quercetin, fruits and veggies, ginseng, turmeric/curcumin, berberine and green and black tea.
AMPK Promotes Longevity And Reduces Fat Storage
  • The science of bioenergetics is producing paradigm-shifting discoveries, including the role of AMPK in regulating the ways our bodies use and transform energy.
  • AMPK is the “switch” that is the link between metabolic disease, inflammation, and longevity. This “switch” tells our cells when to store and generate energy-containing molecules such as fat, and when to “hunker down” and use existing energy stores.
  • When switched “on,” AMPK triggers the use of stored energy from fats, enhances removal of fats and sugar from the blood, increases production of mitochondria, and reduces inflammation and cellular “junk.”
  • Calorie restriction and vigorous exercise activate AMPK, shrinking body fat stores (especially in the belly region), lowering blood sugar and lipid levels, and producing other beneficial effects that retard the aging process.
  • The drug metformin also activates AMPK, with similar body-wide results.
  • A pair of natural botanical extracts have now been found to activate AMPK, reducing belly fat, cholesterol, blood sugar, and insulin levels.
  • Instead of combating longevity threats using multiple drugs, supplementation with AMPK-activating botanicals can address these problems at its source.
  • Age-induced risk factors can be tackled efficiently by boosting AMPK activity with Gynostemma pentaphyllum and trans-tiliroside from rose hips.


And guess what else activates AMPK? Nicotine!!

Guess the weight gain in former smokers isn't all down to a lack of willpower and a propensity for lollypops after all. I've said it before and I'll say it again...if Big Pharma had been able to patent nicotine, we'd all be puffing away. Nicotine really is a miracle drug.

J Biol Chem. 2007 Sep 14;282(37):26793-801. Epub 2007 Jul 16.
Nicotine-induced activation of AMP-activated protein kinase inhibits fatty acid synthase in 3T3L1 adipocytes: a role for oxidant stress.

An Z1, Wang H, Song P, Zhang M, Geng X, Zou MH.
Recent studies suggest that the AMP-activated protein kinase (AMPK) acts as a major energy sensor and regulator in adipose tissues. The objective of this study was to investigate the role of AMPK in nicotine-induced lipogenesis and lipolysis in 3T3L1 adipocytes. Exposure of 3T3L1 adipocytes to smoking-related concentrations of nicotine increased lipolysis and inhibited fatty acid synthase (FAS) activity in a time- and dose-dependent manner. The effects of nicotine on FAS activity were accompanied by phosphorylation of both AMPK (Thr(172)) and acetyl-CoA carboxylase (ACC; Ser(79)). Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation. Inhibition of AMPK using either pharmacologic (insulin, compound C) or genetic means (overexpression of dominant negative AMPK; AMPK-DN) abolished FAS inhibition induced by nicotine or ONOO(-). Conversely, activation of AMPK by pharmacologic (nicotine, ONOO(-), metformin, and AICAR) or genetic (overexpression of constitutively active AMPK) means inhibited FAS activity. Notably, AMPK activation increased threonine phosphorylation of FAS, and this effect was blocked by adenovirus encoding dominant negative AMPK. Finally, AMPK-dependent FAS phosphorylation was confirmed by (32)P incorporation into FAS in adipocytes. Taken together, our results strongly suggest that nicotine, via ONOO(-) activates AMPK, resulting in enhanced threonine phosphorylation and consequent inhibition of FAS.

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