a. Dissipative
Life Context

Author: Gianpiero Pescarmona
Date: 27/03/2007


Life on the earth

Atmospheric Oxygen pO2 Umidita' relativa
"3BMeteo: inquinante":
Oxygen Transport

Healthy Cells have high Acid Production

Atmosphere Evolution


life takes place only in environments with an excess of energy: in our case, in the sunlight. This concept includes the following facts:
• Cells have to feed continuously
• Cells have to breath continuously
• Cells cannot ever stop producing energy
• Cells use energy to keep many ionic gradients (Ca++, Na+, K+, Cl- etc.)
Gradients are necessary for most cell functions (signal transduction, glucose and AA transport, etc.)

Life soundtrack

Energy metabolism


CoQ10 Synthesis
Heme synthesis Heme degradation
Iron storage
Q10 and Lipoic

Heat production (UCPs)

Coenzyme Q and cholesterol

Serum cholesterol

More details about Mitochondria
What happens if respiratory chain rate is low?

Mitochondria in Neurodegeneration: Bioenergetic Function in Cell Life and Death 1999

More details on mitochondria

Heme synthesis

Role of VDAC

Ions asimmetry


Energetic Requirements for Ions asimmetry

ATP driven pumps

It is Na asimmetry driven by ATP powered pump?


Intracellular Protons Gradients

Mitochondrial proton gradient

Acid Vesicles

Protons (H+) driven Reactions



Sodium driven reactions

Clinical Applications

Post-herpetic Pain

Diabetes: insulin and ....

more details....

Regulation of the sodium/sulfate co-transporter by farnesoid X receptor alpha. 2007

2023-10-14T19:07:54 - Gianpiero Pescarmona


2023-10-14T19:07:36 - Gianpiero Pescarmona


2011-05-05T15:33:38 - Gianpiero Pescarmona

Gene expression centroids that link with low intrinsic aerobic exercise capacity and complex disease risk, 2010

  • A strong link exists between low aerobic exercise capacity and complex metabolic diseases. To probe this linkage, we utilized rat models of low and high intrinsic aerobic endurance running capacity that differ also in the risk for metabolic syndrome. We investigated in skeletal muscle gene-phenotype relationships that connect aerobic endurance capacity with metabolic disease risk factors. The study compared 12 high capacity runners (HCRs) and 12 low capacity runners (LCRs) from generation 18 of selection that differed by 615% for maximal treadmill endurance running capacity. On average, LCRs were heavier and had increased blood glucose, insulin, and triglycerides compared with HCRs. HCRs were higher for resting metabolic rate, voluntary activity, serum high density lipoproteins, muscle capillarity, and mitochondrial area. Bioinformatic analysis of skeletal muscle gene expression data revealed that many genes up-regulated in HCRs were related to oxidative energy metabolism. Seven mean mRNA expression centroids, including oxidative phosphorylation and fatty acid metabolism, correlated significantly with several exercise capacity and disease risk phenotypes. These expression-phenotype correlations, together with diminished skeletal muscle capillarity and mitochondrial area in LCR rats, support the general hypothesis that an inherited intrinsic aerobic capacity can underlie disease risks.
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