Hunger itself regulates GI apoptosis through sympathetic nerves

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This study is fascinating, and I am not sure whether or not I believe it entirely, but there is a mechanism delineated in the full-text that makes some sense, especially in light of recent findings regarding adrenergic signalling and the regulation of forkhead transcription factors..... [ http://tinyurl.com/ck4o6 ]

In any case, the basic story is this. When you are hungry, apoptosis is reduced. When you are "full", apoptosis increases. Apply this logic to your stem cells, and you might have a bonafide "hunger slows aging" mechanism within arm's reach. However, things are not that simple, for instance, apoptosis is thought to be "enhanced" in caloric restriction, and this is part and parcel of the anti-cancer effect commonly ascribed to dietary interventions thought to forestall the aging process.

However..many have already discussed the vexing influence of the Sirtuins on p53 function, and the observation that sirtuin-mediated deacetylation of p53 negatively influences apoptosis has led some (including myself) to speculate that this represents a cellular version of "bracing against the drought".

I would take things a step further, and say that "frank starvation" (which I consider CR to be) is a pro-apoptotic influence, and there are cellular adaptations that occur to prevent the realization of apoptosis. In other words, p53 isn't killing the cells so much under starvation, but "something else" is. That "something else" is starvation-mediated "stress". In fact, the cells that are the "most troubled" will be culled at an accelerated clip under such conditions. This may represent a long-term "quality control" mechanism, where one uses starvation to cull the weak members from the pack, leaving cells that are indestructible.

In any case, my point is that the simple fact that hunger and satiety influence apoptosis in different ways leads one "once again" to the possibility that hunger itself is going to end up having some sort of significant influence on "aging" and "disease".

The "central mechanism" described in this paper invovles the sympathetic nervous system. Once again, the theme of "stressed for life" emerges..........maybe this activity has no influence on "aging", but it sure is "spooky" even if you try to disregard it.

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J Gastroenterol Hepatol. 2005 Aug;20(8):1285-91.

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Apoptosis in rat jejunal mucosa is regulated partly through the central nervous system, which controls feeding behavior.Lin T, Sakata H, Ootani A, Fujise T, Tsunada S, Amemori S, Danjo A, Yokoyama F, Sakata Y, Iwakiri R, Toda S, Fujimoto K.Department of Internal Medicine, Saga Medical School, Nabeshima, Saga, Japan."Abstract Aim: The aim of this study was to investigate whether central nervous system-related feeding behavior regulates mucosal apoptosis in rat small intestines.....The test solutions, which elicited feeding (0.24 and 24 micromol/rat of chlorpheniramine and 2-deoxy-D-glucose, respectively), suppressed mucosal apoptosis in the rat jejunum 1 h after cerebroventricular infusion. In

contrast, the test solutions, which suppressed feeding (8 and 24 micromol/rat of leptin and 1-deoxy-D-glucosamine, respectively), induced jejunal mucosal apoptosis 3 h after infusion. The effects of the test solutions on feeding behavior and changes in apoptosis were not affected by truncal vagotomy. Conclusion: The central nervous system, which regulates feeding behavior, might control intestinal function through the regulation of intestinal apoptosis."PMID: 16048579 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstract & list_uids=16048579

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Endocrinology. 2005 Jul 14; [Epub ahead of print]

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"In contrast, the alpha1-adrenergic receptor agonist, phenylephrine (50 microM), did not phosphorylate Akt and caused dephosphorylation of FOXO1 acutely and increased FOXO1 expression with chronic exposure. Phenylephrine, but not EGF, caused nuclear translocation of FOXO1, a response that is associated with dephosphorylation. " - PMID: 16020479

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Science. 2005 Jul 15;309(5733):481-4.

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"Accumulation of mtDNA mutations was not associated with increased markers of oxidative stress or a defect in cellular proliferation, but was correlated with the induction of apoptotic markers, particularly in tissues characterized by rapid cellular turnover. The levels of apoptotic markers were also found to increase during aging in normal mice. " - PMID: 16020738

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