e. Competitive
Life Context

Author: Gianpiero Pescarmona
Date: 27/03/2007


As biological systems tend to expand exponentially in a finite environment, they become - sooner or later - limited in their growth due to a shortage in some essential factor ("nutrient").
The competition for the limiting nutrient will locally drive the selection.

Concept of "essential" nutrient (Metal ions (Zn, Cu, Fe, Se), Inorganic phosphate, selected aminoacids, Vitamins (why eating vitamins is better than producing them by themselves)

Competition is an universal feature of living organisms at any scale (from microscopic to social scale) and for almost any nutrient

Competion take places between different agonists:

  • Between species (host/parasite)
  • Between members of the same species (war)
  • Between organelles (mitochondria, nucleus, cytoplasm, ribosomes)
  • Between parts of the same large cell (autophagy)
  • Between genes

Competition pattern for essential nutrients


Vitamin K

Host against Parasite

Vitamin K in humans is a cofactor of glutamic acid Carboxylases.
As Vitamin K is a respiratory pigment of many aerobial bacteria (it plays the role of Coenzyme Q in respiratory chain) its presence in blood is sign of an infection.
The Thrombin activation by Vitamin K therefore may be a anti infection mechanism, devoted to avoid spreading of the infection into the whole body.

Interaction between vitamin K nutriture and bacterial overgrowth in hypochlorhydria induced by omeprazole 1998

Parasite against Host

The Vitamin K-Dependent Carboxylase Has Been Acquired and Adapted by Leptospira Pathogens with a loss of function but still successfully competing with the host for Vit.K and leading to host depleton of Vit.K. Inhibition of host proteins carboxylation leads to haemorrage.
The Vitamin K-Dependent Carboxylase Has Been Acquired and Adapted by Leptospira Pathogens for a Role Other Than Protein Carboxylation 2005


Protein synthesis

N-Formylmethionine is a proteinogenic amino acid found in Bacteria and related Prokaryotic organelles. It is a derivative of the amino acid methionine in which a formyl group has been added to the amino group. It is specifically used for initiation of protein synthesis, and may be removed after.

fMet plays a crucial part in the protein synthesis of bacteria, mitochondria and chloroplasts. It is not used in cytosolic protein synthesis of eukaryotes, where eukaryotic nuclear genes are translated. It is also not used by Archaea. In the human body, fMet is recognized by the immune system as foreign material and stimulates the body to fight against potential infection.

A similar effect has N-Formylmethionine leucyl-phenylalanine


Visfatin - PBEF A New Natural Insulin-mimetic Adipokine

2007-05-07T16:02:44 - Gianpiero Pescarmona

A Role for Milk Proteins and their Peptides in Cancer Prevention.

Evidence of mitochondrial dysfunction in obese adolescents. 2009

Abstract Aim: Although obesity and weight gain generally are anticipated to be caused by an imbalance between energy intake and energy expenditure, the significance of thyroid hormones (TH) remains unclear. Examination of mitochondrial function may reflect intracellular thyroid hormone effect and elucidate whether a lower metabolic rate is present. Methods: In a group of 34 obese adolescents (age <16 years and body mass index above the age-related 95th percentile), and an age- and gender-matched group of 32 lean adolescent, thyroid stimulating hormone (TSH) and basal oxygen consumption were measured and mitochondrial function in peripheral blood monocytes was determined by flow cytometry. Results: Significant increase in TSH (3.06 +/- 1.56 mU/L vs. 2.33 +/- 0.91 mU/L, p < 0.05) and a decrease in VO (129 +/- 16 mL O(2)/m(2)*min vs. 146 +/- 15 mL O(2)/m(2)*min, p < 0.05) were observed in obese adolescents compared with lean adolescents. Flow cytometry analysis demonstrated a lower mitochondrial mass (6385 +/- 1962 a.u. vs. 7608 +/- 2328 a.u., p < 0.05) and mitochondrial membrane potential (11426 +/- 3861 a.u. vs. 14017 +/- 5536 a.u., p < 0.05) in obese adolescents compared with lean adolescents. These results are even more pronounced in adolescents with obese mothers. Conclusion: In obese adolescents, the increased TSH and lowered VO propose a lowered basal metabolic rate and the impaired mitochondrial function suggests a decreased thyroid hormone stimulation of mitochondrial energy production. The maternal in-heritage is suggestive of a basal metabolic defect or mitochondrial resistance for TH.

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