About that abstract.....

[Guest guest]

I forgot to actually bring up that abstract from that meeting, http://www.americanaging.org/2005/jones.pdf .

The actual protocol described features using monosodium-glutamate to "fry" the neurons in the brain that mediate the experience of hunger. Upon doing so, the investigators found that the hormonal changes seen under situations of "nutrient withdrawal" (caloric restriction) were attenuated.

If one accepts the notion that hormones are mediating much of calorie restriction's benefits, then this is a pretty important determination. If one tends to emphasize thermodynamic considerations when thinking about the benefits of calorie restriction, then perhaps it is entirely meaningless. I tend to lean towards the former, but goodness knows that there are plenty of folks that would bet the summer house that it is latter.

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FEBS Lett. 2004 Nov 19;577(3):357-60.

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Effect of IGF-1 on the balance between autophagy of dysfunctional mitochondria and apoptosis.Gu Y, Wang C, Cohen A.Division of Immunology and Allergy, Departments of Pediatrics and Immunology, Infection, Immunity, Injury and Repair Program, Research Institute, The University of Toronto, Ont., Canada M5G 1X8.Mutations in mitochondrial DNA (mtDNA) cause excessive production of mitochondrial reactive oxygen species (ROS) and shorten animal life span. We examined the mechanisms responsible for removal of mitochondria with deleterious mtDNA mutations by autophagy. Incubation of primary cells and cell lines in the absence of serum promotes autophagy of mitochondria with deleterious mtDNA

mutations but spares their normal counterparts. The effect of serum withdrawal on the autophagy of dysfunctional mitochondria is prevented by the addition of IGF-1. As a result of the elimination of mitochondria with deleterious mutations, excessive ROS production, characteristic of dysfunctional mitochondria, is greatly reduced. Mitochondrial autophagy shares a common mechanism with mitochondrial-induced cell apoptosis, including mitochondrial transition pore formation and increased ROS production.PMID: 15556609 [PubMed - indexed for MEDLINE]

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Mol Cell Neurosci. 2005 Jan;28(1):42-54.

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"Real-time whole cell fluorescence video microscopy was utilized to analyze mitochondrial inner membrane potential (Delta Psi(m)), which drives ATP synthesis, in cultured adult sensory neurons. These adult neurons do not require neurotrophic factors for survival. Insulin and other neurotrophic factors increased Delta Psi(m) 2-fold compared with control over a 6- to 24-h period (P < 0.05). Insulin modulated Delta Psi(m) by activation of the phosphoinositide 3-kinase (PI 3-K) pathway. Insulin also induced rapid and long-term (30 h) PI 3-K-dependent phosphorylation of Akt and cAMP response element binding protein (CREB). Additionally, insulin elevated the redox state of the mitochondrial NAD(P)H pool, increased hexokinase activity (first committed step of glycolysis), and raised ATP levels. This study demonstrates that insulin utilizes the PI 3-K/Akt pathway to augment ATP synthesis that we propose contributes to the

energy requirement for neurotrophic factor-driven axon regeneration."PMID: 15607940 [PubMed - indexed for MEDLINE]

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J Hypertens. 2005 Jul;23(7):1285-309.

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A forkhead in the road to longevity: the molecular basis of lifespan becomes clearer.

"FINDINGS: In diverse species transcription factors belonging to the forkhead/winged helix box gene, group O (FOXO) subfamily have been found to be crucial in downstream suppression of the life-shortening effects of insulin/insulin-like growth factor-I receptor signalling pathways that, when upregulated, accelerate ageing by suppression of FOXO." - PMID: 15942449

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstract & list_uids=15942449

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Mech Ageing Dev. 2005 May 7; [Epub ahead of print]

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Overview of caloric restriction and ageing.Masoro EJ.

"While the Reduction of Metabolic Rate Hypothesis is not supported by experimental findings, it nevertheless still has advocates. Currently, the most popular concept is the Oxidative Damage Attenuation Hypothesis; the results of several studies provide support for this hypothesis, while those of other studies do not. The Altered Glucose-Insulin System Hypothesis and the Alteration of the Growth Hormone-IGF-1 Axis Hypothesis have been gaining favor, and data have emerged that link these two hypotheses as one. Thus, it may now be more appropriate to refer to them as the Attenuation of Insulin-Like Signaling Hypothesis. Finally, the Hormesis Hypothesis may provide an overarching concept that embraces several of the other hypotheses as merely specific examples of hormetic processes. For example, the Oxidative Damage Attenuation Hypothesis probably addresses only one of likely many damaging processes that underlie aging. It is proposed that low-intensity

stressors, such as CR, activate ancient hormetic defense mechanisms in organisms ranging from yeast to mammals, defending them against a variety of adversities and, when long-term, retarding senescent processes."=-=-=-=-=-=

T. pct35768@...

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