While browsing PubMed for more AMPK articles, I found this short article published in August of 2007 about AMPK and it’s hypothalamic control of energy balance. Since I felt it worded some things well, and contributed to my understand of AMPK in the hypothalamus, I decided to pass on this information.

This article is short and easy to read, but I want to highlight some of the parts I considered to be key information in case you don’t want to flip to the article right now.

** AMP-activated protein kinase (AMPK) has emerged as a metabolic “fuel gauge,” which oscillates between anabolic and catabolic processes that ultimately influence energy balance.

** [T]he 5? AMP-activated protein kinase (AMPK) pathway has been identified as a key molecular signaling pathway in the coordinated control of energy balance. This is due in large part to the ability of the enzyme to link changes in the AMP/ATP ratio to coordinated cellular responses.

** Increases in AMPK activity contribute to fatty acid oxidation and increased glucose transport concomitant…Moreover, AMPK activation leads to decreased hepatic glucose production and lipid synthesis but increased lipid oxidation in the liver and decreased glucose-dependent insulin secretion in pancreatic islet ? cells

** [A] decrease in hypothalamic AMPK activity is sufficient to reduce food intake and weight gain, while constitutive AMPK activation leads to hyperphagia [abnormally increased appetite] and obesity

I found this a quick, but interesting read. In the refrences, I found a paper about hypothalamic energy singling and mTOR, and decided to add it into this post.

For those following CRON, mTOR deactivation is a good thing to happen. While this paper does not mention Calorie Restriction, it does cover mTOR and how it responds to nutrient availability.This paper’s main focus is on how mTOR activity in the hypothalamus affects food intake. However, while the information in this paper is interesting, it also has AMPK snippets of info in there in addition to all the hypothalamus talk, hence my interest.

** The ability of L-leucine to activate mTOR in the hypothalamus and to inhibit food intake may be an example of CNS circuits using an evolutionarily conserved signaling mechanism as a fuel sensor rather than as an amino acid sensor.

** Conceivably, the inhibition of mTOR signaling may block leptin’s anorectic effect by suppressing the hormone’s synaptic remodeling activity.

And, here we go for the final interesting bit that ties in AMPK and mTOR:
** Other fuel-sensitive kinases have been implicated in the hypothalamic control of energy balance. Like mTOR, AMP-activated protein kinase (AMPK) is regulated by intracellular AMP/ATP ratios. However, in contrast to mTOR, AMPK activity is increased during fuel deficiency and inhibited by leptin and nutrient signals. AMPK overexpression in the hypothalamus increases food intake and body weight, and its down-regulation inhibits feeding. Moreover, the activation of AMPK-dependent mechanisms leads to the inhibition of mTOR activity. Thus, AMPK and mTOR may have overlapping and reciprocal functions.

So, that’s your zen moment of the morning. Enjoy! :-)