INT204332

Context Info Confidence 0.67 First Reported 2007 Last Reported 2008 Negated 0 Speculated 0 Reported most in Body Documents 7 Total Number 7 Disease Relevance 1.42 Pain Relevance 0.07

cytosol (PPARGC1A) mRNA processing (PPARGC1A) RNA binding (PPARGC1A) mitochondrion organization (PPARGC1A) nucleus (PPARGC1A) protein complex assembly (PPARGC1A)

Anatomy Link Frequency body 1 PPARGC1A (Homo sapiens)

Pain Link Frequency Relevance Heat Hippocampus 1 71.84 Intracerebroventricular 1 69.04 anesthesia 6 5.00 Bioavailability 5 5.00 cINOD 2 5.00 long-term potentiation 1 5.00 Inflammation 1 5.00 ischemia 1 5.00

Disease Link Frequency Relevance Heat Syndrome 2 99.36 Stress 62 98.00 Overweight 36 97.40 Aging 51 96.64 Alzheimer's Dementia 9 84.48 Obesity 67 78.60 Disease 43 74.20 Targeted Disruption 7 74.08 Apoptosis 6 70.92 Chronic Disease 12 66.00

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Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

Six months of caloric restriction caused an increase in the expression levels of TFAM and PPARGC1A and induced mitochondrial biogenesis.

Positive_regulation (increase) of PPARGC1A

1) Confidence 0.67 Published 2007 Journal PLoS Medicine Section Body Doc Link PMC1808482 Disease Relevance 0.31 Pain Relevance 0

The mammalian ortholog of Sir2, known as sirtuin 1 (SIRT1), deacetylates and activates PPARGC1A [11,14], suggesting a direct link between SIRT1 and mitochondrial bioenergetics.

Positive_regulation (activates) of PPARGC1A

2) Confidence 0.67 Published 2007 Journal PLoS Medicine Section Body Doc Link PMC1808482 Disease Relevance 0.19 Pain Relevance 0

In support of this concept, SIRT1 mRNA was increased in the CR and CREX groups in proportion to the increase in PPARGC1A mRNA, consistent with the potential role of SIRT1 as a direct regulator of PPARGC1A activity [11,14].

Positive_regulation (increase) of PPARGC1A

3) Confidence 0.67 Published 2007 Journal PLoS Medicine Section Body Doc Link PMC1808482 Disease Relevance 0.07 Pain Relevance 0

We show, to our knowledge for the first time, that in overweight nonobese humans, short-term caloric restriction lowers whole-body energy expenditure (metabolic adaptation), in parallel with an induction in mitochondrial biogenesis, PPARGC1A and SIRT1 mRNA, and a decrease in DNA damage.

Positive_regulation (induction) of PPARGC1A in body associated with overweight

4) Confidence 0.49 Published 2007 Journal PLoS Medicine Section Body Doc Link PMC1808482 Disease Relevance 0.18 Pain Relevance 0

In line with these studies, resveratrol appears to be protective against the dysregulation of energy homeostasis observed in mouse models for metabolic syndromes by a mechanism implicating the activation of SIRT1, PGC-1?

Positive_regulation (activation) of PGC associated with syndrome

5) Confidence 0.45 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2604890 Disease Relevance 0.45 Pain Relevance 0.07

Six months of caloric restriction caused an increase in the expression levels of TFAM (the principal transcription factor involved in regulating mtDNA transcription) and PPARGC1A (Figure 1A and 1B), suggesting an induction of mitochondrial biogenesis.

Positive_regulation (increase) of PPARGC1A

6) Confidence 0.45 Published 2007 Journal PLoS Medicine Section Body Doc Link PMC1808482 Disease Relevance 0 Pain Relevance 0

Participants in the CR and CREX groups had increased expression of genes encoding proteins involved in mitochondrial function such as PPARGC1A, TFAM, eNOS, SIRT1, and PARL (all, p < 0.05).

Positive_regulation (increased) of PPARGC1A

7) Confidence 0.20 Published 2007 Journal PLoS Medicine Section Abstract Doc Link PMC1808482 Disease Relevance 0.22 Pain Relevance 0

General Comments

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